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1. INFECTIONS > judith (L26) > Flashcards

judith (L26) Flashcards

1
Q

How do you diagnose viral infections?

A

Clinical history and examination

Detection of the virus
Live virus, viral particles, viral antigens or nucleic acid

Detection of the body’s response to infection
Usually virus specific antibodies

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2
Q

Principle of immunofluorescence

A

Look for viral antigens expressed in infected cells.
Fix infected cells to slide.
Add virus-specific antibody eg mouse anti-HSV.
Incubate.

Wash.
Add ‘tagged’ anti-antibody eg rabbit anti- mouse with fluorescent label.
Incubate.

Wash.
Visualise under UV light.
Look for apple-green fluoresence.

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3
Q

diagnosis of virus infections

A

Antigen detection (by immunofluorescence)
Virus isolation (attempt to grow virus in cell culture, can be followed by antigen detection for typing and confirmation)
Direct visualisation of virus particles (electron microscopy)
Genome detection
Virus-specific antibodies

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4
Q

define genome detection

A

Usually involves genome amplification
eg polymerase chain reaction assay (PCR)
Highly sensitive assays
For HSV assays can be type-specific eg by using type-specific probes or melting curve analysis
Can be made quantitative ie how much virus is there?
eg monitoring of HIV viral load in response to therapy

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5
Q

examples of virus-specific antibodies

A

Virus specific antibodies ie serology
eg IgG or IgM antibodies to HSV
or type-specific antibodies to HSV-1 or HSV-2

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6
Q

types of HSV infection

A 
Primary (first encounter with HSV)
Initial or 1st episode (first encounter with ‘the other’ virus)
Reactivation of either virus
Endogenous reinfection (another site)
Exogenous reinfection (another strain)

Recurrent oral-labial herpes simplex virus-1 infection
Neonatal HSV
Eczema herpeticum
HSV encephalitis

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7
Q

complications

A

VZV pneumonia
recurrent infection - herpes zoster or shingles
sight threats - Opthalmic zoster
( worse if immunocompromised )

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8
Q

VZV - therapy with aciclovir

A

Chicken-pox

  • Adults, including pregnant women
  • Complications eg pneumonia
  • Immunocompromised child

Shingles

  • Early treatment can reduce post herpetic neuralgia
  • Ophthalmic
  • Immunocompromised patient
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9
Q

causes of viral gastroenteritis

A

Rotaviruses (Reoviridae)
Enteric adenoviruses (group F Adenoviridae)
Noroviruses and Sapoviruses (Caliciviridae)
Astroviruses (Astroviridae)

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10
Q

diagnosis methods

A

Antigen detection
- ELISA for rotavirus and enteric adenoviruses.

Genome detection
- eg norovirus - most sensitive & specific

Electron microscopy
- now rarely used - slow, expensive, need 106 particles/ml.

Serology and virus isolation not used

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11
Q

MERS-CoV in what countries

A

Countries in or near the Arabian Peninsula with Cases
Saudi Arabia, United Arab Emirates (UAE), Qatar, Oman, Jordan, Kuwait, Yemen, Lebanon, Iran.

Countries with Travel-associated Cases
United Kingdom (UK), France, Tunisia, Italy, Malaysia, Philippines, Greece, Egypt, United States of America (USA), Netherlands, Algeria, Austria, Turkey, Germany, Republic of Korea, China, Thailand.
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12
Q

MERS-CoV

A

First identified September 2012 in a Qatari man who had recently travelled to Saudi Arabia.
Once sequence known a diagnostic PCR could be developed.
The nearest relatives are bat coronaviruses.
Camels have a high prevalence of MERS-CoV infection – not just camels across the Arabian Peninsula.
All known viruses are closely related, belong to the same serotype and all may originally stem from Africa.

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13
Q

ways in which one may acquire a zoonotic MERS-CoV infection

A

from an actively infected camel

  • Camel calves excrete the virus at higher concentrations than adult camels.
  • Detectable levels of antibodies do not prevent reinfection of adult camels.

camels are infectious (by sneezing on you, drinking their milk, cleaning after them)
if it is unwell, it is taken somewhere to take care of it but could spread

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14
Q

diagnosis of viral respiratory tract infection

A

Rapid tests for viral antigen (RSV and Flu A) - less sensitive than PCR.
Immunfluoresence.
Virus isolation – slow, now rarely used outside reference laboratories.
PCR - increasingly used but expensive
Serology – complement fixation tests – retrospective diagnosis.

