Faeco-oral transmission. Global distribution.
Incubation 4/52, can be asymptomatic in young children. Non-specific fever, malaise, possibly RUQ pain before jaundice appears, usually with rapid relief in symptoms. Up to 1% however have fulminant disease with hepatic failure.
Post exposure prophylaxis for hepatitis A with hepatitis A vaccine reduces secondary infection rate from 13% to 2.8% (NNT=18).
See also viral hepatitis.
Plus the newer D (faeco-oral as A, particularly severe in pregnant women) and E (a co-factor in Hepatitis B infection).
But a range of other viruses can cause hepatitis eg EBV, Varicella.
Oseltamivir and Zanamivir licensed for treatment and the former also for post-exposure prophylaxis.
Cochrane review 2014 found little evidence of benefit. But this was based on community studies in healthy populations.
“Use of neuraminidase inhibitors in influenza” [October 2015, Academy of Medical Sciences] indicates that the use of antivirals can be beneficial in certain situations, but of limited use in others. Additionally, a recent review “Expert opinion on neuraminidase inhibitors for the prevention and treatment of influenza – review of recent systematic reviews and meta-analyses” August 2017, European Centre for Disease] supports use as treatment and prophylaxis.
UKHSA therefore recommends:
“Complicated” influenza defined as
Risk factors include:
Oseltamivir (Tamiflu) PO or NG is first line, unless severe immunosuppression and A(H1N1) variant prone to resistance dominant – then zanamavir.
Presumes flu-like illness and circulating influenza, CMO publishes advice when surveillance levels cross threshold. Highly virulent strain would change things, of course. Further details including use of anti-virals at HPS.
Oseltamavir dose is twice daily for 5 days. Oral only, capsules can be opened and added to something sugary (very bitter). Liquid preparation available but limited supply, prioritise for infants. Give by NG if necessary. Licensed for treatment at all ages now, prophylaxis only over 1 yr. Diarrhoea and vomiting are the only significant side effects.
The earlier it is started the better: starting within 12 hours reduced duration of illness by 3 days, start within 48 hours and only 1 day benefit. 5% of childhood infections will become resistant whereas this is unusual in adults, probably due to kids having higher viral loads in primary infection. Consider resistance if no benefit after 5 days treatment.
Zanamivir used for adolescents 12 years and older – taken again twice daily for 5 days by diskhaler (age less important than ability to use device!). No resistance, very low rate of side effects (wheeze!). Zanamavir is preferred in severely immunocompromised AND (probable) A(H1N1)pdm09 disease, as resistance is higher . Unlicensed IV form of zanamavir is available on compassionate named patient basis.
For prophylaxis, vaccination best! But consider using anti-virals (NICE recommendations) for post-exposure prophylaxis with Oseltamivir where:
Dose is once daily for 10 days. Treatment for up to 6 weeks might be required during an epidemic.
Amantadine not recommended – targets M2 protein, only effective against type A influenza, rapid resistance and side effects common.
2 adolescents in Japan have committed suicide while on oseltamavir, plus there have been a number of other neuropsychiatric reports.
Peramivir is IV preparation with marketing authorization in EU, not yet available in UK.
A good proportion of healthy children will have palpable lymph nodes in the neck. Mostly these will be under 1cm in diameter. Acute enlargement as part of an upper respiratory tract infection is usually accompanied by tenderness, and affected nodes will reduce in size over 4-6 weeks.
Guidance from NICE and the Scottish Government provide criteria when children with lymphadenopathy should be urgently referred for suspected cancer.
These criteria include the following:
But caveat is “Always refer any patient with Repeat presentations (3 or more times) of any physical symptoms which do not appear to be resolving or following a normal pattern, taking into account parental and patient concern”.
No need to do bloods in the absence of any of these criteria. Not that cancer is the only concern – differential includes developmental lesions (branchial cysts etc), TB, Cat-scratch disease, non-tuberculous mycobacterial infection (esp in neck). These are always more than 2cm and there may also be systemic features and/or overlying skin discolouration too.
Malignancies often present in the head/neck region. Hodgkins lymphoma usually affects teenagers, Non-hodgkins tends to affect school age children, neuroblastoma tends to affect pre-school children. B-symptoms (recurrent fever, weight loss, night sweats, pruritus, lethargy) are only seen in a minority but does suggest more advanced disease, of course. Airway or voice changes, swallowing difficulty, Horner’s syndrome, superior vena cava syndrome may all be seen due to mass effect. Most neuroblastomas have an abdominal mass. Nasopharyngeal carcinomas are seen so look in the nose/throat.
