Pediatric Infectious Diseases
Infection is what most sick children in India have, and the paper knows it. The difficulty is not that paediatric infections are obscure. It is that a small number of organisms produce an enormous number of presentations, and the same organism behaves differently at two weeks, two years and twelve years of age.
Adult infectious disease can often be approached by asking which organ is involved and which organism lives there. In children that approach fails early, because the commonest presentation is a febrile child with nothing localising at all.
1. Timing Is the Diagnostic Instrument
The organising tool for this chapter is that timing carries more diagnostic information in paediatric infection than in almost any other field, and it does so in three separate senses.
Timing of acquisition divides infection into congenital and postnatal. An infection acquired across the placenta at ten weeks of gestation damages organs that are still forming, and produces a pattern of malformation that no postnatal infection can imitate.
Timing of the rash against the fever separates the exanthems from one another almost completely. The organisms are unrelated; the temporal signatures are distinctive and reproducible.
Timing of clinical deterioration decides disposition. A child with dengue is most at risk not at the height of the fever but as the fever settles, and a child in compensated shock looks deceptively stable until the moment they do not.
Hold these three axes and most stems resolve before you have identified the organism.
2. Recognising the Sick Child Before Naming the Disease
A child's cardiovascular reserve is larger than an adult's, and this is dangerous rather than reassuring. A child in shock maintains blood pressure by tachycardia and intense vasoconstriction, and can do so until a very large fraction of circulating volume is lost.
The consequence is that hypotension in a child is a preterminal sign, not an early one. Waiting for it means waiting too long.
The signs that appear before it are tachycardia, cool peripheries, prolonged capillary refill, reduced urine output and altered mental state. The last is the one that families notice and clinicians discount.
IMNCI and the danger signs
The Integrated Management of Neonatal and Childhood Illness approach exists because most sick children in India are first seen by someone who cannot investigate. It replaces diagnosis with classification into coloured action bands.
The general danger signs in a child aged two months to five years are inability to drink or breastfeed, vomiting everything, convulsions, and lethargy or unconsciousness. Any one of them mandates urgent referral whatever the presenting complaint.
In the young infant under two months the list widens, because sepsis in this group is non-specific: poor feeding, movement only on stimulation, temperature instability in either direction, severe chest indrawing, and a bulging fontanelle.
Fever is an unreliable guide to severity in the newborn, who may be hypothermic instead. Temperature instability, not fever, is the signal.
3. Fever Without a Focus
The management of the febrile child without localising signs is decided almost entirely by age, because the risk of serious bacterial infection falls steeply with it.
| Age | Risk | Approach |
|---|---|---|
| Under 28 days | Highest | Full sepsis evaluation including lumbar puncture, admit, empirical antibiotics |
| 1 to 3 months | Intermediate | Investigate; low-risk criteria may permit closer observation |
| Over 3 months, immunised | Low | Clinical assessment, urine testing, selective investigation |
Urinary tract infection is the commonest occult serious bacterial infection in a young febrile child, and it is missed because nobody examines urine in a child with no urinary symptoms. Infants with urinary infection present with fever, vomiting and poor feeding, never with dysuria.
The landscape changed with conjugate vaccines. Occult pneumococcal bacteraemia was once the central concern of this topic; widespread pneumococcal and Haemophilus type b conjugate vaccination has made it uncommon in fully immunised children, which is why immunisation status is part of the risk assessment and appears in stems deliberately.
4. The Exanthems: Reading the Rash Against the Fever
| Disease | Agent | Temporal signature |
|---|---|---|
| Measles | Measles virus | Three to four days of prodrome, Koplik spots, then rash while fever continues |
| Rubella | Rubella virus | Mild or absent prodrome, rash with tender posterior auricular and occipital nodes |
| Chickenpox | Varicella zoster | Crops in successive waves, so all stages coexist at once |
| Scarlet fever | Group A Streptococcus | Sandpaper rash with sore throat, strawberry tongue, later desquamation |
| Roseola | Human herpesvirus 6 | Three days of high fever, then rash appears as fever disappears |
| Erythema infectiosum | Parvovirus B19 | Slapped cheek, then lacy rash; child is no longer infectious once the rash appears |
| Hand, foot and mouth | Coxsackie A16, enterovirus 71 | Oral ulcers with vesicles on palms, soles and buttocks |
Three of these carry a rule that is examined far more often than the rash itself.