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15
Q

respiratory PCR panel

A 
Influenza A
Influenza B
RSV A & B
HMPV A & B
Parainfluenza virus 1-4
Adenovirus
Rhino/enteroviruses
Bocavirus
Coronaviruses 229E, NL63, OC43, HKU1 (not MERS-CoV)
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16
Q

influenza vaccine efficacy

A

Efficacy in adults last winter was extremely low, particularly in the elderly, due to a combination of factors:
- Poor response to H3N2 component of the vaccine
More flu B – not covered by trivalent vaccine

For this season:
- adjuvanted trivalent vaccince for ≥ 65 and quadrivalent vaccine for other at risk groups.

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17
Q

who is offered flu vaccine?

A

Health and social care workers – to protect themselves, their patients and colleagues
Chronic neurological, hepatic, renal, pulmonary and chronic cardiac disease
Diabetes mellitus
Severe immunosuppression because of disease or treatment
HIV infection – regardless of immune status
Age over 65 years
Residents of residential or nursing homes
Carers
Household contacts of immunosuppressed patients
Pregnant women
Young children – live vaccine programme

Morbid obesity (BMI ≥40) not on list despite being high risk for complicated influenza
Outside this list vaccination available but not free
18
Q

complications of EBV infection - acute infection and long term

A

Acute infection

  • Respiratory obstruction
  • Hepatitis – don’t drink alcohol
  • Rupture of spleen – avoid contact sports

Long term - association with various malignancies because EBV can ‘transform’ cells

  • Burkitt’s lymphoma
  • Nasopharyngeal carcinoma
  • Hodgkins disease
  • Lymphomas in AIDS and transplant patients
19
Q

viral hepatitis

A

Acute hepatitis

  • Hepatitis A, B, E (rarely C or D)
  • Herpes viruses - EBV and CMV
  • Yellow Fever
20
Q

hepatitis A virus

A

Faecal-oral route of transmission

  • Entry via contaminated food or water
  • Excreted in faeces
21
Q

hepatitis E virus

A

Incubation period – range 15-60 days (average 40 days).

Symptomatic infections are rare, < 1% & the disease is usually mild. Uncertain whether infection confers lifelong immunity.

Infections during pregnancy are associated with 30% mortality rate in mothers & poor neonatal outcome. This is seen in hyperendemic areas where G1 viruses circulate.

Infection in patients with pre-existing chronic liver disease is associated with a 70% mortality rate. Alcohol consumption is an important risk factor.

22
Q

epidemiology

A

HEV infection & the disease it causes, hepatitis E, are found worldwide.

HEV is a family of ≥ four closely related viruses referred to as genotypes 1 to 4 (G1-4) each with distinct host preferences & patterns of illness.

HEV is hyper-endemic through much of the developing world where sanitation & food hygiene may be poor.

Infections in the developing world are usually linked to G1 (South Asia, Middle East and Africa) and G2 viruses (Mexico).

In these countries HEV causes sporadic cases of hepatitis but also large water-borne outbreaks associated with faecal contamination of water.

23
Q

HBV modes of transmission

A

Sexual
Vertical transmission - mother to child
Parenteral - unsafe injections and transfusion
NB Largely preventable by vaccination

24
Q

natural history of HBV infection - adults

A

Acute infection

  • subclinical infection
  • acute hepatitis with jaundice
  • fulminant hepatitis (1%) – may die or survive by Tx
  • chronic infection (10%)

Chronic infection

  • healthy carrier
  • chronic hepatitis
  • cirrhosis
  • hepatocellular carcinoma
25
Q

Diagnosis of HBV infection

A

Clinical

  • History of exposure
  • Signs & symptoms

Serology

  • Viral antigens (HBsAg, eAg)
  • Antibodies (anti-HBc, anti-Hbe, antiHBs)

Genome detection
- HBV DNA

26
Q

treatment of HBV infection

A
  • Interferon
  • Nucleoside analogues - use HBV DNA to monitor response
  • Liver transplant
27
Q

outcome of HCV infection

A

25% spontaneous clearance

75% chronic infection
80% asymptomatic
20% cirrhosis
1-2% hepatocellular carcinoma

Progression to cirrhosis or cancer takes decades

28
Q

HCV diagnosis

A

Relative few diagnosed in acute phase as symptoms often absent
or minimal

Detection of anti-HCV - marker of infection at some time

Detection of HCV antigens - marker of current infection

Detection of HCV RNA - marker of current infection

What do we do?
Test for antibodies to HCV
If positive ‘reflex test’ for HCV RNA

Result reporting
‘HCV RNA detected – evidence of current HCV infection;
Please refer to a hepatologist.’

