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Year 2 - Clinical Pathology > Viral and Prion Pathogens > Flashcards

Viral and Prion Pathogens Flashcards

1
Q

what are viruses

A

simple micro-organism not capable of independent existence

require energy and enzymes from host

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2
Q

what are the 4 components that make up a virus

A

genome (RNA or DNA)
Capsid (protein coat)
envelope (lipid bilayer)
(some carry their own enzymes)

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3
Q

what is the 8 step life cycle of a virus

A 
attachment 
entry 
uncoating 
4-6 synthesis 
assembly 
release
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4
Q

what are the classifications of virus

A

genetic material - DNAvsRNA, single vs stranded
single, positive, negative

presence or absence of an envelope

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5
Q

what is the structure of the herpes virus and how many types are there

A

double stranded enveloped DNA virus

herpes simplex 1
herpes simplex 2
varicella zoster 
epstein barr
cytomegalovirus 
6a 
6b 
7 
8
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6
Q

what is the herpes virus characterised by

A

its ability to establish latency and reactivation

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7
Q

what is the difference between simplex 1 and simplex 2 of herpes

A

HSV-1 cold sores - leading cause of encephalitis, high mortality rates

HSV-2 - genital herpes which can be followed by meningitis

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8
Q

what is the exposure difference between HSV 1 and 2

A

1 about 80% have experienced

2 about 10-20 of population

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9
Q

what is the mode of transmission of herpes

A

direct skin, sexual contact, eye contact with fluid vesicle,

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10
Q

describe the latency in HSV-1 vs 2 in sensory neurones

A

1 - trigeminal nerve ganglion hence face outbreak

2 - sacral ganglia hence outbreak on pubis

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11
Q

what are the 4 clinical syndromes associated with herpes

A

ulcers to skin
encephalitis (HSV1)
meningitis (HSV2)
neonatal herpes - give to child which can cause sepsis of child

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12
Q

what is varicella zoster virus

A

type of herpes (3)

chicken pox is primary and reactivation is shingles or herpes zoster

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13
Q

what is the mode of transmission of varicella zoster virus

A

respiratory droplet from person with primary

vesicle fluid with primary or reactivation

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14
Q

what is the latency established by in varicella zoster

A

dorsal root ganglion across CNS as reactivates across the body

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15
Q

what are the clinical syndromes of varicella zoster

A

chicken pox - widespread rash - potential complications of pneumonia, encephalitis

shingles - reactivation causing unilateral vesicles in a dermatomal distribution

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16
Q

what is epstein barr known as

A 
herpes virus (4) 
glandular fever or infectious mononucleosis
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17
Q

what is the mode of transmission of EBV

what is it associated with

A

virus is shed in saliva and genial secretions (kissing disease)

associated with b cell malignancy (abnormal proliferation)

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18
Q

what are the two clinal syndromes associated with EBV

A

primary infection glandular fever - sore throat, fever, lymphadenopathy, atypical WBC’s - mononucleosis

reactivation - latency in B cells, risk for immunocompromised - lymphoproliferative disorder

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19
Q

what CMV and what is the mode of transmission

A

CMV - cytomegalovirus - herpes virus (5)

salvia or genital secretions
donated blood, stem cells or organs

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20
Q

what is the latency associated with in CMV

A

monocytes, dendritic cells and myeloid progenitors

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21
Q

what are the clinical manifestations of CMV

A

infectious mononucleosis

congenital CMV - produce babies with retinitis, deafness, microcephaly, cause distinct rash

immunosuppressed transplant recipients

people with advanced HIV - reactivation of latent CMV causing colitis

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22
Q

what is rhino virus - mode of transmission and clinical aspects

A

respiratory virus
common cold
aerosolised respiratory secretions and droplets from nose and eyes
symptoms - sneezing, nasal obstruction, sore throat, cough, headache, fever

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23
Q

what is respiratory syncytial virus, epidemiology, transmission and clinical aspects

A

RSV
comments in young children, mainly occurs in winter
aerosolised in respiratory secretions
bronchiolitis - affects children under 2 - inflammation of small airways - cough, wheeze, hypoxia and fever

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24
Q

what is the epidemiology of HIV and mode of transmission

A

36.7 mil global - 70% sub-saharan
about 0.25% of uk

virus present in blood, genital secretions
breast milk
ie transmitted vertically, sexually and needlestick

25
Q

what is the clinical course of HIV

A

targets helper T lymphocytes (CD4)
2-6 weeks after transmission patent develop acute seroconversion illness ie fever sore throat and lymphadenopathy

can have asymptomatic chronic infection

26
Q

when does HIV become AIDS and how can this be fatal

A

increase in viral load and fall in CD4 where patient can be killed by opportunistic infections: TB, pneumonia, meningitis, cerebral toxoplasmosis

27
Q

what are the 5 hepatitis viruses and what are the two classes they are split into

A

face-oral:
Hep A/E

Blood borne:
Hep B/C
Hep D but defective and can only survive with Hep B

28
Q

what is the epidemiology of Hep A compared to E

A

A: mainly children under 5 in endemic countries
E: mainly young adults, asia and africa
geno 1 and 2 = water
geno 3 associated with pigs and meat (pork)

29
Q

what is the mode of transmission of Hep A and Hep E

A

face-oral virus - virus shed in faeces of infected individual

30
Q

what are the clinical symptoms of hep A and E

A

nausea, myalgia, arthralgia, fevers

jaundice and right upper quadrant pain

31
Q

what are the symptomatic populations of hep A vs E

A

A: infection in children is sally asymptomatic but 50% adults show symptoms

E: majority asymptomatic and only show in 2-5%

32
Q

what are special considerations of Hep A and E

A

A: associated with lower socio-economic groups, returning tourists and MSM

E: high mortality in pregnant women (25%)
more severe in older males with liver disease

