viral and prion pathogens Flashcards

1
Q

what is a basic virus?

A

DNA coated in protein - capsid

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2
Q

what are viruses?

A

they are simple micro-organisms that cannot exist independently and need a host cell to survive. They steal the energy, metabolic intermediates and enzymes from the host to replicate

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3
Q

what is the envelope of viruses made of?

A

it is made of a lipid bilayer

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4
Q

what do viruses do when they enter a cell?

A

they remove their protein coat to replicate

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5
Q

what are examples of human DNA and RNA viruses?

A

DNA - adenovirus

RNA - rhabdovirus

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6
Q

what is the process of viral infections?

A
  1. adsorption - interaction between the host receptor molecule and the virus ligand
  2. penetration - through receptor mediate endocytosis or cell membrane fusion
  3. uncoating - nucleic acid is liberated from the phagosome and/ or the capsid but complex enzymatic process or receptor mediated process
  4. synthesis - nucleic acid and protein synthesis mediated by the host and or the virus enzymes. takes place in the cytoplasm or the nucleus
  5. assembly - assembly or viral components that is mediated by the host or viral enzymes
  6. release - complete virus particles are released by budding of host cell membrane or disintegration of host cell
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7
Q

how are viruses classified?

A

the presence or absence of an envelope or the genetic material inside them (DNA, RNA, single, double stranded, positive (5 to 3’) or negative sense)

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8
Q

how many human herpes viruses are they and what are they?

A
9 
1/2 - herpes simplex 1/2
3 - varicella zoster 
4 - epstein barr 
5 - cytomegalovirus 
human herpes virus 6A/B, 7 and 8
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9
Q

what are herpes viruses?

A

they are double stranded DNA enveloped viruses that are characterised by their ability to establish latency and then reactivate

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10
Q

what is herpes simplex 1?

A

it is characterised by a cold sore which is when inoculation starts. It is transmitted through direct contact with the fluid in the vesicles. it can result in genital and encephalitis which can be severe. Latency is established in the trigeminal nerve ganglia after the cold sore has healed with periodic reactivations

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11
Q

what characterises herpes 1?

A

there are vesicles or ulcers on skin or mucous membranes and encephalitis which is fatal or severe - commonest cause of viral encephalitis worldwide

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12
Q

what is the epidemiology of HSV1?

A

up to 80% of the UK population will experience in life time - seen globally, humans only known reservoir

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13
Q

what does HSV2 commonly cause?

A

genital herpes

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14
Q

what are the complications of HSV2 in pregnancy?

A

if there is an outbreak in the mother (worse if first time) then can cause severe illness to baby when giving birth - severe disseminated viralaemia - vertical transmission

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15
Q

what are the differences between HSV1 and 2?

A

lower proportion of HSV2 - 10-20% of population

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16
Q

what are the similarities between HSV1 and 2?

A

same latency mechanism and transmission mechanism and reactivate down a sensory nerve. can see same vesicles

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17
Q

what is the risk of genital herpes outbreaks?

A

can cause meningitis

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18
Q

what is the primary and secondary infection of varciella zoster?

A

primary - chicken pox - high proportion of the population have had by 20 y/o
secondary - shingles

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19
Q

what is the mode of transmission for VZV?

A

respiratory droplet transmission - highly infectious or direct contact from fluid in vesicles

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20
Q

where is latency established in VSV?

A

dorsal root ganglia of entire CNS and reactivates down sensory nerves (shingles in unilateral vesicles in dermatomal distribution)

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21
Q

what is the epidemiology?

A

higher prevalence in temperate climates,, this falls towards to equator

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22
Q

what is a common syndromic infection from epstein barr?

A

glandular fever and infectious mononucleosis

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23
Q

what is the epidemiology of epstein barr and what is the transmission?

A

95% infected by 25y/o and 50% by 5y/o

virus is shed in the saliva and through genital secretions

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24
Q

what are the symptoms ans signs of infectious mononucleosis?

A

tonsilitis, fever, hepatosplenomegaly and lymphadenopathy. On a blood film the lymphocytes are atypical and will look like a monocyte

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25
Q

how does reactivation occur?

A

through latency in B cells - if unwell or immunosupressed, and is associated with malignant B cell lymphoproliferative disorders

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26
Q

what is the prevalence of cytomegalovirus?

A

equal to the decade age

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27
Q

how is latency established in cytomegalovirus?

A

many cells of the immune system will establish latency in the myeloid progenitors, monocytes or dendritic cells

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28
Q

what happens when the mother has an infection of cytomegalo in pregnancy?

A

can be transmitted in utero - usually on primary infection

29
Q

how is CMV transmitted?

A

donated blood, stem cells or solid organs, saliva or genital secretions

30
Q

what are the important clinical syndromes of CMV?

A

infectious mononucleosis, reactivation in immunosupressed patients resulting in pneumonitis, retinitis or colitis and congenital CMV infection - retinitis, deafness, microcephaly, hepatosplenomegaly in neonate

31
Q

what are examples of respiratory viruses/

A

influenza, rhinovirus and syncytial respiratory virus

32
Q

what is rhinovirus/?