Roseola is the one where the rash appears as the fever breaks. The parent describes three days of alarmingly high fever in a child who was otherwise well, then a rash on the day the child improved. That sequence is diagnostic and nothing else reproduces it.
Chickenpox is the one where lesions of all stages are present simultaneously, because crops appear over several days. This is the classical discriminator from smallpox, in which lesions were uniform in stage.
Parvovirus B19 is the one that is infectious before the rash and harmless after it. Excluding these children from school is pointless. The clinical importance lies elsewhere: the virus infects erythroid precursors, causing aplastic crisis in children with haemolytic anaemia and hydrops in the fetus.
5. Measles and India's Elimination Effort
Measles deserves separate treatment because it remains a major cause of childhood death and because it is under active elimination effort.
The prodrome is the three Cs, cough, coryza and conjunctivitis, with high fever. Koplik spots on the buccal mucosa appear one to two days before the rash and are pathognomonic, but they fade quickly and are frequently gone by the time the child is brought in.
The rash begins behind the ears and at the hairline, spreads downwards over three days, and fades in the same order leaving brownish staining and fine desquamation.
The fever continuing after the rash has appeared is the sign of complication, most often pneumonia, which is the commonest cause of death, or otitis media, or diarrhoea.
Two late complications are examined. Acute post-measles encephalitis occurs within days. Subacute sclerosing panencephalitis occurs seven to ten years later, presenting with declining school performance and myoclonic jerks, and is uniformly fatal. Risk is highest when measles is contracted under two years of age.
Vitamin A is given to every child with measles, on two consecutive days, with a third dose later if there is eye disease. It reduces mortality substantially, and the biological reason is that measles depletes vitamin A stores at the moment they are most needed for epithelial repair and immune function.
India has repeatedly reset its measles and rubella elimination target, missing 2015, 2020 and 2023, and is now working to a 2026 goal under the National Zero Measles-Rubella Elimination Campaign launched in April 2025. Coverage stands near 94 percent for the first dose and 92 percent for the second, with measles cases falling by roughly 73 percent in 2024, though district outbreaks continue.
6. Congenital Infection: Acquired Before Birth
The TORCH group is toxoplasmosis, others including syphilis, rubella, cytomegalovirus and herpes simplex. They are grouped because they share a route rather than a biology.
Gestational timing determines the damage. Infection in the first trimester, when organs are forming, causes malformation. Infection later causes inflammation and growth restriction rather than structural defects, which is why congenital rubella syndrome is a first-trimester disease.
| Infection | Discriminating features |
|---|---|
| Congenital rubella | Cataract, sensorineural deafness, patent ductus arteriosus or pulmonary artery stenosis |
| Cytomegalovirus | Periventricular calcification, microcephaly, deafness that may be progressive |
| Toxoplasmosis | Diffuse intracranial calcification, hydrocephalus, chorioretinitis |
| Congenital syphilis | Snuffles, desquamating rash on palms and soles, osteochondritis, later Hutchinson teeth |
| Herpes simplex | Usually acquired during delivery, not in utero; skin, eye and mouth disease, or disseminated |
The calcification pattern separates cytomegalovirus from toxoplasmosis, and it is the single most examined discriminator in this section. Cytomegalovirus calcifies around the ventricles; toxoplasmosis calcifies diffusely throughout the parenchyma.
Cytomegalovirus is the commonest congenital infection and the commonest infectious cause of sensorineural deafness. Most infected infants are asymptomatic at birth, and deafness may appear later, which is the argument for newborn hearing screening.
Herpes simplex is the exception to the grouping, because it is usually acquired during passage through the birth canal rather than transplacentally. Disseminated neonatal herpes carries very high mortality and is treated with high-dose intravenous aciclovir.
7. Tuberculosis in Children
Childhood tuberculosis is not adult tuberculosis in a smaller person, and the differences are almost all consequences of one fact: children have paucibacillary disease.
