The physical signs of measles are nearly the same as those of smallpox, but nausea and inflammation is more severe. The rash of measles usually appears at once, but the rash of smallpox spot after spot . .
Chickenpox has become much less common since the introduction of the varicella vaccine in 2000 and its inclusion on the National Immunisation Program in 2005, because of both individual and herd immunity.1 Prior to this, nearly all children acquired it (<80% of the Australian population were seropositive by their teens). Chickenpox has a complication of only 1%, and is often thought of as not being a serious disease—which mostly it isn’t—but because it was so common prior to the vaccine’s introduction it resulted in 1500 hospital admissions and 7–8 deaths a year.1
Chickenpox is a highly contagious infection caused by the varicella zoster virus, a DNA virus within the herpes virus family. Primary infection causes chickenpox (varicella), with the virus establishing latency in the dorsal root ganglia. Reactivation leads to herpes zoster (shingles), which is relatively uncommon in children and can be more difficult to diagnose as it often presents with only a few lesions.
Note: shingles can happen in childhood.
The clinical features of varicella are shown in TABLE 93.1 and the complications in TABLE 93.2. Children are not normally very sick but tend to be lethargic and have a mild fever. Adults have an influenza-like illness. The typical distribution is shown in FIGURES 93.1 and 93.2.
Table 93.1Clinical features of varicella ||Download (.pdf) Table 93.1 Clinical features of varicella
Children: no prodrome
Adults: prodrome (myalgia, fever, headaches) for 2–3 days
Centripetal distribution, including oral mucosa (see FIG. 93.1)
Lesions can become infected
‘Cropping’ phenomenon: vesicles, papules, crusting lesions present together
Degrees of severity
Number of vesicles can vary from fewer than 10 to thousands (usually 200–500)1
Mild cases can be missed
More severe in adults and the immunocompromised
Viral pneumonia rare in children, uncommon in adults
Death rare except in the immunocompromised and neonates with congenital varicella
Table 93.2Complications of varicella ||Download (.pdf) Table 93.2 Complications of varicella
Bacterial infection of cutaneous lesions (usually staphylococcal or streptococcal); can take form of cellulitis or bullous impetigo
Can leave pitted scars
Birth defects with neonatal infection
Acute cerebellitis (ataxia, normal mental state)
Varicella (chickenpox) in a 12-year-old girl showing a maculopapular vesicular rash with a centripetal distribution
Chickenpox: typical distribution
Congenital varicella syndrome can occur from varicella in pregnancy, and may result in skin scarring, limb defects, ocular anomalies and neurological malformations, with the risk highest in the second trimester. Intrauterine exposure also increases the risk of shingles in infancy. Severe neonatal varicella infection can result from perinatal varicella in the mother (especially if contracted from 5 days before the birth to 2 days after).
Treatment is symptomatic and usually no specific therapy is required. Antiviral therapy is used in patients with complications or those at high risk (e.g. immunocompromised people). Many people, especially parents, worry about scarring but the lesions invariably heal, leaving normal skin, unless they become infected.
The patient should rest until feeling well.
Give paracetamol for the fever (avoid aspirin in children due to the possibility of Reye syndrome).
Daub calamine or a similar soothing lotion to relieve itching, although the itch is usually not severe.
Avoid scratching; clean and keep the fingernails short. Provide cotton mittens if necessary.
Daily bathing is advisable, with the addition of mild antiseptic or sodium bicarbonate if pruritic (add half a cup to the bath water). Pat dry with a clean, soft towel; do not rub.
Antihistamines can be prescribed for itching. Aciclovir or similar agents can be life-saving in the immunocompromised host. Antibiotics (e.g. flucloxacillin/dicloxacillin) are reserved for bacterial skin infection. Use hydrogel for sore wounds.
Exclusion is recommended until the blisters have dried, usually at least 5 days in unimmunised children but possibly shorter in those immunised. Except for immunocompromised children, contacts should not be excluded from school.
Exclusion and incubation times for chickenpox (and other basic childhood infectious diseases) are given in TABLE 93.3.
