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)
who is given the hep B vaccination?
children born in the uk are now vaccinated as part of routine vaccination
at risk groups shoul be vaccinated
what is the hep B vaccine?
contains HBsAg adsorbed onto aluminum hydroide adjuvant and is prepared from yeast cells using recombinant DNA technology
what are the risk factors for adults failing to respond to vaccine?
over 40 years obesity smoking alcohol excess immunosupression
what kind of virus is hepatitis C and what is the incubation period?
hepatits c is a flavicirus
incubation period is 6-9 weeks
it is mainly spread via blood
***NO VACCCINE FOR HEP C
what are the features of hep c?
a transient rise in serum aminotransferases - jaundice
fatigue
arthralgia
what are the risk factors for hep C
unsafe medical practice IV or intranasal drug use blood transfusion or organ transplant heavy alcohol use HIV
what investigations would you perform for hep C?
hep c virus (HCV) antibody enzyme immunoassay (EIA)
hep c virus RNA PCR
serum aminotransferases
what are the outcomes of hep C infection?
around 15-45% of patients will clear the virus after acute infection
the majorty will develop chronic infection (55-85%)
and 20-30% will go on to develop cirrhosis with in 20 years
there is and increased risk of hepatocellular carcinoma
how is chronic hep c defined?
the persistence of HEP C RNA in the blood for more that 6 months
what are the complications of chonic hepatitis c?
rheumatological problems: arthralgia, arthritis eye problems - sjogren's syndrome cirrhosis hepatocellular cancer cryoglobulinaemia - typically type II porphyria cutanea tarda membranoproliferative glomerulonephritis
how is hep c managed?
recent infection - initiate antiviral therapy
chronic infection
- treatment should depend on the viral genotype - this should be tested prior to treatment
- currently a combination of protease inhibitors (e.g. daclatasvir plus sofosbuvir or sofosbuvir plus simeprevir) with or without ribavirin are used
what is hepatitis D?
it is a single stranded RNA virus
It is an incomplete RNA virus that requires hepatitis B surface antigen to complete its replication and transmission cycle
what are the different types of hep D infection?
co-infection - when hep B and D infection at the same time
superinfection - patient has hep B and the subsequently develops hep D infection - superinfection is associated with a high risk of fulminant hepatitis, chronic hepatitis an cirrhosis
how is hep D diagnosed?
HDV IgM and IgG = active infection (IgG is not protective)
HDV RNA PCR
what doe IgG and IgM mean in hep A and E?
IgM = active infection IgG = recovery/protective
hepatitis E what kind of virus? incubation period? pregnancy? acute/chronic? vaccine?
RNA hepevirus
spread by the faecal-oral route
incubation period 3-8 weeks
common in central and SE asia, north and west africa and in mexico
carries significant mortality during pregnancy
does not cause a chronic disease and does not increase risk of hepatocellular carcinoma
currently no vaccination
what are the different intra-abdominal infections that can occur?
acute diverticulitis cholecystitis (with secondary infection) ascending cholangitis appendicitis spontaneous bacterial peritonitis intra-abdominal abscess
what are the common causes of intra-abdominal infections?
anaerobes - bacteroids and clostridium E.coli Klebsiella Enterococcus streptococcus
what antibiotics can be used for intra-abdominal infections?
co-amoxiclav - provides good gram positive, negative and anaerobic cover, does not cover pseudomonas or atypical bacteria
Quinolones (ciprofloxacin and levofloxacin) - reasonable gram postive and negative and also cover atypical bacteria however the do not cover anaerobes so are usually paired with metronidazole when treating abdo infections
Metronidazole - excellent for anaerobic bacteria but does not provide any cover against aerobic bacteria
Gentamicin - very good gram negative cover with some gram positive cover particularly against staph.