33
Q

what is the epidemiology and mode of transmission of Hep B

A

more than 500,000 deaths annually

vertical, sexual and parenteral transmission

34
Q

what is the clinical course of Hep B

A

acute clinical hepatitis
90% children and 50% young adults are asymp
Hep B is cleared or chronic
the older you are when you acquire it the less likely it will turn chronic
chronic hep = cirrhosis = heptocellular carcinoma

acute hep doesn’t cause long term damage

35
Q

what is the epidemiology and mode of transmission of Hep C

A

170 mil infected, causes highest % of carcinomas
low prevalence in developed countries

IVDU (drug users), needlestick injuries, transfusion
vertical and sexual transmission but less common

36
Q

what are the important clinical aspects of Hep C

A

after transmission about 25% develop acute clinal hepatitis

15% clear but most become chronic which then causes cirrhosis and hepatocellulr carcinoma

37
Q

what is norwalk virus

A

norovirus - ssRNA virus (positive sense singleton’s stranded)

38
Q

what is the epidemiology of norwalk virus and mode of transmission with its main clinical aspect

A

common - 90% infected at some point, short lived immunity less than a year and associated with point-source outbreaks

ingestion/inhalation of aerosolised vomit particles

vomiting is dominant feature

39
Q

what is rotavirus

A

dsRNA - looks like wheel on election microscope

40
Q

what is the epidemiology of rota virus and mode of transmission with its main clinical aspect

A

childhood virus 1-3 y/o
major cause of infant mortality in developing world

face-oral aerosolised in water and food

fever, vomiting, watery diarrhoea

41
Q

what are enteroviruses - give examples

A

more than 70 types
it replicate sin the GI tract but no GI symptoms

poliovirus, coxsackie A and B, enterovirus and echoviruses

42
Q

what is the epidemiology and mode of transmission of enteroviruses

A

worldwide, peak in sumer, 75% in 15 y/o or under, 90% asymp or mild symp

43
Q

what is the mode of transmission of enertoviruses and pathogenesis

A

energetic route, feaco-oral, contaminated food/water
replicate in GI but no GI symptoms
from gut to lymph nodes to blood - vireamia

44
Q

what are the clinical symptoms of enteroviruses and give specific examples

A

fever-rash, hand, foot, mouth, cold symps,
meningitis (most cases of men are caused by entero)
encephalitis

herpangina - Cox A
Pericarditis - Cox B

45
Q

what is the epidemiology and transmission of mumps

A

childhood infection peaking in winter

virus shed in saliva and respiratory secretions via droplet transmission

46
Q

what are the three clinical aspects associated with mumps

A

acute parotitis - inflammation of parotid glands

orchitis - inflammation of testicles (20-30% of males)

meningitis occurs in about 15% which can lead to deafness

47
Q

what is the epidemiology and mode of transmission of measles

A

occurs in unvaccinated children

droplet transmission, highly infectious (still present in environment after 2 hours)

48
Q

what are the 3 clinical aspects of measles

A

primary - fever, cough, conjunctivitis, kopliks spots on inside of cheek
maculopapular rash

acute post infection encephalitis 1:1000 - high mortality, immune mediated - 7-10 days after infection

subacute sclerosing pan-encephalitis - 7-10 years after infection, progressive and fatal

49
Q

what is the epidemiology of measles and mode of transmission

A

german measles - vaccinated but previously common

droplet transmission - respiratory

50
Q

what are the 3 clinical aspects of measles

A

primary postnatal rubella: mild illness, rash, fever, arthritis occurs in 30% adults

congenital rubella: triad: bilateral cataracts, sensorineural deafness and microcephaly (similar to CMV)

foetal malformation is highest in first 12 weeks preg

51
Q

what is parvovirus B19, epidemiology and mode of transmission

A

slapped cheek syndrome, fifth disease

later winter, early summer, 50% infected by 15, 90% by 90

droplet, respiratory

52
Q

what is the specific pathology of parvovirus B19

A

infects and destroys erythrocyte progenitors cells causing transient anaemia

53
Q

what are the clinical aspects of parvovirus B19

A

erythema infectosium - fever, fiery red rash on cheeks

transient aplastic crisis - affects those with high RBC turnover such as sickle cells
dyspnoea, confusion

infection in pregnancy - 7-10 % foetal loss, hydrops fettalis (severe fetal anaemia, ascites)

54
Q

what is a prion

A

small infectious pathogen containing protein but not nucleic acid

55
Q

where do we normally find prions

A

in natural cells, gene mutation leads to changes in folding pattern which becomes resistant to protease enzyme, accumulates and becomes pathogenic

56
Q

what are the two types of abnormal prions

A

inherited (genetic) or transmitted by infected meat/ material

57
Q

what properties are shared by human prion diseases

A

pathologic manifestations confined largely to CNS
produce spongiform change in brain tissue
long incubation times
progressive and fatal

58
Q

what is new variant CJD

A

nvCJD - sopradic cruz felt jacobs disease - rare, 1 in mil

progressive ataxia, depression dementia and death

59
Q

what is nvCJD linked to

A

BSE - bovine spongiform encephalopathy - same structure prion - consumption of infected beef

Year 2 - Clinical Pathology (67 decks)

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