Depending on geographic location, different viruses cause viral meningitis. In some areas, arthropod borne viruses are important.
With new diagnostic methods, more of these cases are being given a specific aetiology.
Very unusual. Some small studies have suggested that early enterovirus meningitis linked to later language problems. Deafness is debatable – some large studies have not found any cases, yet antenatal infections and subclinical viral infections are felt to be causes for deafness in other clinical situations!
Tonsillitis, pharyngitis. See SIGN guideline.
“Doughnut lesions” – multiple small erythematous papules with clear centres – associated with group A streptococcus.
See also pharyngitis treatment.
FeverPAIN scoring system – possibly better than Centor at avoiding antibiotics. For primary care settings, children over 3 and adults.
3 points gives 40-50% risk of strep, so treat at 4 points, consider delayed antibiotics for 3 points. Not for under 3s, and beware worsening after 3 days which might indicate more severe infection. [PRISM study 2014]
Centor and McIsaac scores to predict group A streptococcal pharyngitis. One point for each of the following:
Centor score is sum (0-4). The McIsaac score (1998) is an adjustment of +1 to account for the increased incidence of GAS in children <15yr and -1 for decreased incidence in those 45+ years. CDC advises treat empirically at score 3+ or at score 2 if rapid testing positive.
Original studies used small samples, but national US study confirmed validity in 65 000 patients aged 3-14yrs presenting to primary care. For children, GAS positive rates were:
AUC was 0.71 for McIsaac score across all ages.
Fine and Nizet, Archives of Internal Medicine. 172(11):847-52, 2012 Jun 11. PMID 22566485
Other clinical decision rules include:
Rapid antigen test performs better, 85% sensitivity (similar to Abu Reesh rule) but much better PPV (48%).
VZV encephalitis presentation not different from usual, viz fever, headache, altered consciousness, etc. But can be subacute onset.
The more common neuro manifestation of VZV in young children is post-infectious cerebellitis – usually mild and self limiting, child not unwell but risk of secondary
hydrocephalus in more severe cases.
There is also a well recognized association in childhood between VZV infection and stroke, usually presents after the rash has cleared – typically 3 months [London study, Miravet & Danchaivijitr 2007). Post-VZV thromboembolism also seen rarely eg lower limb DVT.
Encephalitis can present early, even before rash (which may
not be very obvious either). PCR for VZV DNA in the CSF is positive in around a third of patients; VZV specific IgG seen in 90% in CSF. Compare levels to serum as a way
of confirming CNS involvement.
Usually (not for cerebellitis), steroids given eg 60-80 mg of prednisolone daily for 3 to 5 days) is given (Gilden & Kleinschmidt-DeMasters 2000) esp where MRI evidence of vasculitis.
[encephalitis article, source?]
A systemic viral illness characterised by widespread vesicles. Like other herpesviruses, it retains the ability to lie dormant in ganglions after initial infection, possibly reactivating in the future as Herpes Zoster (= shingles).
Age and immunodeficiency are the most important predictors of severity, with adults and infants having more severe disease. Cellular rather than humoral immunodeficiency is associated with more severe disease. Nonetheless, most cases of severe disease (and 90% of the deaths) occur in previously healthy people.
Average age is falling, now under 5 (presumably increased day care) cf underdeveloped countries, where average age is older eg teens. Peak incidence March to May.
There are 3 genotypes but they are virtually identical, and only 1 circulates in Europe; it remains theoretically possible, therefore, to get chickenpox twice! But more likely is that one or more episodes were due to another virus eg enterovirus.
Starts as small spots, spreading over the trunk within 24 hr. There is usually no prodrome in children, can be 1-2 days in adults. Within 24-48 hours the classic vesicles, followed by pustules, develop. Burst to leave a scab which falls off after 4-5 days. There may be several crops of these blisters which follow the same pattern. The classical distribution is on the trunk but lesions can be widespread and can affect the mouth, the eyes and the urethra.
Onset of the rash is often associated with fever and other systemic symptoms. The disease can however be subclinical (or at least unrecognized) in some cases. Secondary cases in a household on the other hand tend to be more severe, probably due to increased viral load.
