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HYMS Block 9 > Viral, Fungal and Parasitic Infections > Flashcards

Viral, Fungal and Parasitic Infections Flashcards

1
Q

Describe the following viral shapes

  1. icosahedral
  2. helical/spherical
  3. enveloped
  4. complex
A
  1. outer shell is made from 20 flat sides. Structure of most viruses
  2. capsid is shaped into a rod. a central cavity that encloses its nucleic acid.
  3. capsid is encased in a baggy membran that can change shape
  4. capsid is neither purely helical or icosahedral. May possess extra structures
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2
Q
  1. What is the nucleocapsid?
  2. what is a virion?
  3. what is a naked virus?
  4. what are the consequences of being naked?
  5. what are the consequences of being enveloped.
  6. What are spikes? What are they involved in?
  7. Name the spikes found on the influenza virus
A
  1. genome contained within a protein capsule (capsid; comprisded of capsomeres)
  2. infective viral particle
  3. virus not contained within an envelope. Viral particle is nucelocapsid
  4. more stable in face of environmental stress; spreads more easily; survives gut
  5. must stay wet to remain infectious; v. sensitive to detergents
  6. protein/glycoprotein structures that often protrude from the surface of viral particles; involved in contact with host cell
  7. Haemagluttin receptor (H)
    Neuraminidase (N)
    both are susceptobnle to antigenic drift and shift, resulting in new strains; also implicated in effectiveness of vaccines
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3
Q
  1. Describe the infection process of a virus?
  2. which viruses replicate outside the nucleus?
  3. which viruses replicate within the nucleus?
  4. which viruses are released by budding?
  5. which viruses are released by cell lysis?
A
  1. attatchment → penetration → uncoating → replication → assembly → release
  2. RNA viruses
  3. retroviruses and DNA viruses
  4. RNA viruses and retroviruses
  5. DNA viruses
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4
Q
  1. name 3 effects of viral infection

2. name 6 clinical problems with viral infections

A
  1. Infection (lytic, latent, chronic); tumourigenesis; necrosis
2. few drugs available and drug resistance
high mutagenic rates
emerging infectious diseases
re-emerging infectious diseases
latent and persistent infection
public health issues
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5
Q

MODES OF VIRAL TRANSMISSION

  1. examples transmitted by droplets (2)
  2. examples transmitted by saliva (2)
  3. examples transmitted via mucosa (2)
  4. examples transmitted cutaneously (1)
  5. blood borne viruses (2_
  6. examples of congenital infections
  7. what are perinatal infections
  8. What are zoonoses?
  9. ingestion zoonoses
  10. animal bites
  11. arboviruses
A
  1. influenza, rhinovirus, RSV; rashes (measles, rubella, chicken pox)
  2. cytomegalovirus; epstein barr
  3. Herpes simplex; HIV
  4. HPV
  5. HIV; Hep B and C
  6. cytomegalovirus, rubella, varicella
  7. overlap with blood borne/mucosal viruses that are transmitted during birth
  8. viruses transmitted by animals
  9. Hepatitis E; hantaviruses; lassa
  10. rabies
  11. denuge fever, zika
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6
Q
  1. why are viruses difficult to treat?

Describe the MOA and give examples of the following:

  1. nucleoside reverse transcriptase inhibitors
  2. non nucleoside reverse transcriptase inhibitors
  3. DNA polymerase inhibitors
  4. Protease Inhibitors
  5. Neuraminisase Inhibitors
  6. Integrase Inhibitors
A
  1. because they subvert host machinery to replicate, therefore it is difficult to intervene without damaging the host. They are also very diverse.
  2. compete with endogenous triphosphate substrates in reverse transcriptase, so that viral RNA is not retrotranscribed to DNA
    e. g. zidovudine
  3. block the active site of reverse transcriptase; viral RNA is not retrotranscribed into DNA
    e. g. etravirine
  4. prevent the replication of viral RNA by mimicking nucleotides and acting as chain terminators
    e. g. aciclovir
  5. prevent cleavage of viral polypeptides during viral replication
    e. g. aprenavir
  6. neuraminidase is used by influenza virus to bud from the cell. These drugs inhibit this therefore prevent viral infection.
    e. g. tamiflu; zanamivir
  7. prevent integration of viral genome into host genome
    e. g. raltegravir
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7
Q
  1. which immune mediators are important in host immune response to viruses? (2)
  2. how are viral antigens presented?
  3. Which antibodies are implocated? How?
  4. How are interferons implicated in fighting viruses?
A
  1. cytokines and interferons
  2. viral antigens are presented by MHC I to CD8 T cells
  3. IgM - aggregation of viral antigens
    IgG - neutralisation of viral antigens; persist for immune memory
  4. stimulate production of host restriction factors; activate NK cells and macrophages; stimulate other cytokines
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8
Q

