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Case 16 > Theme 3: Infectious disease > Flashcards

Theme 3: Infectious disease Flashcards

1
Q

how is measles transmitted?

A

respiratory route- contact with infectious secretions
extremely contagious- R- approx. 18
infectious from 4 days before rash till 4 days after it disappears

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2
Q

what are the clinical features of measles infection?

A

incubation period- 10-12 days
prodromal phase- 2-4 days- high fever (39-40), rhinorrhoea, cough, malaise, conjunctivitis, diarrhoea, kolpiks spots (small red spots with white centre on buccal mucosa- pathognomic to measles)
rash- 4-10 days- morbilliform (measles like), erythamtous, maculopapular (flat, raised), appears first on face (behind ears), forehead, neck, trunk, limbs, hands feet last

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3
Q

what are the complications of measles infection?

A

susceptible to opportiuistic infection- diarrhoea, otitis media, pneumonia
CNS- encephalitis, blindness, subacute sclerosis panencephalitis
death

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4
Q

what are the clinical features of rubella?

A

transmission- respiratory route, infectious for 1 week before symptoms till 4 days after rash diappears
usually mild disease- lymphadenopathy, maculopapular rash
complications in pregnancy- congenital rubella syndrome

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5
Q

what are the clinical features of mumps?

A

transmission- respiratory route, infectious 6 days before symptoms till 4 days after
symptoms- fever, parotitis (inflammation of parotid glands)
complications- swollen testicles, viral meningitis, encephalitis

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6
Q

how can measles, mumps and rubella be prevented?

A

MMR vaccine

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7
Q

what are the principles of vaccines?

A

vaccines are biological preparations which improves immunity to a particular disease by triggering an immune response.
B- cell response- produces antibodies against the antigen and produce memory cells>
T cell response- kills infected cells, helps with B cell response and produces memory T cells- generally only induced by live vaccines

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8
Q

what are the types of vaccine available?

A

inactivated vaccines- killed bacteria/virus, viral sub-unit, peptide or polysaccharide, inactivated toxin, viral like peptide or RNA vaccines
live vaccines- mostly attenuated or can be virulent

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9
Q

what are adjuvants?

A

substances used in combination with a specific antigen in a vaccine to produce a more robust immune response.
used in weakly immunogenic vaccines

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10
Q

what is the rationale behind vaccine programmes?

A

they can save millions of pounds in healthcare costs

successful vaccination programmes help protect each vaccinated person and provides herd immunity

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11
Q

what are the stages of the virus life cycle?

A
  1. attachment
  2. entry
  3. replication and protein synthesis
  4. assembly
  5. release
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12
Q

what are the routes of transmission?

A

respiratory- rhinovirus, influenza, COVID-19, chickenpox, smallpox
faecal-oral- picornaviruses (poliovirus, hep A), norovirus
sexual- HIV, HPV, HSV
mechanical- parenteral: IVD, blood transfusion, biting insects
vertical- moter to foetus- HIV, rubella
conjunctiva

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13
Q

what is pathogenicity?

A

pathogenicity is the severity of the disease a virus causes

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14
Q

what are pathogenicity factors?

A

a pathogenic virus must be able to enter the host, replicate, evade the immune system, dissemination, further replication and shed (spread )

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15
Q

how do generalised infections disseminate?

A

virus infects epithelial surface and replicates
spreads to regional lymph nodes and enters blood (primary viraemia)
virus enters tissues (liver, spleen, bone marrow) and replicates further
virus reenters bloodstream,(secondary viraemia)
multiplication and shedding from target organ

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16
Q

what is the definition of incubation period?

A

the the time between viral exposure and onset of illness (symptoms becoming apparent)

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17
Q

what is reproduction number R0?

A

the number of subsequent infections in a susceptible population caused by a viral illness in one individual during its infective period

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18
Q

what are the general patterns of viral disease?