Table 93.3Basic childhood infectious diseases: incubation periods, minimum exclusion periods from school, preschool and child care centres (times in days)1,2 ||Download (.pdf) Table 93.3 Basic childhood infectious diseases: incubation periods, minimum exclusion periods from school, preschool and child care centres (times in days)1,2
| ||Incubation period (days) ||Patient exclusion (least time from onset of rash or symptoms) (days) ||Contact exclusion (days) |
|Measles ||10–14 ||4 ||14 in non-immunised |
|Glandular fever ||? 30–50 ||Nil ||Nil |
|Mumps ||12–25 ||9 ||Nil |
|Pertussis ||7–20 ||5 (after starting antibiotics) or 21 from onset of cough ||Non-immunised household contacts—until have had 5 days of antibiotics or 21 days after exposure finishes |
|Parvovirus B19 (erythema infectiosum) ||4–20 ||Nil ||Nil |
|Roseola infantum ||7–17 ||Nil ||Nil |
|Rubella ||14–21 ||4 ||Nil |
|Scarlet fever ||1–7 ||24 hours (after starting antibiotics and feeling well) ||Nil |
|Impetigo ||1–3 for strep, 4–10 for staph ||Until treatment commenced (cover sores) ||Nil |
|Meningococcus ||1–10 (commonly 3–4) ||Until antibiotic therapy complete ||Check with consultant |
|Varicella and zoster ||10–21 ||Until blisters have dried ||Only those immune deficient |
|A ||15–50 ||7 or recovery ||Nil |
|B ||45–180 ||Nil ||Nil |
|C ||14–180 ||Nil ||Nil |
|Infective diarrhoea ||Varies ||24 hours after cessation of diarrhoea ||Nil |
Prevention in contacts who are immunocompromised or at high risk (e.g. neonates) and in contact with varicella, is possible with zoster immune globulin (ZIG). An attenuated live virus vaccine is available and suitable for healthy children from the age of 12 months up to and including 13 years. It is given routinely at 18 months with the immunisation schedule. Vaccination of household contacts and post-exposure vaccination will reduce risk and also result in less serious disease if it does occur.
Reye syndrome and aspirin
There is concern over children with febrile illness ingesting aspirin because of the suspected causal relationship between aspirin and Reye syndrome, particularly in those with varicella, influenza and other viral diseases. The syndrome includes nausea and vomiting with the rapid development of encephalopathy, hepatic failure, seizures and coma.
Measles (rubeola) is a highly contagious disease caused by an RNA paramyxovirus. It presents as an acute febrile exanthematous illness with characteristic lesions on the buccal mucosa called Koplik spots (tiny white spots like grains of salt, opposite the molars).
The disease is endemic throughout the world and complications are usually respiratory in nature. If an acute exanthematous illness is not accompanied by a dry cough and red eyes, it is unlikely to be measles. Laboratory diagnosis is by serology, with IgM rising 3–5 days after the onset of the rash.
Measles is transmitted by patient-to-patient contact through oropharyngeal and nasopharyngeal droplets expelled during coughing and sneezing.
The incubation period is 10–14 days and the patient is infectious until about 4 days after the onset of the rash, but especially just before the appearance of the rash. Morbidity and mortality are high in countries with substandard living conditions and poor nutrition.
Immunity appears to be lifelong after infection. Measles, like smallpox, could be eradicated with public health measures. While vaccination programs have been very successful worldwide, there has been a recent resurgence of measles in developed countries due to falling vaccination rates in some areas.
The clinical presentation can be considered in three stages.
Prodromal stage. This usually lasts 3–4 days. It is marked by fever, malaise, anorexia, diarrhoea and ‘the three Cs’: cough, coryza and conjunctivitis (see FIG. 93.3). Sometimes a non-specific rash appears a day before the Koplik spots.
Exanthema (rash) stage. Identified by a typically blotchy, bright red maculopapular eruption; this stage lasts 4–5 days. The rash begins behind the ears; on the first day it spreads to the face (see FIG. 93.4), the next day to the trunk and later to the limbs. It may become confluent and blanches under pressure. The patient’s fever usually subsides within 5 days of the onset of the rash.