Name 3 ways in which viruses can evade the immune system

A
  1. subversion of the immune system by inhibiting synthesis or sequestering cytokines
  2. interfering with the surface protein markers in infected cells
  3. interfering with apoptotic pathway
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9
Q
  1. describe the structure of the HIV virion

2. which 3 proteins does the HIV virion contain?

A
  1. enveloped ssRNA virus. Envelope also has surface molecules such as gp120
  2. reverse trasncriptase, integrase, protease
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10
Q
  1. Describe how the HIV virus enters cells

2. Describe the HIV replication cycle

A
  1. gp120 on the viral envelope interracts with CD4 and then CCR5, both cell surface receptors on CD4 T cells.
    This interraction facilitates virus-lymphocyte fusion > the virus can then deliver its molecular package into the cell
  2. viral reverse transcriptase makes a DNA copy of viral RNA
    cDNA translocates to the nucleus
    viral integrase integrates viral DNA into the host genome
    viral DNA is transcribed into mRNA and translated to produce proteins
    viral particles then assemble in cytoplasm and released by budding as mature HIV virion
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11
Q
  1. How does HIV infection deplete CD4 cells?
  2. during primary infection, where does a large proportion of CD4 loss occur?
  3. what is responsible for the latency period?
  4. what CD4 count is associated with increased risk of opportunistic infection?
  5. name 4 opportunistic infections associated with HIV immunodeficiency
A
  1. Exhaustion > apoptosis
    chronic immune activation > bystander killing of non infected CD4 cells
  2. Gut associated lymphoid tissue
  3. CD8 cells are able to control the virus to some extent which drives down viral load
  4. <200
  5. Kaposi’s sarcoma, pneumocystis jjorveci pneumonia, toxoplasmosis, CMV retinitis
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12
Q
  1. what is pneumocystis jjroveci pneumonia caused by?

2. how is it treated?

A
  1. Pneumocystis jjroveci fungi - attacks interstitial fibrous tissue of lung
  2. Antibiotics (does not respond to antifungals) - trimethoprim-sulfamethoxazole
    steroids given as adjuctive therapy
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13
Q

Name the 6 classes of drug used to treat HIV

A 
NRTIs
NNRTIs
Protease Inhibitor
Boosting agent
CCR5 inhibitor
Integrase Inhibitor
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14
Q
  1. what is active immunisation?

2. What is passive immunisation?

A
  1. inducing a state of immunological readiness so that first infection with given pathogen is recognised as though it were a second infection by the same pathogen
  2. the transfer of preformed immunological mediators into a normal individual to generate a state of enhanced immunity
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15
Q
  1. what types of live vaccines are there? (2)

2. what types of non living vaccines are there? (3)

A 
1. naturally attenuated (e.g. using a related strain or species)
artificially attenuated (most)
  1. killed whole organisms (inactivated vaccines)
    antigenic components of the organism (subunit vaccines)
    DNA vaccines (not yet licenced)
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16
Q
  1. what type of virus is small pox?

2. why was small pox eradication possible through vaccination (5)

