Viruses Flashcards
(40 cards)
RF for blood borne viruses
IVDU
steroid injections
Tattoo
Sex
Do you need to contact public health in Hep A infections?
Yes
Blood results in HIV seroconversion
low WCC and low platelets
What viruses cause atypical lymphocytes?
CMV, EBV, toxoplasma
Advice in glandular fever
avoid contact sports for 2 months - spleen may rupture
Influenza treatment
- options
- mechanism of action
- SE
Influenza: Oseltamivir; zanamavir
No substitute for vaccination
Neuraminidase inhibitors
- Prevent release of new virions during shedding from infected cells
- Influenza A & B virus (treatment & post-exposure prophylaxis)
Oseltamivir
- H1N1 (influenza A) often resistant
- Hepatic metabolism (pro-drug)
- Renal excretion
- Oral
Zanamavir
- Inhaled (poor oral bioavailability)
- May cause bronchospasm
- Reaches high concentration in respiratory mucosa
SE
Minimal
Nausea
Rare – arrhythmia, seizures
Controversy over efficacy
- Reduced mortality
- Early treatment (within 48hrs) better
- Prophylaxis use results in reduced acquisition
Herpes treatment
- options
- mechanism of action
- SE
Herpes: Aciclovir; ganciclovir
Aciclovir
- Activated via prophorylation by viral thymidine kinase
- Active form inhibits viral DNA polymerase
- used for Herpes simplex virus; Varicella Zoster virus
Use
- Oro-labial HSV infection “cold sore” (Topical in immunocompetent)
- Genital HSV infection - Oral (IV if severe)
- HSV encephalitis (IV)
- Shingles (VZV)- Oral (IV if severe)
SE:
Neurotoxicity (1-4% if IV)
Nephrotoxicity (1-5% if IV)
Ganciclovir
- Nucleoside analogue
- Phosphorylated by CMV kinase then inhibits viral DNA elongation
- Active against CMV (gamma-herpes virus)
Route
- Ganciclovir – IV
- Valganciclovir – oral
Use:
- CMV infections – Retinitis; Hepatitis; pneumonitis; colitis
- Prophylaxis of CMV infection in immunosuppressed transplant recipients → oral valganciclovir
SE
- Myelosuppresion
- Headache, confusion, seizures
- Nephrotoxicity
- Hepatotoxicity
Possible viral causes of abnormal LFT in young adult?
EBV, CMV
Possible viral causes of abnormal LFT in older adult?
drug induced hepatitis, Hep E
Possible viral causes of lymphadenopathy?
EBV
CMV
Toxoplasma
HIV
Possible viruses involved in immunosuppressed?
CMV
Adenovirus
Haemophagocytic lymphohistiocytosis (HLH)
- what is it?
- causes
- epidemiology
- clinical features
- treatment
- prognosis
THINK HLH IF:
- fever and splenomegaly
- and at least 2 blood lineages affected
Uncommon but severe
Activated macrophages engulfing erythrocytes, leukocytes, platelets and their precursor cells
May be diagnosed in association with malignant, genetic or autoimmune disease but also linked to EBV infection
Epidemiology
Primary HLH: Familial form
- Autosomal recessive, long arms of chromosomes 9 and 10
Secondary HLH:
- Virus associated HLH (VAHS)
- Malignancy associated HLH (MAHS)
- Possibly due to excessive activation of monocytes by cytokines (such as interferon, interleukin and tumor necrosis factor)
Difficult to distinguish between familial and HLH associated with viral infection
Clinical features
- Fever, splenomegaly most common
- May have hepatomegaly, lymphadenopathy, jaundice, rash
- CNS manifestations → encephalopathy, meningisms, seizures
- Cytopenia – low Hb, low platelets, low neutrophils
- Hypertriglyceridemia and/or hyofibrinogenemia
Treatment
- Dexamethasone, Etoposide (toxic to macrophages), Cyclosporin
- Intrathecal methotrexate (neurological symptoms)
Prognosis
- Treat underlying infection
- Supportive care associated with recovery in 60-70%
- EBV associated HLH almost universally fatal if untreated
- Death usually due to haemorrhage, infection or multi-organ failure
Adenovirus
- presentation
- treatment
- rare presentation
Presentation
- conjunctivitis
- nasal congestion
- diarrhoea
- hepatitis
Treatment: Cidofovir
- IV with probenecid and fluids
- Loading dose – 2 doses a week apart
- Maintenance dose – a dose every 2 weeks
- Until get 2 negative results
Rare presentation = adenoviral hepatitis
- Jaundice, dark urine, diarrhoea, drowsiness, enlarged liver; haemorhaggic cystitis
- May have history of nasal congestion, red eyes, watery discharge, enlarged lymph nodes
- Treatment: IV cidofovir
CMV
- treatment
1st line - IV ganciclovir BD for 14 days
- 100% bioavailability
2nd line – IV Foscarnet BD
Alternative = oral therapy – Valganciclovir
- No need for admission (QoL)
- No IV access
- Good bioavailability – 60%
- Generally well tolerated
- Used commonly in sold organ transplant cases
RSV
- symptoms
- diagnosis
- treatment
Coryza, afebrile
Direct immunofluorescence of nasopharyngeal aspirate
Aerolised ribavirin & IV HNIG
Severe = IV ribavirin
Community acquired pneumonia
- children - what microbiology is involved?