A

it is the common cold - worldwide distribution, epidemics in autumn, winter and spring

33
Q

what is the mode of transmission and important clinical syndromes for rhinovirus?

A

MOT: aerosolised respiratory droplets and secretions from nose and mouth, and common cold

34
Q

what is unusual about influenza?

A

infects humans and animals and can spread between species

35
Q

what is the epidemiology of influenza?

A

it peaks in winter anually, there are 3 distinct types - A, B and C
A mutates regularly - new strain every year

36
Q

what is on the surface of the influenza virus?

A

two important surface proteins - H and N with many variables (H3N2 is seasonal, H1N1 is swine)

37
Q

what are important clinical syndromes of influenza?

A

primary influenza illness - fever and myalgia and then headache, cough, sore throat and nasal discharge
post-influenza secondary bacterial lung infection with S. aureus etc

38
Q

what is the epidemiology for RSV?

A

worldwide and epidemics in winter - commonest in children - 70% infected and 30% have had in first year of life

39
Q

what is the important clinical syndrome of RSV?

A

bronchiolitis - children under 2y/o

inflammation of the smallest airways causing cough, wheeze, apnoea and hypoxia

40
Q

why is bronchiolitis not such an issue in adults?

A

we have larger airways so swelling is not such an issue

41
Q

what is the basis of HIV?

A

the CD4 cells are being destroyed but are regenerating in a cycle - eventually this will plummet - immunocompromised - loss of immune system main cause of death

42
Q

What is the epidemiology of HIV?

A

70% of global cases are in subsaharan africa

43
Q

what is the mode of transmission for HIV?

A

the virus is present in blood, genital secretions and breast milk, and can be passed through vertically, sexually or needlestick

44
Q

what is the clinical course of HIV?

A

the HIV targets T helper lymphocyte CD4 cells as part of cell mediated immune response. 2-6 week after transmission the patient develops an acute seroconversion illness and then an asymptomatic chronic infection follows

45
Q

what lasts for 5-15 years?

A

the steady state between the immune system and the virus

46
Q

what is AIDS?

A

when there is a rise in viral load and a fall in the patients CD4 count resulting in opportunistic infections - defining infections are Paoski’s sarcoma, pneumocystic pneumonia and cryptococcus meningitis

47
Q

many viruses can induce hepatitis as part of a wider clinical syndrome. What is hepatitis?

A

liver inflammation from 5 primary hepatotropic viruses

48
Q

what happens in hepatitis?

A

there is liver inflammation and death of hepatocytes

49
Q

how are the viruses transmitted?

A

D can only be present with B, A and E are usually fecal oral but there is increasing evidence that E can be transmitted through organ donation or through thyraemia. C and B are blood borne

50
Q

how is at risk in the fecal oral hepatitis viruses?

A

for A - lower socioeconomic groups

E - pregnant women

51
Q

what is the MOT for B?

A

sexual, parenteral - vertical

52
Q

what is the clinical course of B?

A

after transmission, an acute hepatitis may occur however 90% of children are asymptomatic and 50% of young adults are aswell. It is then cleared or becomes chronic.

53
Q

what is the relationship between chronicity and age in hep B?

A

chronicity and age of first infection are inversely related - 90% of perinatally acquired infection becomes chronic and less than 5% in adult infections

54
Q

what can chronic hepatitis cause?

A

cirrhosis and then hepatocellular carcinoma

55
Q

what are the symptoms of acute Hep B infection?

A

fever, myalgia and jaundice

56
Q

which is more prevalent B or C?

A

B - 250m worldwide compared to 170m in C

57
Q

which group in the UK population is at risk of hepatitis C (up to 50% showing evidence?)

A

people who inject drugs

58
Q

what is the most common MOT for hep C?

A

sharing needles, needlestick injury and transfusion on contaminated products

59
Q

of those who have the acute clinical hepatitis what percentage will develop chronic hep C?

A

85%

60
Q

what are GIT viruses?

A

norovirus, rotavirus and enteroviruses

61
Q

what is a point source?

A

for norovirus, it is a contained area with many people in - single source

62
Q

which GIT virus is a major cause of infant mortality in the developing world?

A

rotavirus

63
Q

immunity to what is short lived and what is this time?

A

norovirus and less than a year

64
Q

what is the MOT for rotavirus and norovirus?

A

inhalation of aerosolised vomit particles and ingestion for noro
for rota - fecal oral or inhalation or aerosolised vomit or faeces

65
Q

what are the dominant features in noro and rota?

A

noro - vomiting

rota - vomiting, fever and watery diarrhoea

66
Q

when do enteroviruses peak?

A

they have a worldwide distribution but in the UK peak in summer or autumn

67
Q

what is the course of enteroviruses?

A

they replicate in the gut but do not cause GI disturbances, from the gut they go to the lymph nodes and then the blood

68
Q

what are the important clinical syndrome in enteroviruses?

A

fever rash syndromes in children e.g. hand foot and mouth, viral meningitis, sever disseminated disease in neonate