A

acute infections- normally short lived and self limiting e.g. common cold, flu
subclinical infections- no signs or symptoms e.g. polio- 99% asymptomatic
persistent and chronic- acute or subclinical infections that are non terminated by an immune response
latent infections- acute infection followed by a persistent latent infection, virus becomes dormant in cells. chicken pox, HSV
slowly progressive disease- virus replicates at normal rate but disease takes many years to manifest.

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19
Q

what are the antivirals used in hepatitis B and C?

A
  1. HCV- antivirals used in chronic disease
    weekly pegylated interferon A- establishes non-specific antiviral state in infected cells, enhances host immune response
    ribavirin- stops viral RNA synthesis
  2. HBV- antivirals only used in chronic cases
    pegylated interferon A
    oral antivirals- tenofavir and entecavir- inhibits HBV DNA polymerase
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20
Q

what are the antivirals used in HPV?

A

lopinavir- reduces HPV precancerous lesions

cidofavir- inhibits HPV DNA polymerase

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21
Q

what are the antivirals used in herpesviruses?

A

aciclovir- given in unmodified form- activated by viral enzyme (thymidine kinase), activated drug inhibits viral polymerase
valaciclovir- prodrug of aciclovir, better oral bioavailability, converted to acyclovir in gut

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22
Q

what is the mechanism of action of ganciclovir?

A

inhibits viral DNA polymerase

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23
Q

what antivirals are used to treat influenza?

A 
only treated if in at risk group 
oral oseltamivir (tamiflu)- neuraminidase inhibitor/ prevents newly formed virions from leaving the cell
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24
Q

what are health protection teams responsible for?

A

local disease surveillance
maintaining alert systems
investigating and managing heath protection incidents and outbreaks
implementing and monitoring national action plans for infectious diseases at local level

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25
Q

how can notifiable diseases be reported to PHE?

A

complete a notification form immediately on diagnosis of a suspected notifiable disease. don’t wait for laboratory confirmation before notification

26
Q

what strategies are used in the prevention and control of viral infections?

A

vaccination
quarantine/isolation of infected individuals
hygiene and sanitation
vector control for arboviruses/ insect repellent
lifestyle changes- STI
postexposure prophylaxis
pre-exposure prophylaxis

27
Q

what are the common structural features of herpes viruses?

A

viral genome- DS DNA genome
spherical capsid
tegument
envelope- deprived from host cell

28
Q

what is the lifecycle of herpes viruses?

A
  1. primary infection-
  2. latency- viral DNA persists in specific cell types, no replication
  3. reactivation- virus reactivates intermittently, actively replicates, can be symptomatic or asymptotic
29
Q

what is the difference between primary and initial infection with herpes simplex virus?

A

primary infection- first infection with HSV1 or HSV2

initial infection- first infection with HSV1 OR HSV2 in a patient who has already been infected with the other HSV

30
Q

what is the pathogenesis of HSV?

A

virus infects epithelial cells and undergoes lytic replication (causes cell destruction) leading to the vesicular rash. visions are shed and infect sensory neurones and travel up spiralganglions to the nerve cell bodies where they enter a latent state. the virus reactivates periodically and replicates, travel down spiral ganglions and re-infect epithelial cells starting the process again.

31
Q

what are the clinical features if HSV1 and HSV2 infection?

A

primary oral heprpes- usually HSV1, usually asymptomatic, may get initial prodrome or cold sores which last 10-14, can present with gingivomatitis in children
reactivation of oral herpes- almost always HSV1, normally asymptomatic or cold sores
genital herpes- usually HSV2, primary infection usually more severe (fever, malaise, dysuria, discharge, small blisters), can be asymptomatic

32
Q

how is HSV diagnosed and managed?

A

diagnosis- normally by detection of viral DNA by PCR, sample taken by swab, CSF or blood or histology
management- supportive care (analgesia, fluids), or antivirals (acyclovir, valaciclovir) oral or topical

33
Q

what is the pathogenesis of varicella zoster virus?

A

infection via respiratory mucosa/ conjunctiva, replication in regional lymph node, primary viraemia, replication in liver and spleen, secondary viraemia, dissemination to skin (chickenpox rash), latency in dorsal root ganglion, reactivation= zoster (shingles)

34
Q

when is varicella infectious?