Convalescent stage. The rash fades, leaving a temporary brownish ‘staining’. The patient’s cough may persist for days, but usually good health and appetite return quickly, with recovery in about 7–10 days.
Measles showing the typical blotchy, bright red maculopapular rash on the face of a miserable child with the three Cs (cough, coryza and conjunctivitis)
Measles typical symptoms. Note the 3Cs: cough, coryza, conjunctivitis.
Measles is often a serious disease, and complications are common.1 These include otitis media (9%), pneumonia (6%) and diarrhoea (8%). Children under 5 and adults and patients with chronic disease are more prone to complications. For every 1000 children who get measles, 1 to 2 will die,3 with the majority of deaths occurring from pneumonia. Infection during pregnancy can lead to miscarriage or premature delivery, but is not associated with congenital malformation.
Encephalitis has an incidence of 1 in 1000, and has a mortality of 10–15% and also a high rate of permanent brain damage. Subacute sclerosing panencephalitis (SSPE) is a late complication, occurring on average 7 years after infection in 0.5–1/100 000 cases, and is manifested by universally fatal progressive brain damage.
There is no specific treatment although some symptoms can be relieved (e.g. a linctus for the cough, paracetamol for fever). The patient should rest quietly, avoid bright lights and stay in bed until the fever subsides. Oral vitamin A has been reported to reduce complications.
Vaccination should be given to any child over 12 months, or any teenager or adult born since 1966 who does not have a documented record of 2 MMR-containing vaccines (or serological evidence of protection for measles, mumps and rubella).1 Live attenuated measles virus vaccinations combined with mumps and rubella (MMR) are recommended at the age of 12 months and then MMRV (with varicella) at 18 months. Consider normal immunoglobulin for infants under 12 months and the immunocompromised when MMR is contraindicated, given as soon as possible after exposure.
Rubella (German measles) is a viral exanthema caused by a togavirus. It is a minor illness in children and adults, but devastating when transmitted in utero. Congenital rubella syndrome (CRS) occurs in up to 90% of infants born to mothers contracting rubella in the first trimester. Multiple features of CRS are usually evident, which include intellectual disabilities, cataracts, deafness, cardiac abnormalities, intrauterine growth disorders (IUGR) and inflammatory lesions of the brain, liver, lungs and bone marrow. It is completely preventable. The risk declines rapidly after the first trimester.
All women of child-bearing age should have 2 documented doses of rubella-containing vaccines and if not their immune status should be assessed serologically. If not immune, they should be vaccinated and retested 6–8 weeks later and revaccinated if they have negative or low levels. No antibody response to 2 doses may represent a false negative result. Rubella-containing vaccinations are contraindicated in pregnant woman and pregnancy should be avoided for 28 days after vaccination.1 Once the baby arrives, postpartum vaccination of those mothers not fully immune should be done immediately (breastfeeding is not a contraindication).
CRS is rare in Australia due to vaccination. Only 2.5% of women of child-bearing age are seronegative, though the risk is higher in women born overseas. Intra-uterine infection occurs via the placenta.
Approximately one-third of infections are asymptomatic (subclinical). Infection usually confers lifelong immunity. Incubation period is 14–21 days.
The clinical features of rubella are presented in TABLE 93.4 and FIGURE 93.5 and the complications in TABLE 93.5.
Table 93.4Clinical features of rubella ||Download (.pdf) Table 93.4 Clinical features of rubella
There is no prodrome.
A generalised, maculopapular rash, sometimes pruritic, may be the only evidence of infection.
Other symptoms are usually mild and short-lived.
There is often a reddened pharynx but sore throats are unusual. An exudate may be seen as well as palatal exanthem.
Fever is usually absent or low-grade.
Other features: headache, myalgia, conjunctivitis and polyarthritis (small joints).
Lymphadenopathy may be noted; usually postauricular, suboccipital and postcervical.