A
  1. dsDNA virus
  2. no subclinical infections - disease is obvious
    vaccine was highly effective at inducing sterile immunity
    no animal reservoir
    vaccination was coupled with active surveillance and containment
    there is only one serotype/strain
17
Q
  1. what type of virus is polio?
  2. describe how it replicates
  3. name and describe the disease it causes
  4. why is vaccination possible
  5. what form was the inactivated vaccine given?
  6. give 2 advantages and 2 disadvantages of the inactivated vaccine
  7. Give 2 advantages and 2 disadvantages of the live attenuated vaccine
A
  1. +ssRNA; icosahedral
  2. RNA acts as mRNA which is translated. RNA polymerase transcribes viral RNA into -ssRNA, which is used as a template for new +ssRNA
  3. pyelomyelitis - targets nerve cells leading to paralysis, including of respiratory muscles
  4. symptoms appear quickly
    no non primate reservoir
  5. sugar cube
    • safe for immunocompromosed individuals.
      + effective
      - infection of gut remains (nappies were infected)
      - higher community vaccination levels and booster vaccines required
    • induces immune resistance similar to natural infection
      + boosters not required
      - vaccine induced pyelomyelitis
      - unsafe for immunocompromised individuals
18
Q
  1. which vaccines are the gold standard and why?
  2. name 5 examples of live attenuated vaccines
  3. name 3 examples of inactivated whole organisms
  4. name an example of a subunit vaccine
  5. name considerations with the following vaccines:
    a) live attenuated vaccines
    b) inactivated whole organisms
    c) subunit vaccines
A
  1. live attenuated vaccines. they are more immunogenic
  2. Oral polio vaccine; BCG; MMR; yellow fever; varicella
  3. Rabies, Influenza, Hep A
  4. DTP

5a) can revert back to virulence
5b) can’t revert back to patogenic form; decreased immunogenicity
5c) may require adjuvants

19
Q

why are fungi and parasites harder to treat?

A

they are eukaryotic organisms therefore closer to humans on a cellular level. They are also more complex

20
Q
  1. what are saprophytes?
  2. are the majority of fungi obligate or opportunistic pathogens?
  3. which group of people are more prone to fungal infections?
  4. Why are fungal infections so rare despite fungi being ubiqutious (6)
A
  1. organisms which obtain nutrients directly from dead organic matter
  2. opportunistic (very few are pathogenic)
  3. immunocompromised
  4. not well adapted to growth at 37 degrees C
    enzymatic pathways function most efficiently at redox potentials found in non living substates
    poorly adapted to human nutrients
    host defence mechanisms are efficient at dealing with invading fungi
    slow growing
    do not need to infect humans as they are highly successful in the environment
21
Q
  1. are moulds unicellular or multicellular?
    2 how do moulds grow?
  2. in respect to moulds, what are mycelium?
  3. how do moulds reproduce?
  4. name a mould which causes infection?
  5. are yeasts unicellular or multicellular?
  6. how do yeasts reproduce?
  7. what is the shape of yeasts?
  8. name an important pathogenic yeast
  9. what are dimorphic fungi?
  10. name a pathogenic dimorphic fungi
A
  1. multicellular
  2. formation of fillaments - hyphae
  3. entangled mass of hyphae
  4. sexually and asexually
  5. aspergillus
  6. unicellular
  7. budding
  8. round
  9. candidia
  10. fungi that grow as yeasts or moulds
    - yeast form causes infection; mould form is saprophytic
  11. coccididomycoses
22
Q

1-3 name 3 reactions of tissue to fungal infections

  1. what are mycotoxins and what can they cause?
  2. name 2 examples of hypersensitivity reactions caused by fungi
A
  1. minimal tissue reaction (superficial skin infections)
  2. acute inflammation (mucosal fungal infections)
  3. granulomatous formation (deep subcutaneous and systemic infection)
  4. toxic substances caused by a fungus. can cause ergotism
  5. asthma; farmer’s lung
23
Q
  1. what are mycoses
  2. name an example of a superficial mycoses
  3. what are cutaneous mycoses?
  4. give an example of a cutaneous mycoses
  5. what do subcutaneous mycoses usually occur after?
  6. what do subcutaneous mycoses infect/involve?
A
  1. diseases caused by fungi
  2. tinia versicolour
  3. mycoses that extend deeper into the dermis; no tissue is invaded but a host response is elicited
  4. dermatophytosis - ring worm or tinea
  5. traumatic inocculation (piercing trauma which allows the fungi to enter)
  6. dermis, subcutaneous tissue, muscle and fasica
24
Q
  1. name the most common deep/systemic mycoses
  2. how does this infection occur? (route of inocculation)
  3. how can this infection become systemic?
  4. which fungi causes murmycoses
  5. which tissues does this fungi infect?
  6. how does this become systemic?
A
  1. aspergillus fumigatus
  2. inhalation of spores
  3. invasion of blood vessels; dissemination from lung
  4. mucorales
  5. sinuses, brain, lungs
  6. invasion of blood vessels, which results in formation of blood clots > hypoxia and necrosis
25
Q
  1. why are antofungal agents toxic?
  2. how do -azole antifungals work?
  3. name 2 examples of -azoles
  4. name 2 other examples of antifungal drugs
A
  1. because they cross react with human elements
  2. inhibit Ianosterol methylase, which interrupts ergosterol biosynthesis
  3. flucanozole; voriconazole
  4. amphoteraxin echinocandins
26
Q
  1. what are protazoa?
  2. what are helminths?
  3. what are arhtopods?
A
  1. unicellular eukaryotic organisms
  2. multicellular parasitic worms
  3. vertebrate with exoskeleton (e.g. insects)
27
Q