A

2 days before rash till rash has fully crusted over (5 days after onset)

35
Q

what are the clinical characteristics of chicken pox and shingles?

A

chicken pox- prodrome (fever, malaise, headaches, fussiness, loss of appetite), rash (starts as macules, papules, vesicles, pustules), very itchy
shingles- prodrome (abnormal sensation in skin- tingling, burning, pain) rash (dermatomal, never crosses midline, vesicular)

36
Q

how is chickenpox and shingles managed?

A

chickenpox- children rarely need treatmentt, sometimes symptomatic relief (calamine lotion, antihistamine), adult - antivirals (aciclovir, valaciclovir) and close monitoring, may need hospitalisation if complicated/ pregnant
shingles- antivirals, pain relief

37
Q

how is varicella and zoster prevented?

A

there is a varicella vaccine- live attenuated not given routinely in UK, only given to susceptible healthcare workers and susceptible contacts of immunocompromised children
zoster vaccine- live attenuated, higher conc. of VZV compared to varicella vaccine, boosts immune system to prevent shingles, reduce severity and prevent post herpetic neuralgia (pain after shingles)

38
Q

what are the clinical features of otitis external?

A

red swollen ear canal and/ or external ear
can have discharge and inflamed ear drum
itchy and painful ear, tenderness when moving jaw
can be acute or chronic (>3weeks)
can be localised (folliculitis), diffuse (skin and subdermis), malignant (rare, invasive, destructive, seen in diabetics), fungal (spores seen in ear)

39
Q

what are the common causes and treatment of otitis externa?

A

localised acute OE- staph aureus
acute diffuse- staph aureus and psuedomonas aeruginosa
malignant- polymicrobiology
fungal- aspergillus, Candida albicans
treatment:
localised/diffuse- treatment rarely required, flucloxacilin if antibiotic given
chronic fungal OE- clotrimazole solution, acetic acid spray

40
Q

what are the clinical characteristics of acute otitis media?

A

can be with or with our effusion

rapid onset of symptoms- ear pain, dulled hearing, fever, irritable baby, perforation of ear drum

41
Q

what are the common causes and management of acute otitis media?

A

bacterial- strep. pyogenes, moraxella catarhallis, strep. Pneumoniae, haemopilis influenzae
viral- respiratory syncytial virus (RSV), rhinovirus, adenovirus, infulenza
management- if systemically unwell 5-7 days of amoxicillin, hospitalisation in symptoms worsen

42
Q

what is otitis media with effusion?

A

glue ear
similar to AOM but no acute infection
low grade chronic bacterial or viral infection
generally resolves in 6-10 weeks

43
Q

what is vestibular neuritis/labrynthitis?

A

inner ear infection
sudden onset of symptoms- vertigo, nausea/vomiting
usually viral after an URTI
bacterial more severe

44
Q

what is sinusitis?

A

inflammation of the paranasal sinuses
usually resolves within 10 weeks (chronic >10 weeks)
acute sinusitis is normally caused by viral URTI (rhinovirus, RSV, influenza)can be followed by bacterial infection (strep. pneumoniae, haemopillius influenzae, maraxella catarhalis)- anitbiotic if high risk (phenoxymethyl penecilin)

45
Q

what are the common causes of sore throat?

A

virus (most common)- rhinovirus, coronavirus, parainfluenza, influenza A/B
bacteria- group A betahaemolytic strep

46
Q

what is a Quincy?

A

peritonsilar abbess commonly caused by strep. pyogenes, staph aureus, haemophiliac influenzae
requires ENT referral and drainage

47
Q

what is epiglottitis?

A

inflammation of the epiglottis
symptoms of sore throat but rare
stridor in children- emergency
main causes B-haemolytic strep, staph. aureus, strep. pneumoniae

48
Q

what are the symptoms of meningitis?

A

rapid onset
fever, headache, stiff neck, rigid back, building fontanelle (infants), photophobia, altered mental state, unconcious, seizures, non-blanching rash

49
Q

what are the major classes of bacteria causing CNS infection?