The patient is infectious for a week before and at least 4 days after the onset of the rash.
A discrete pale pink maculopapular rash (not confluent as in measles).
Starts on the face and neck—spreads to the trunk and extremities.
Variable severity: may be absent in subclinical infection.
Exaggerated on skin exposed to sun.
Brief duration—usually fades on the third day.
No staining or desquamation.
Rubella: typical symptoms
Table 93.5Complications of rubella ||Download (.pdf) Table 93.5 Complications of rubella
Polyarthritis, especially in adult women (this complication abates spontaneously)
Congenital rubella syndrome
Treatment is symptomatic, especially as rubella is a mild disease. Patients should rest quietly until they feel well and take paracetamol for fever and aching joints. Prevention is by vaccination, recommended at 12 and 18 months.
The child is usually excluded until fully recovered or for at least 4 days from the onset of the rash.
Viral exanthema (fourth syndrome)
This mild childhood infection may be caused by a number of viruses, especially the enteroviruses, and produces a rubella-like rash that may be misdiagnosed as rubella. The rash, which is usually non-pruritic and mainly confined to the trunk, does not desquamate and often fades within 48 hours (see FIG. 93.6). The child may appear quite well or can have mild constitutional symptoms, including diarrhoea.
Viral exanthema (fourth syndrome). This mild rubella-like maculopapular rash, which may be caused by a number of viruses, is usually non-pruritic
Parvovirus B19 (erythema infectiosum, fifth disease)
Parvovirus, also known as ‘slapped cheek’ syndrome, is a childhood exanthem caused by parvovirus strain B19. It occurs typically in young school-aged children. The incubation period is 4–20 days. Non-specific prodromal symptoms (fever, runny nose, headache, nausea) are followed 2–5 days later by the rash. The bright macular rash erupts on the face first (see FIG. 93.7) then, after a day or so, a maculopapular rash appears on the limbs.1 The rash lasts for only a few days but may recur for several weeks. By the time the rash appears the individual usually is no longer infective.
Parvovirus, showing the typical slapped cheek appearance
Mild fever (30%) and malaise
Runny nose, headache, nausea
Possible lymphadenopathy (especially cervical)
The rash (see FIG. 93.8):
Parvovirus: typical distribution of rash
bright red flushed cheeks with circumoral pallor for 2–3 days
maculopapular rash on limbs (especially) and trunk (sparse)
reticular appearance on fading
may be pruritic
Typically, the cheeks become reddened again for the next few weeks on exposure to sunlight or wind or after a hot bath. Adults can be infected and the side effects, especially arthritis, can be quite severe.
Erythema infectiosum is a mild illness but, if the parvovirus infection occurs during pregnancy, fetal complications including miscarriage can occur. It is advisable to avoid close contact with pregnant women (see CHAPTER 108). Some 50% of young adult females are susceptible to parvovirus infection. About 50% of susceptible household contacts will become infected, and around 20% of classroom contacts.
Pregnant women should be tested for parvovirus IgM and IgG if:
The results are interpreted as:
IgG alone detected—immune
IgM detected—false positive or early infection. Repeat in 2 weeks to see if rising IgG levels
IgM and IgG not present—susceptible. If susceptible and becomes unwell, repeat test
If infection occurs in the first half of pregnancy, the fetus may become anaemic (the virus replicates in erythroid progenitor cells) and hydrops fetalis and miscarriage can occur. Women in this situation should be reassured that <5% of women will miscarry, though ultrasound monitoring is recommended. Parvovirus in pregnancy is not associated with fetal anomalies. If exposure or infection is suspected in the second half of pregnancy, investigation is still warranted as there may be errors in the gestational age and the risk to other pregnant women in health settings needs to be managed.
Treatment is symptomatic.
Ample fluid intake
Paracetamol for fever
If itchy, daub a soothing anti-itch lotion such as Pinetarsol or calamine lotion
Wear a broad-brimmed hat when outside
Adults may need stronger analgesics or NSAIDs for arthralgia (more common in adult women).