29
Q

treatment of HCV

A

Interferon and ribavirin were mainstay of treatment for
many years – but unpleasant drugs with limited efficacy.

New direct-acting antivirals are now available - these are very much more effective and length of treatment is shorter – restrictions due to high costs are gradually being eased.

So many drugs in the pipeline that drug companies regard HCV as ‘cured’ & are focusing on HBV.

Liver transplantation

30
Q

testing strategy for acute hepatitis

A

History (unsafe sex, sharing needles, travel etc) & examination (lymphadenopathy) may (or may not) suggest a specific viral aetiology but laboratory testing is required for confirmation.

Epidemiology of viral infections has changed – sanitation, vaccination, infection control practices.

This has necessitated review of the testing protocol.

More testing for hepatitis E, less testing for hepatitis A.

31
Q

diagnosis of meningitis

A

Bacterial meningitis likely if:

  • CSF glucose level low cf blood glucose
  • CSF protein raised
  • Raised WBC, particularly if neutrophils

Viral meningitis more likely if: -

  • Normal protein and glucose
  • Moderately raised WBC, particularly if lymphocytes
32
Q

causes of viral meningitis

A

Very commom
- Enteroviruses and Parechoviruses

Fairly common

  • Herpes simplex virus (HSV)
  • Mumps

Rare

  • Lymphocytic choriomeningitis virus
  • Varicellar zoster
  • Human herpesvirus type 6
  • Influenza
  • West Nile
33
Q

picornaviridae family and genus

A

FAMILY: the Picornaviridae are a large and diverse family of non-enveloped RNA viruses has been reclassified into 9 genera based on acid lability, serum neutralization, and sequence homologies.

GENUS: the Enterovirus genus contains human rhinoviruses A-C and human enteroviruses A-D (based on RNA sequence and their order of identification). Enteroviruses and rhinoviruses share an identical genomic organization and have high sequence homology but different phenotypic characteristics.

GENUS: contains human parechoviruses 1-16.

34
Q

picornaviridae types

A

Cytopathic viruses causing tissue-specific cell destruction.

EV-A71: most neuropathogenic non-polio enterovirus in humans.

EV-D68: spectrum of disease ranges from asymptomatic to acute respiratory infection including hospitalisation with severe respiratory disease and, sporadically, to neurological symptoms and death.

HPeV 3 cause more severe illness in young infants, particularly neonates, including sepsis and CNS infections.

35
Q

EV D68

A

In summer and autumn 2014, the USA and Canada experienced an outbreak of EV-D68 associated with severe respiratory illness.

There were 1 153 cases in the USA over a 5 month period of respiratory illness caused by EV-D68.

There was a significant increase in acute flaccid myelitis cases in 2014 in the USA and Canada which coincided with this outbreak of severe respiratory illness caused by EV-D68.

EV-D68 was not detected in CSF. Definitive causation between EV-D68 and AFM was not established but case controlled studies support the hypothesis.

36
Q

diagnosis and treatment

A

diagnosis

  • virus isolation
  • pcr - new gold standard

treatment

  • aciclovir when appropriate
  • supportive
  • stop antibiotics
37
Q

HIV routes of transmission

A

Sexual

Mother-to-baby

  • Antenatally: transplacental
  • Perinatally: in birth canal, exposure to maternal blood
  • Postnatally: in breast milk

Blood or blood products

  • Sharing needles
  • Haemophiliacs
  • Blood transfusions
38
Q

diagnosis of HIV infection

A

Detection of anti-HIV antibodies by immunoassay

Detection of HIV antigens eg p24 by immunoassay

Most laboratory screening tests are 4th generation ‘combo’ assays
ie they detect antibody and p24 antigen

Many POCT and self-test kits are antibody only

Detection of viral genome by PCR

39
Q

HIV stages of infection

A

Acute infection – often associated with “seroconversion illness” 6-8 weeks after infection

Asymptomatic phase

Evidence of declining immune function eg oral candida,TB, shingles, generalised lymphadenopathy

AIDS: AIDS is a very carefully defined disease.

40
Q

HIV: Clinical presentations

A 
acute HIV rash
oral candidiasis
TB
crytococcal meningitis
pneumocystis
primary cerebral lymphoma

1. INFECTIONS (17 decks)

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