A

Meningococcal disease- can cause meningitis and sepsis, peticheal rash highly suggestive of meningococcal disease. caused by- neisseria meningitidis (common serotypes A, B, C and Y, W on rise)
pneumococcal disease- can cause meningitis and pneumonia. rash not common. cause- strep pneumoniae
group B streptococci- most common cause of meningitis in newborns

50
Q

what is the treatment of bacterial meningitis?

A

meningococcal- benzylpenicilin/ cefotaxime
pneumococcal- cefotaxime
haemophilus influenzae B- cefotaxime

51
Q

what is the causative agent of lyme disease and how is it transmitted?

A

borrelia burgdorferi

deer/sheep ticks

52
Q

what are the clinical features of stage 1 and 2 Lyme disease?

A

stage 1- early, localisednLyme disease, erythema migrans-circular bullseye rash at site of tick bite within 3-36 days
stage 2- disseminated Lyme disease- flu like illness, neurological disorders, unilateral/bilateral facial nerve palsies, meningism/ meningitis, mild encephalitis

53
Q

what are the causes and treatement of viral meningitis?

A

most common cause non-polio enteroviruses (coxsackie, echovirus)
other causes- herpesviruses, HIV, EBV
treatment- generally milder than bacterial and self limiting- should be treated as bacterial until confirmed.
generally supportive, acyclovir for herpes infection

54
Q

what are the causes of viral encephalitis?

A

HSV1 (2), VZV, enteroviruses, EBV, CMV measles, mumps

55
Q

what are the features of herpes simplex encephalitis?

A

most commonly HSV1 in children and adults, HSV2 most common in neonates
symptoms- altered conciseness, focal and generalised seizures, raised intracranial pressure (papilloedema), focal neurological signs, psychiatric symptoms
if untreated HSE is progressive and often fatal
treatment- IV acyclovir for 10 to 21 days

56
Q

what are the clinical characteristics of rabies infection?

A

incubation- 3-12 weeks
prodromal stage- virus enters CNS, non-specific symptoms, 2-10 days
disease- 2 forms: furious rabies (80%)- aggressive, muscle spasms, hallucinations, seizures.
paralytic, ‘dumb’, apathetic rabies- muscle weakness, paralysis, bladder dysfunction
almost all who develop symptoms die

57
Q

what is the blood brain barrier and its function?

A

the blood brain barrier is a layer of endothelial cells surrounding the blood vessels in the brain which are linked together by tight junctions which provide a physical barrier preventing unwanted substances passing through. there is a second layer of protection made up of glial cells called astrocytes which have specific transporters so only allow specific nutrients into the brain.
the blood brain barrier keeps out pathogens, unwanted chemicals and immune cells from passing into the brain

58
Q

where is CSF produced?

A

the ependymal cells which line the ventricles and form the choroid plexus

59
Q

describe the flow of CSF

A

CSF is produced in the enclosed spaces of the ventricles which produces a small amount of pressure. this pressure forces CSF to move from the lateral ventricles through the interventricular foramen into the third ventricle. it then moves down the cerebral aqueduct to the fourth ventricle. the CSF flows out into the cisterna magna through the lateral apertures (of luschka) and median aperture (of sylvius). from here is moves across the whole outer surface of the brain. it also flows down the central canal of the spinal cord to surround the spinal cord tissue. CSF is removed by flowing into the blood stream through the arachnoid granulations of the meninges.

60
Q

what is the role of CSF?

A

allows brain to float and reduces traction on nerves and blood vessels connected to the brain.
protection- cushioning
removes waste metabolites
provides a stable ionic envrionemtn for the CNS

61
Q

what is the role of lumbar puncture?

A

abnormal levels of proteins, nutrients, waste products, electrolytes etc. in the CSF could be indicative of disease
may be used as an early diagnostic tool for neurodegenerative diseases (Alzheimers, Parkinson’s)
used to diagnose CNS infections such as meningitis and encephalitis- cloudy CSF with low glucose, high protein and high WCC is indicative of bacterial meningitis

Case 16 (3 decks)

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