Roseola (roseola infantum, exanthema subitum or sixth disease)
Roseola is a viral infection (human herpes virus 6) of infancy, affecting children at the age of 6 months and 2 years; 95% of children have had it by this time, and it is rare after this. Constitutional symptoms are generally mild.
Sudden high fever (up to 40°C)
Temperature falls after 3 days (or so) then
Red macular or maculopapular rash appears
largely confined to the trunk and limbs (see FIG. 93.9)
usually spares face
appears as fever subsides
blanches on pressing
disappears within 2 days
mild cervical lymphadenopathy
Roseola: typical distribution of rash
The infection runs a benign course, although a febrile convulsion can occur. The child will no longer be infectious by the time the symptoms appear. Treatment is symptomatic. Encourage high fluid intake.
Hand, foot and mouth (HFM) disease
This is a mild vesicular eruption caused by enteroviruses, the most common being Coxsackie A-16, with EV-71 being less common. HFM disease affects both children and adults but typically children under the age of 10. Sometimes referred to as ‘crèche disease’, it often occurs among groups of children in child care centres. Transmission is through respiratory secretions, touch contact with the blistered areas or faeco-oral transmission (hand washing after changing nappies is important to reduce transmission).
Incubation period 3–5 days
Initial fever, headache and malaise
Sore mouth and throat
The rash appears after 1 or 2 days
Starts as a red macule, then progresses to vesicles
Vesicles lead to shallow ulcers on buccal mucosa, gums and tongue
Greyish vesicle with surrounding erythema
On hands, palms and soles (usually lateral borders)
May appear on limbs especially buttocks and genitals
Lesions resolve in 3–5 days
Healing without scarring
Virus excreted in faeces and saliva for several weeks
Children are infectious until the blisters have disappeared
Diagnosis is clinical, investigations usually unnecessary
Scarlet fever results when a Group A Streptococcus pyogenes organism produces erythrogenic toxin. The prodromal symptoms prior to the acute exanthem comprise malaise, sore throat, fever (may be rigors) and vomiting. A throat swab should be taken.
Appears 12–24 hours after the start of the fever
First appears on neck
Punctate and red, a ‘boiled lobster’ or sunburnt appearance
Blanches on pressure
Prominent on neck, in axillae, cubital fossa (Pastia lines), groin, skinfolds (see FIG. 93.10)
Absent or sparse on face, palms and soles
Feels like fine sandpaper
Lasts about 5 days
Scarlet fever: typical presentation of rash
Phenoxymethylpenicillin (dose according to age) for 10 days with rapid resolution of symptoms, although resistance is increasingly common. Children can return to school 24 hours after taking antibiotics and feeling well.
This is an uncommon but important systemic vasculitis that typically affects the coronary arteries, usually in children under 5 years of age and likely caused by an infection, though the presumed agent remains unknown. It is characterised by an acute onset of fever >39°C of 5 days or more and accompanied by 4 out of 5 of the following features:
bilateral (non-purulent) conjunctival infection
mucous membrane changes, e.g. reddened or dry cracked lips, strawberry tongue, diffuse redness of oral or pharyngeal mucosa
peripheral changes, e.g. erythema of the palms or soles, oedema of the hands or feet (and in convalescence desquamation)
an ‘unusual’ nappy rash
cervical lymphadenopathy (>15 mm diameter, usually unilateral, single, non-purulent and painful)
Diagnosis is basically a clinical one. Other diseases with similar signs should be excluded (e.g. staph or strep infections, measles, viral exanthems, drug reactions or JRA).
Kawasaki disease can be elusive as there are variations with atypical or incomplete manifestations. Think of it in a miserable child with a high fever ≥5 days and arrange for paediatric review if suspicious. Blood results will also help contribute to the diagnosis and management decisions (e.g. ESR and CRP usually raised, thrombocytosis often raised in second week, neutrophilia, normochromic normocytic anaemia, hypoalbuminuria, abnormal LFTs).