name pharmacological targets for:

  1. protazoa (4)
  2. helminths (3)
A
  1. nucleic acid synthesis; protein synthesis; metabolic pathways; detoxification mechanisms
  2. neuromuscular co-ordination; carbohydrate metabolism’ microtubular integrity
28
Q
  1. which parasites cause malaria?
  2. how are these parasites transmitted?
  3. describe the life cycle of the malaria parasite
  4. which stage parasites are responsible for the clinical manifestations of the disease?
A
  1. plasmodium - falciparum, vivax, ovale and malariae
  2. via the female anopheles mosquito
  3. 1) infected anopheles mosquito inoculates sporozoites into the human host
    2) sporozoites infect liver cells
    3) in the liver, sporozoites mature into schizoints, which rupture and release merozoites
    4) merozoites infect RNBCs and undergo asexual reproduction
    5) ring stage trophozoites mature into schizoints, which rupture and release merozoites
    6) some parasites differentiate into sexual gametocytes
    7) gametoxytes are ingested by anopheles mosquito during blood meal - generate zygites in stomach
    8) Male and female gametocytes fuse and form a fertilised motile zygote, which developer into new sporozoites and migrate to the insects salivary glands.
  4. blood
29
Q
  1. how is malaria diagnosed?
  2. describe clinical signs and symptoms of malaria
  3. what can severe malaria cause?
  4. what is cerebral malaria?
A
  1. blood film
  2. flu like symptoms with fluctuating fever
  3. cerebral malaria, acidosis and severe anaemia
  4. manifestation of severe malaria; unrousable coma; infected RBCs are sequestered in vasculature
30
Q
  1. name 2 classes of traditional antimalarials and their MOA

2. name a class of new antimalaria and how it works

A
  1. quinolones - block the parasitic detoxification of haem which is required for parasite survive
    antifolates - distupt parasitic folate metabolsim
  2. ARTEMISININ COMPOUNDS
    generate free radicals that alkylare and oxidise proteins and lipids within infected RBCs
31
Q
  1. What is the causative agent of African Typanosomiasis? (sleeping sickness?)
  2. how is it transmitted?
  3. describe symptoms
  4. What is the causative agent of South American Typanosomiasis (chagas disease?
  5. how is it transmitted?
  6. describe symptoms
A
  1. Typanosomabrucei rhodesiense
    Typanosomabrucei gambiense
  2. tsetse fly
  3. infects CNS causing neurological disturbacnes > coma > death
  4. typanosoma cruzi
  5. triatomine insects (infection via insect faeces)
  6. cardiac, digestice and neurological alterations
32
Q
  1. What causes leishmaniasis?
  2. how is it transmitted?
  3. what causes Toxoplasmosis?
  4. how is it transmitted?
  5. what group of people are particularly susceptible?
A
  1. Leishmania genus
  2. female phebotomise sandflies
  3. toxoplasma gondii
  4. ingestion of inadequately cooked meat, oocysts from cat faeces, maternal to child transmission
  5. immunocompromised; foetus
33
Q
  1. how do helminth infections usually occur?
  2. how is schistosomiasis transmitted?
  3. what are symptoms caused by?
  4. what is a pathogenic effect of lymphatic filariasis?
  5. what is a pathogenic effect of dracunculiasis?
A
  1. by larvae or eggs
  2. contaminated water
  3. body’s response to eggs
  4. blockage of lymphatic vessels
  5. causes pain as they move around, particularly through joints

HYMS Block 9 (9 decks)

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