Infectious disease 2 Flashcards
what diseases does varicella zoster cause?
chicken pox = varicella zoster
shingles = herpes zoster
what are the symptoms of chickenpox?
- flu-like prodrome followed by a vesicular rash
- not contagious after lesions scab
what is the management of chicken pox?
calamine lotions
aciclovir if in adults, immunocompromised or pregnant
what is shingles and what are the symptoms?
shingles in zoster reactivation due to decreased immunity/stress
painful vesicular rash in dermatomal distribution
- thoracic and ophthalmic most common
- may be multi-dermatomal - disseminated in the immunocompromised
post-herpetic neuralgia - severe dermatomal pain
Ramsay Hunt - ear zoster, facial palsy, decreased taste, decreased hearing
how do you manage shingles?
aciclovir PO/IV
or
famciclovir or valaciclovir
what diseases does EBV cause ?
glandular fever/infectious mononucleosis Burkitt's Lymphoma PTLD oral hairy leukoplakia primary brain lymphoma nasopharyngeal cancer
what causes infectious mononucleosis?
Infectious mononucleosis (glandular fever) (EBV, also known as human herpesvirus 4, HHV-4) in 90% of cases. Less frequent causes include cytomegalovirus and HHV-6. It is most common in adolescents and young adults.
what are the symptoms of infectious mononucleosis?
classic triad of
- pyrexia
- sore throat
- lymphadenopathy
*symptoms usually resolve after 2-4 weeks
other features include
- malaise, anorexia, headache
- palatal petechiae
- splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture
- hepatitis, transient rise in ALT
- lymphocytosis: presence of 50% lymphocytes with at
least 10% atypical lymphocytes
- haemolytic anaemia secondary to cold agglutins (IgM)
- a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
how do you diagnose glandular fever?
heterophil antibody test (Monospot test) - NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever.
you can also perform:
- FBC
- EBV specific antibodies
- LFTs
how do you manage infective mononucleosis?
- rest and fluids
- avoid alcohol
- simple analgesia for aches and pains
- avoid sport of 8 weeks as increased risk of splenic rupture
what is Burkitt’s lymphoma?
Burkitt’s lymphoma is a high-grade B-cell neoplasm. There are two major forms:
- endemic (African) form: typically involves maxilla or mandible
- sporadic form: abdominal (e.g. ileo-caecal) tumours are the most common form. More common in patients with HIV
he Epstein-Barr virus (EBV) is strongly implicated in the development of the African form of Burkitt’s lymphoma and to a lesser extent the sporadic form.
macroscopy findings: starry sky appearance - lymphocyte sheets interspersed with macrophages containing dead apoptotic tumour cells
what patterns of disease does CMV have?
congental CMV infection (growth retardation, pinpoint petechial blueberry muffin skin lesions, microcephaly, sensorineural deafness, encephalitiis and hepatosplenomegaly)
CMV mononucleosis - infective mononucleosis like illness - may develop in mmunocopetent individuals
CMV retinitis - common in HIV patients with low CD4 count (<50), presents with visual impairment e.g. blurred vision - fundoscopy shows retinal haemorrhages and necrosis - often called pizza retina- IV ganciclovir is the treatment of choice
CMV encephalopathy - seenm in patients with HIV who had low CD4 count
CMV pneumonitis
CMV colitis
hepititis A
- transmission?
- incubation period?
hepatitis A is a RNA picornavirus
It only cause acute disease - no chronic disease
it is transmitted by the faecal oral route - more prevelant in enviroments with improper hygiene.
incubation period is 2-4 weeks
what are the clinical features of hepatitis A?
flu like prodrome fever malaise nausea and vomiting jaundice hepatomagaly RUQ pain clay coloured stools
what investigations would you perform for HEP A?
serum transaminases - raised
serum bilirubin - raised
blood urea - will be elevated in fulminant hepatitis
serum creatinine - will be elevated in fulminant hepatitis
IgM antibody - positive in active infection
IgG antibody - recovery/protective - will rise after IgM levels rise and stay elevated throughout the persons lifetime
how do you manage Hep A?
unvaccinated people with recent exposure to hep A (<2weeks) give Hep A vaccine or immune globulin
confirmed HEP A - supportive care and avoid alcohol
who should get be vaccinated against HEP a?
people travelling or going to reside in areas of high or intermediate prevelence, if aged >1 year people with chronic liver disease patients with haemophilia men who have sex with me IV drug users individuals at occupational risk people infected with HIV
how is hep B spread?
infected bodily fluids
what kind of virus is hep B?
it is a DNA virus
what are the features of Hep B?
fever
jaundice
elevated liver transaminases
what are the complications of hep B infection?
chronic hepatitis - ground glass hepatocytes may be seen on light microscopy fulminant liver failure hepatocellular carcinoma glomerulonephritis polyarteritis nodosa cryoglobulinaemia
what investigations should you perform for hep B?
bloods - LFTs, FBC, U&E
HBsAG - Hep B surface antigen - indicates active infection - will be detected around 4 weeks after exposure to virus and usually become undetectable after 4-6 months. If persistence >6 months it implies chronic HBV infection.
Hep B surface antigen antibody - IgG - indicates past infection and in most patients provides life long immunity - also detectable in those with hep B vaccination
Hep B core antigen antibody - IgG and IgM - IgM anti-HBc appears within weeks of acute infection and remains detectable for 4-8 months. During the window period (several weeks or months) after the disappearance of HBsAg and before appearance of antibody to hep B surface antigen, detection of IgM anti HBc may be the only way to make the diagnosis of acute hep b infection. however some patients who have a reactiviation of chronic hep b may have positive IgM antiHBc so it is not an absolutely reliable marker for acute infection. In the chronic infection IgG anti HBc will be detactable.
Hep B e antigen - viral protein found in serum in the early part of acute hep B virus infection - it usally disappears at or soon after the peak in ALT levels. Its presence >3 months after onset of ilness indicates high lkelihood of chronic infection.
If HBsAg plus HBeAg = high infectivity with high level of viral activity
Hep B e antigen antibody - if positive good indicator that the virus has be cleared
if immunised they will be antiHBs positive and all others will be negative (anti- HBc will be negative)
how do you manage Hep B?
acute - supportive care. If severe or if there is acute lover failure - antiviral therapy (entecavir) and assess for liver transplant
chronic - antiviral therapy (entecavir or pegylated interferon alpha - not used as often anymore)