•Children – viruses in 30-67%; more common in those under 1 years
Older children – bacterial causes
- S. pneumonia > Mycoplasma > chlamydial pneumonia
Rhinovirus
- what type of virus is this?
- presentations
Picornaviridae family; enterovirus genus
- Non-enveloped; SS + sense RNA
- > 100 serotypes
- Species – viral capsid sequencing
Presentations URTI Bronchiolitis (children) Exacerbations – asthma, COPD Pneumonia – young children, adults
Neonatal HSV
- what HSV virus is involved?
- transmission
- what places the neonate at risk?
- presentation if perinatal/post natal infection
- presentation if intrauterine infection
- 75-85%-HSV-2;15-25%HSV-1
Transmission:
- 85% - Peripartum
- ~10% - Post partum (including family contacts)
- ~5% - Intrauterine (identified in first 48 hours)
Risk to neonate:
- Primary maternal HSV (esp – third trimester)
- Prolonged rupture of membranes
- Vaginal delivery
- Fetal scalp electrodes
Involvement:
Perinatal / Postnatal:
- SEM (Skin, Eye, Mucous membrane) (33-47%)
- CNS disease (33%)
- May include SEM lesions
- No other organs involved
- Disseminated (~25%) - 75% also show CNS involvement
Intrauterine:
- Apparent at birth
- Triad:
(1) Skin vesicles/ skin scarring
(2) Eye (Kerititis / Keratoconjunctivitis)
(3) Microcephaly / hydranencephaly
Viruses which cause a macula-papular rash
Measles
Rubella
Parvovirus
Viruses which cause a vesicular rash
VZV
Herpes
Paracox
What type of virus is HIV?
ss+ve RNA
Clinical course of HIV infection
Most infected individuals experience acute glandular fever-like symptoms 3-6 weeks’ post-infection
- rapid rise in concentration of HIV virus in blood; seeding of lymphoid organs ALSO have decline in number of CD4 cells
High levels of virus leads to development of HIV-specific immune response
- infection brought under degree of control
- concentration of virus falls (HIV RNA) to a “viral setpoint”
- Viral setpoint – reflects strength of primary immune response & varies among individuals
- Higher viral setpoint = more rapid decline in CD4 cell count
- Lower viral setpoints = remain immunologically stable for longer
- HIV-infected individuals do not usually experience symptoms for years after initial infection BUT virus continues to multiply at high rate in absence of treatment
- Progressive destruction of CD4 cells
CD4 cell count measurement used to measure the extent of immune system damage.
Measurement of viral load in plasma reflects activity of virus and predictive of risk of disease progression and death.
HIV-infected individuals are infectious even when they have no symptoms – as virus is present in blood and genital secretions
- Seroconvert <12 weeks post-infection
When does seroconversion occur in HIV?
4-12 weeks post infection
Prognosis in untreated adults and children
In untreated adults
- Clinical latency lasts on average 8-10 years
- AIDS sets in at the end of latency
- Leads to death in up to 2 years from severe opportunistic infections and/or neoplasms
Disease progression is considerably faster in untreated children