Vancomycin - very good gram positive cover including MRSA - it is often combined with gentamicin to cover gram negative and metronidazole to cover anaerobes
cephalosporins - broad spectrum against gram positive and gram negative but not effective against anaerobes - they are often avoided due to the risk of developing c.diff infection
Tazocin and meropenem - piperacillin/Tazobactam (tazocin) and meropenem are heavy hitting antibiotics that cover gram positive, gram negative and anaerobic bacteria - usually reserved for patients who are very unwell and are not responding to other antibiotics
who does spontaneous bacterial peritonitis usually occur in?
patients with liver failure
what different types of plasmodium cause malaria?
Plasmodium falciparum
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
what causes the most severe form of malaria??
plasmodium falciparum - it is also the most common type of malaria it accounts for 75% of cases
what can be protective against malaria?
sickle cell trait
G6PD deficiency
HLA- B53
absence of duffy antigens
which plasmodium can lie dormant in the liver for several years?
p. vivax and p. ovale
what is the life cycle of malaria?
when a mosquito bites human the sporozoites are injected into the human by the mosquito they the travel to the liver where they can lie dormant as hypnozoites for several years if they are p.vivax or p. ovale.
They mature in the liver into merozoites which enter and infect red blood cells. In red blood cells, the merozoites reproduce over different time periods depending on the species. After they reproduce the red blood cells rupture releasing more merozoites into the blood causing haemolytic anaemia.
This is why people with malaria have high fever spikes, every time the blood cells rupture they get spike - may be 48 hours or 72 hours depending on the species.
what are the features of severe malaria?
schizonts on a blood film parasitaemia >2% hypoglycaema acidosis temp >39 severe anaemia
what are the complications of malaria?
cerebral malaria - seizures and coma acute renal failure - blackwater fever, secondary to intravascular haemolysis acute respiratory distress syndrome hypoglycaemia DIC
how does malaria present?
non-specific symptoms - fever, sweats and rigours malaise myalgia headache vomiting
signs
- pallor due to anaemia
- hepatosplenomegaly
- jaundice as bilirubin is released during the rupture of RBCs
how is malaria diagnosed?
Giemsa-stained thick and thin blood stains - thick films are more sensitive for detect parasites where as thin films permit species identification and parasitameia - 3 samples should be sent over 3 consecutive days to exclude malaria due to the cycle of malaria being released into the blood from the blood cells
rapid diagnostic tests FBC clotting profile U&Es LFTs blood glucose
what is the most common cause of non-falciparum malaria?
plasmodium vivax
which form of malaria is associated with nephrotic syndrome?
plasmodium malariae
which malaria may relapse following treatment?
ovale and vivax have a hypnozoite stage where they can stay dormant in the liver for months/years so therefore may relapse following treatment
how do you manage plasmodoium falciparum - uncomplicated disease?
if sensitive to chloroquine and non pregnant
- chloroquine or hydroxychloroquine
if chloroquine-resistant
- ACTs - artemisinin-based combination therapies (artemether with lumefantrine (riamet))
how do you manage severe plasmodium falciparum ?
parenteral antimalarial regimen
- artesunate
other options include artemether or quinine
supportive care and admission to intensive care
if parasite count is greater than 10% the exchange transfusion should be considered
how do you manage plasmodium ovale, vivax, malariae or knowlesi ?
either an ACT or chloroquine
if pregnant in first trimester and chloroquine resistant then treat with quinine
what antimalarial medications can be given to prevent infections?
proguanil and atovaquone (malarone) - taken daily 2 days before, during and 1 week after being in endemic area, most expensive - around £1 per tablet, best side effect profile
Mefloquine - taken once weekly 2 weeks before, during and 4 weeks being in enemic area - can cause bad dreams and rarely psychotic disorders and seizures
Doxycycline - taken daily 2 days before, during and 4 weeks after being in endemic area - borad spectrum antibiotic so causes side effects like diarrhoea and thrush, also makes patients more sensitive to the sun causing a rash and sunburn.