Because there are few organisms, sputum smear is usually negative, and children under about eight cannot produce sputum in any case. Gastric aspirate or induced sputum is used instead, and diagnosis frequently rests on the combination of contact history, symptoms, tuberculin testing and chest radiography rather than on bacteriological confirmation.
Because immunity is immature, children progress from infection to disease more often and faster, and are far more likely to develop disseminated and meningeal disease, particularly under two years of age.
The classical presentation is not cough but persistent unremitting fever, failure to gain weight, and loss of playfulness, in a child with a household contact.
Tuberculous meningitis is the presentation that must not be missed. It develops over weeks rather than days, with a prodrome of irritability and behaviour change before meningism, and outcome depends almost entirely on the stage at which treatment starts.
Two current points are worth carrying. WHO recommends a four-month regimen for non-severe drug-susceptible disease in children and adolescents aged 3 months to 16 years, on the strength of the SHINE trial, which found four months non-inferior to six. And tuberculosis preventive therapy for household child contacts is a programme priority, because the child who is contact-traced today is the meningitis case avoided next year.
8. Diarrhoea and Dehydration
Diarrhoea kills by dehydration, not by infection, and the entire management follows from that.
Assessment is clinical. Two of the following place a child in some dehydration: restless or irritable, sunken eyes, drinks eagerly, skin pinch returns slowly. Lethargy, inability to drink and a very slow skin pinch indicate severe dehydration.
| Plan | Applies to | Treatment |
|---|---|---|
| A | No dehydration | Extra fluids at home, continued feeding, zinc |
| B | Some dehydration | Oral rehydration solution over four hours under supervision |
| C | Severe dehydration | Intravenous Ringer lactate immediately, then oral rehydration |
Low-osmolarity oral rehydration solution replaced the older formulation because it reduces stool output, vomiting and the need for unscheduled intravenous fluid. Its mechanism is the sodium-glucose co-transporter in the small intestine, which continues to work in most infective diarrhoea, so water follows sodium into the circulation even while secretion continues.
Zinc is given for 14 days in every case. It shortens the episode, reduces stool volume, and reduces the incidence of further episodes over the following two to three months.
Feeding is continued throughout, including breastfeeding. Withholding feeds prolongs recovery and worsens nutritional status.
Antibiotics have almost no place. The exceptions are cholera and dysentery, meaning visible blood in stool, which is treated as shigellosis. Antimotility agents are contraindicated in children.
9. Pneumonia and Acute Respiratory Infection
Pneumonia remains a leading cause of under-five death, and its recognition in the field rests on counting breaths.
| Age | Fast breathing threshold |
|---|---|
| Under 2 months | 60 or more per minute |
| 2 to 12 months | 50 or more per minute |
| 12 months to 5 years | 40 or more per minute |
Fast breathing alone classifies as pneumonia and is treated with oral amoxicillin at home. Lower chest wall indrawing or any general danger sign classifies as severe pneumonia and requires referral with injectable antibiotics and oxygen.
The reason a respiratory rate outperforms auscultation in this setting is practical: it requires no equipment, no training in interpretation, and no cooperation from the child.
Bronchiolitis is the important mimic in infants under one year, typically respiratory syncytial virus, with wheeze and hyperinflation following a coryzal prodrome. It is managed with oxygen, feeding support and nothing else. Antibiotics, bronchodilators and steroids do not help.
10. Dengue and the Febrile Child in the Tropics
Dengue is classified by the 2009 WHO system into dengue, dengue with warning signs, and severe dengue.
The warning signs are abdominal pain or tenderness, persistent vomiting, clinical fluid accumulation, mucosal bleeding, lethargy or restlessness, hepatomegaly greater than 2 cm, and a rising haematocrit with a falling platelet count.
The counterintuitive point, and the one examined, is that the critical phase begins as the fever settles, around days three to seven. Plasma leakage through capillaries is what causes shock, and it occurs at defervescence.
A child whose fever has broken but who is now quiet, cold and tachycardic is not recovering. Platelet count is a poor guide to severity; haematocrit and clinical state are the guides.