The disease is often benign and self-limiting but it is important to make an early diagnosis because early treatment may prevent complications (which also occur in the atypical cases). The major complication is vasculitis, which causes coronary aneurysms and ectasia in 15–25% of untreated cases, and which can lead to ischaemic heart disease and sudden death either at the time or years later. The aneurysms usually develop between the second week and the second month of the illness. Early treatment with immunoglobulin, oral aspirin and possibly IV methylprednisolone has been shown to be effective in reducing the prevalence of coronary artery abnormalities. Echocardiography is used to detect the aneurysms and determine prognosis.
Mumps is an acute infectious disease caused by a paramyxovirus with an affinity for the salivary glands and meninges. It is usually transmitted by respiratory secretions or saliva. A third of infections are asymptomatic, and most of the others have non-specific symptoms, such as fever, headache, malaise, myalgia and anorexia. The classic parotitis occurs in only two-thirds of clinical cases and is usually bilateral. The submandibular and sublingual glands are less commonly involved. About 6% of patients will have presternal oedema resembling cellulitis of the neck.
Mumps can result in spontaneous abortion if contracted in the first trimester of pregnancy. Maternal infection is not associated with an increased risk of congenital malformations.
Prior to vaccination, cases peaked in the 5–9-year age group; however, since 2000 it is now most commonly seen in adolescents and young adults. Recent outbreaks have occurred in the developed world in areas of declining vaccination rates.
Enlargement of the cervical lymph glands can be mistaken for parotitis but the correct diagnosis is indicated by the anatomy of this area. Lymph nodes are posteroinferior to the ear lobe; the parotid gland is anterior and, when enlarged, obscures the angle of the mandible.
Bacterial (suppurative) parotitis is associated with toxaemia and results in a high leucocyte count. The skin over the parotid gland is tense and shiny and the Stensen duct might discharge pus.
Rare disorders such as Sjögren syndrome can be misdiagnosed as mumps.
The complications are summarised in TABLE 93.6.
Table 93.6Complications of mumps ||Download (.pdf) Table 93.6 Complications of mumps
Meningeal symptoms (10%)
Abdominal pain (transient)
Arthritis (one or several joints)
Deafness (usually transient)
Orchitis, usually unilateral, occurs in 15–30% of postpubertal males, developing 3–4 days after parotitis. Subsequent sterility is rare, even if both testes are affected.
Aseptic meningitis is common but benign. Many patients suffer transient abdominal pain and vomiting.
Treatment is symptomatic. Paracetamol may be prescribed for fever, meningitis and orchitis. The patient with orchitis should use supportive underwear. Children should be excluded until 9 days after the onset of the parotitis.
Although glandular fever is more common in adolescents and young adults, it can occur in young children but is often asymptomatic or atypical. The differential diagnosis includes cytomegalovirus infection and acute lymphatic leukaemia. Diagnosis is confirmed by specific antibody tests. Refer to CHAPTER 28.
Pertussis (whooping cough) is a respiratory infection (a bronchitis) caused by Bordetella pertussis and occurs worldwide. Other organisms (Bordetella parapertussis, Mycoplasma pneumoniae, Chlamydia pneumoniae) can cause a pertussis-like syndrome. Despite vaccination, pertussis remains prevalent in Australia, and is the least well-controlled vaccine-preventable disease. Between 2000 and 2010 multiple epidemics caused over 139 000 confirmed cases.
The greatest risk of severe infection and complications is to infants with their soft and easily damaged airways, especially before the first 2 vaccine doses are administered. Adolescents and adults with waning immunity (both from vaccination and previous infection) are often the source of infection, in particular the parents (>50% of identified primary cases).
Pertussis is highly infectious, with B. pertussis spreading to >90% of household contacts. The incubation period is 7 to 20 days. The classical paroxysmal cough followed by an inspiratory whoop is less common in older children and adults, or children who have partial immunity from vaccination. A prolonged cough may be the only presenting feature, and in local epidemics every cough needs to be approached with the suspicion of pertussis.