In the immunocompromised, there may be a prodrome ie symptoms at the time of initial viraemia, around day 7 of the incubation period. The classic prodrome is of abdominal symptoms and/or hyponatraemia, and can precede the classic vesicular rash by several days (up to 3 weeks). Abdominal manifestations include severe pain, diarrhoea, or vomiting which are explained by hepatitis, gastritis, oesophagitis, pancreatitis, and paralytic ileus owing to viral spreading from the posterior nerve roots that supply abdominal organs. The mechanism of hyponatraemia is presumed to be SIADH.
See Congenital varicella for infection in pregnancy and neonatal period.
Usually clinical. If in doubt, PCR and culture can be done on skin scrapings (particularly from the base of lesions, but potentially also from the crust) or from other sites eg CSF.
IgM can be positive from as early as 1-2 days after appearance of the rash. But serology is not 100% sensitive. Antibodies persist lifelong and are useful for indicating previous exposure and hence immunity; they may however be passed on passively through transfusion. Not very good for confirming response to vaccination, as levels are 10 times lower than after disease.
Complications of varicella occur in the immunocompetent, as well as the immunocompromised :
See also Congenital varicella.
Incubation period is 10-21 days, typically 14 days. Longer in some situations (eg post ZIG). Infectivity (by aerosol spread) begins up to 48 hours before onset of the rash and persists until all lesions have dried (crusted), usually 1-2 weeks but may be longer in the immunocompromised. In theory transmission from a moist spot can occur but infection is generally by respiratory route.
Infectious or isolation period is until all lesions crusted, or else 5 days after the last spot appears. UK HPA guidance is available on exclusion periods from school or nursery on health grounds. Infectivity can persist in the immunocompromised for up to several weeks. Note also that after VZIG administration, incubation period is prolonged.
Chickenpox can be treated with aciclovir or the like. Oral aciclovir in the healthy child reduces fever by 1 day and symptoms by 15-30%; not clear if complications are reduced. NEJM 1991;325(22):1539-44. Not standard practice, however! Adolescents and adults should be offered it.
Oral aciclovir only works if given in first 24 hours; IV most effective if given within 72 hours of onset of the rash.
A variety of topical products are available eg calamine. Antihistamines.
Various studies have found an association between severe soft tissue infection and use of ibuprofen (in children, anyway – rate ratio 4.9 [Br J Clin Pharmacol. 2008 Feb;65(2):203-9. doi: 10.1111/j.1365-2125.2007.02997.x]). Likely to be confounding, but in absence of prospective studies, NICE recommends avoiding non-steroidal anti-inflammatories in varicella [https://cks.nice.org.uk/chickenpox#!scenario].
See Vaccines for details on live attenuated vaccine.
Post-exposure prophylaxis (PEP) is required for at risk groups who have had significant exposure. This includes:
Specific Varicella Zoster Immunoglobulin (VZIG) is effective at reducing the likelihood of disease, and where disease occurs it tends to be less severe. It is given intramuscularly. Should be given within 10 days of exposure. Protection lasts 3 weeks, after which a further dose should be considered if re-exposure occurs and antibody has not persisted. Can prolong period of infectivity though. See Greenbook for more details.
Aciclovir can also be used for PEP.
Varivax vaccine is also licensed for this indication, but of course contraindicated in the type of patient who might need it: 18% of healthy contacts developed varicella compared with 78% who did not get vaccine. Of the vaccine recipients who nonetheless developed varicella, the majority only had mild disease (with less than 50 skin lesions). Evidence only really supports PEP within three days following exposure.
If a pregnant woman is infected during the first trimester (risk extends to 20th week), a fetus has a 1% chance of developing widespread scarring, hypoplastic limbs, cataracts and brain lesions (congenital varicella). Affected infants have a poor neurodevelopmental outlook.
Risk of neonatal VZV (severe, disseminated disease in newborn) if chickenpox is contracted by the mother 4 days before birth, to 2 days after (risk 20%). Before that, good chance that maternal immune response will protect baby, after that the dose of infection transmitted to the baby via the umbilical cord is likely to be small (although will still be exposed to droplets).
See Maternal for advice on varicella exposure in pregnancy and in neonates.
Following varicella vaccine introduction in Australia, coverage of greater than 80% at 2 years of age was achieved, with varicella hospitalizations reduced by almost 70%. 40% of hospitalized children were immunocompromised. Of hospitalized children age-eligible for varicella vaccine, 80% were unimmunized, including all cases (3) requiring intensive care. No deaths.
[Pediatric Infectious Disease Journal. , 17 December 2012]