Two other tropical causes deserve mention. Enteric fever presents with stepwise fever, relative bradycardia in older children, and abdominal symptoms, and blood culture in the first week is the diagnostic test. Malaria must be excluded by rapid test or smear in any febrile child in an endemic district, because severe falciparum malaria in children presents as cerebral malaria or severe anaemia rather than the classical paroxysms.
11. Meningitis and Paediatric HIV
Meningitis organisms vary by age, and this is a standard recall question.
| Age | Common organisms |
|---|---|
| Neonate | Group B Streptococcus, Escherichia coli, Listeria |
| Infant and child | Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae type b |
Neck stiffness is unreliable under 18 months. A bulging fontanelle, irritability that worsens on handling, and refusal to feed carry more weight.
Lumbar puncture is deferred, not cancelled, in raised intracranial pressure, focal signs, cardiovascular instability or coagulopathy. Antibiotics are given first in that situation, because delaying treatment for a test is the greater harm.
Paediatric HIV requires virological testing, not antibody testing, under 18 months, because maternal immunoglobulin G crosses the placenta and a positive antibody test in an exposed infant may simply be the mother's antibody. Early infant diagnosis uses DNA polymerase chain reaction from six weeks of age.
12. Worked Examples
Example 1. A 10-month-old has had three days of fever to 40 degrees with no other findings, and today the fever has gone and a maculopapular rash has appeared over the trunk. Diagnosis?
Roseola infantum, caused by human herpesvirus 6. The temporal sequence is the whole diagnosis: high fever in a child who otherwise looks well, then rash appearing precisely as the fever resolves. In measles the rash appears while the fever continues, and the child looks unwell throughout.
Example 2. A neonate has microcephaly with periventricular calcification and failed newborn hearing screening. Which congenital infection?
Cytomegalovirus. Periventricular calcification distinguishes it from toxoplasmosis, in which calcification is diffuse. Cytomegalovirus is also the commonest congenital infection and the commonest infectious cause of sensorineural deafness, which may be progressive and appear after a normal early assessment.
Example 3. A 6-year-old with dengue has been febrile for four days. The fever has settled today. Pulse 130, capillary refill 3 seconds, haematocrit risen from 36 to 45, platelets 40,000. What is happening?
The child has entered the critical phase and is in compensated shock from plasma leakage. Defervescence marks the onset of leakage, not recovery. The rising haematocrit with falling platelets is the key warning sign; the normal blood pressure is misleading, since children maintain pressure until late. Intravenous crystalloid is required now.
Example 4. An 18-month-old has had fever and weight loss for six weeks. The father is on treatment for pulmonary tuberculosis. Sputum cannot be obtained. What is the approach?
Childhood tuberculosis is paucibacillary, so bacteriological confirmation frequently fails and diagnosis is built from contact history, symptoms, tuberculin testing and chest radiography. Gastric aspirate or induced sputum is attempted. Age under two carries a high risk of disseminated and meningeal disease, so evaluation must be prompt rather than sequential.
Summary
Timing is the diagnostic instrument. Timing of acquisition separates congenital from postnatal infection, timing of the rash against the fever separates the exanthems, and timing of deterioration decides disposition.
Hypotension in a child is preterminal. Tachycardia, prolonged capillary refill and altered mental state come first, and the general danger signs mandate referral whatever the diagnosis.
Fever without focus is stratified by age. The neonate is investigated fully; urinary tract infection is the commonest occult bacterial infection; conjugate vaccination has changed the risk in immunised children.
Roseola's rash appears as the fever breaks, chickenpox shows all lesion stages at once, and parvovirus stops being infectious when the rash starts.
Measles kills through pneumonia, causes subacute sclerosing panencephalitis years later, and requires vitamin A in every case.
Periventricular calcification means cytomegalovirus; diffuse calcification means toxoplasmosis.
Childhood tuberculosis is paucibacillary, so diagnosis is clinical and radiological, meningeal disease is the danger under two, and four months suffices for non-severe disease.
Diarrhoea kills by dehydration, so oral rehydration solution, zinc for 14 days and continued feeding are the treatment, and antibiotics almost never are.
Count the breaths. Fast breathing is pneumonia treated at home; chest indrawing is severe pneumonia requiring referral.
Dengue deteriorates at defervescence, and haematocrit with clinical state, not platelet count, guides management.