B. pertussis accounts for 7% of cough illnesses in adults, and given that each year 25% of adults have a cough ≥5 days duration, many cases go undiagnosed. The primary goal of preventing complications and deaths is centred on protecting children, particularly infants (see Prevention below). The fatality rate in unvaccinated infants less than 6 months is 8 per 1000 cases. The most common cause of death is pertussis pneumonia, sometimes complicated by seizures and hypoxic encephalopathy. Apnoea and cyanosis from coughing spasms are also common in the very young.
Even in adults the cough can be very distressing and prolonged. Pertussis is also referred to as the ‘100 day cough’. This can lead to issues with sleep disturbance, work performance (especially when dealing with machinery or driving) and rarely rib fractures.
Classic whooping cough is characterised by cough and coryza for 1 week (catarrhal phase) followed by paroxysms of a more pronounced cough (paroxysmal phase). Fever is uncommon, there are often no other clinical signs, and children are well between coughing paroxysms. Vomiting may follow a coughing spasm (a ‘cough-vomit’).
As well has having a high index of suspicion with coughing patients (both immunised and non-immunised), particularly in outbreaks, any suspicion should lead to PCR testing of nasopharyngeal aspirate/swab.
Neurological: asphyxia, hypoxia, seizures, cerebral haemorrhages
Pulmonary: atelectasis, pneumonia, pneumothorax, bronchiectasis
Treatment during the catarrhal phase or early in the paroxysmal stage may ameliorate symptoms. Treatment early in the disease will help reduce infectiousness; however, once the cough has been present for 3 weeks there is little risk of infectiousness. Options include:
Cough mixtures are ineffective. Good ventilation is important: avoid dust and smoke, and also emotional excitement and overfeeding during the paroxysmal phase.
All infants under 6 months and older children with complications (e.g. apnoea, cyanosis, pneumonia, encephalopathy) require admission to hospital.
High-risk contacts of a pertussis case (those with close/household contact and who may be vulnerable to complications, or transmit to others who are vulnerable) should be treated with the same medications, dosage and duration as above. There is little evidence that prophylactic antibiotic treatment of contacts reduces secondary transmission outside of household settings (i.e. not in child-care centres, preschools, schools or workplaces). State public health officers should be contacted to determine which contacts require prophylaxis.
Active immunisation with pertussis vaccine is given at 2, 4 and 6 months, then at 4 years as per the NIP schedule. Other strategies to reduce the incidence of pertussis and its complications, particularly in infants, include:
a ‘cocoon’ strategy of vaccinating any adults who are or will be in close contact with an infant. Fathers and other adult contacts can be vaccinated before the birth
mothers should be vaccinated in pre-pregnancy planning or straight after delivery. Alternatively, if more than 5 years has elapsed since their last previous dose, a pertussis vaccine should be given in their third trimester (which will boost maternal antibodies that are transmitted in utero to the about-to-be-newborn)
a single booster dose of pertussis-containing vaccine is recommended in health care workers and other adults in regular contact with young children (booster required after 10 years)
Herpes simplex virus (HSV) infection is common and widespread. Primary HSV infection is usually a disease of childhood readily transmitted through direct contact, with the majority of the population being infected in early childhood. Many cases are asymptomatic or non-specific. The specific gingivostomatitis occurs in 25–30% of cases and can be severe and acute.
Typical clinical features of the primary infection:
children 1–3 years
fever and refusal to feed
ulcers on gums, tongue and palate
prone to dehydration
may be lesions on face and conjunctivae
resolution over 7–14 days
Pushing fluids and monitoring for dehydration is important. Topical lignocaine preparations can help. Paracetamol is often not useful, though if the child is very distressed, combined ibuprofen and paracetamol compounds can be considered. Topical antivirals usually do not contribute and are not recommended.
Serious complications (seek specialist advice):
encephalitis can develop in otherwise healthy children (see CHAPTER 30)
eczema herpeticum—children with eczema can get widespread severe herpetic lesions
disseminated HSV infection in neonates (avoid contact until recovered)
HSV can be a serious issue in the immunocompromised patient
Impetigo (school sores) is a contagious superficial bacterial skin infection caused by Streptococcus pyogenes or Staphylococcus aureus or a combination of these two virulent organisms.
There are two common forms:
vesiculopustular with honey-coloured crusts (either strep or staph)
bullous type, usually S. aureus
If mild with small lesions and a limited area:
soak a clean cloth in a mixture of ½ cup white vinegar and 1 L of tepid water. Apply the compress to moist areas for 10 minutes several times a day then wipe off crusts (alternatively just use soap and water)
antiseptic (povidone iodine, chlorhexadine) or mupirocin (Bactroban), a small amount tds for 10 days. Topical antibiotics other than mupirocin 2% (Bactroban) are not recommended
general measures while still oozing or crusted:
– cover the sores
– avoid close contact with others (especially touch and bathing contact)
– regular hand washing
– use separate towels and cloths
– change and launder clothes and linen daily
If extensive and causing systemic symptoms:
Boils (furunculosis) and carbuncles can use the same treatment as impetigo.
The child should be excluded from child-care settings until antibiotic treatment has commenced. Any sores on exposed skin should be covered with a watertight dressing.2
Head lice is an infestation caused by the louse Pediculus humanus capitis (see FIG. 93.11). The head louse is about 1–3 mm in length, white to grey, wingless and has a flat elongated body. They spread through close contact, and do not jump or fly. The female louse lays eggs (or ‘nits’), which are glued to the hairs a few millimeters from the scalp. The nit moves away from the scalp as the hair grows. They hatch at around 8 days, mature into adults in about 10 days and live for about a month.
Head lice spread from person to person by direct contact, such as sitting and working very close to one another. They can also spread by the sharing of combs, brushes and headwear, especially within the family. Children are the ones usually affected, but people of all ages and from all walks of life can be infested. It is more common in overcrowded living conditions but is not a reflection of poor hygiene. Resistance to the usual agents is becoming a problem.
Infestations can vary from a few dozen to hundreds of lice and eggs.
Asymptomatic or itching of scalp
White spots of nits can be mistaken for dandruff
Unlike dandruff, the nits cannot be brushed off
Diagnosis by finding lice (or nits)
Occasionally the eyelashes can be affected (use physical removal methods outlined below)
‘Wet combing’ (see below) improves detection rate
Treatment can be based on physical methods, chemical methods or both (the most effective).
Inspection—look for both lice and nits behind and above the ears and at the back of the scalp.
Treat all members of family at the same time.
Have ready a metal nit comb (available at pharmacies), a good light, some paper towels or tissues and lots of cheap hair conditioner. Sitting a child in front of the TV will help them keep still (it takes around 30 minutes).
Wet the hair with a handful or two of conditioner.
Work through the hair in sections, removing resistant nits by combing down the hair towards the shaft.
Wipe the conditioner onto tissues or paper towels, where the lice and nits will be visible.
Repeat the combing routine for at least 2 more consecutive nights. Repeat weekly until no lice are found on 3 consecutive nights (nits may persist but do not necessarily mean active infection—they may be empty or dead eggs). Other physical measures include:
machine wash bed-linen, clothes, towels in hot water
items that can’t be washed such as soft toys/helmets should be placed in an airtight plastic bag for two weeks
spray hairbrushes and combs with fly spray
Insecticides used to treat head lice include:
These applications can be irritating to the scalp, so use caution in children prone to atopic dermatitis; following the manufacturer’s instructions carefully is important. A second application 7 days after the first may be required.
Many other methods are used and recommended for head lice, both commercially available or ‘home remedies’, which may or may not be useful. These include suffocating agents (e.g. mayonnaise, olive oil, petroleum jelly), natural oils and cutting the hair short (especially in boys e.g. a No. 1 cut).
Treatment failure and/or reinfestation is common. The former can be from inappropriately applied treatments, resistance to chemical treatments or misdiagnosis of old nits as active infection. Cotrimoxazole can be trialled for resistant head lice. Community or school-wide education programs can also keep infestation rates down.