Specific Infections

What infections does Streptococcus pneumoniae (pneumococcus) cause and who is at highest risk of invasive disease?

S. pneumoniae is commonly carried asymptomatically in the nasopharynx, especially in young children, who spread it via respiratory droplets.
It can cause minor infections (pharyngitis, otitis media, conjunctivitis, sinusitis) as well as invasive disease including pneumonia, bacterial sepsis, and meningitis.

Invasive disease mainly occurs in young infants because their immune systems respond poorly to encapsulated pathogens.

Children at increased risk include those with hyposplenism or asplenism (e.g., sickle cell disease), who should receive daily prophylactic penicillin.

What is Scarlet Fever, what causes it, and how is it treated?

Scarlet fever is caused by an erythrogenic exotoxin released during Group A streptococcal (GAS) pharyngitis.
It presents as a diffuse, erythematous maculopapular rash with a sandpaper texture appearing shortly after pharyngitis, spreading to the face, trunk, and extremities with increased density around the neck, axillae, and groin.
There is circumoral pallor (skin around the mouth is spared).
The tongue is initially white-coated, then desquamates to reveal a red "strawberry tongue" with prominent papillae.
Desquamation of fingertips and toes may also occur.

Treatment: a full 10-day course of antibiotics (penicillin V or erythromycin) is required to eradicate GAS and prevent complications such as rheumatic fever and post-streptococcal glomerulonephritis. Antibiotics hasten recovery by only about 16 hours on average.

What is Impetigo, how does it present, and how is it treated?

Impetigo is a localized, highly contagious skin infection caused by Staphylococcus aureus or Group A Streptococcus, most common in infants and young children, especially those with pre-existing skin disease (e.g., atopic eczema).
Lesions appear on the face, neck, and hands, beginning as erythematous macules that progress to vesicles, pustules, or bullae.
Rupture of these lesions leads to the characteristic confluent honey-coloured crusted lesions. The infection spreads by autoinoculation of infected exudate.

Treatment:
topical antibiotics (e.g., mupirocin) for mild cases;
narrow-spectrum systemic antibiotics (e.g., flucloxacillin) for more severe infections;
co-amoxiclav or cephalexin can also be used for better adherence.
Affected children must not attend nursery/school until lesions are dry.

What is Staphylococcal Scalded Skin Syndrome (SSSS), how does it occur, and how is it managed?

SSSS is caused by an exfoliative toxin produced by Staphylococcus aureus, which cleaves the skin through the granular cell layers of the epidermis.
It mainly affects infants and young children, who develop fever, malaise, and a purulent crusting localized infection around the eyes, nose, and mouth, followed by widespread erythema and skin tenderness.

Key finding:
Nikolsky sign — areas of epidermis separate on gentle pressure, leaving denuded, raw-looking skin that subsequently dries and heals without scarring.
Critical warning: its appearance must NOT be mistaken for a scald from non-accidental injury.

Management: IV antistaphylococcal antibiotics (e.g., flucloxacillin), analgesia, and monitoring of hydration and fluid balance.

What is Panton-Valentine Leukocidin (PVL) S. aureus and what serious diseases does it cause?

Panton-Valentine Leukocidin is a toxin produced by fewer than 2% of S. aureus strains (both MSSA and MRSA). It targets leukocytes and causes severe tissue destruction.

Clinical manifestations:
(1) Recurrent skin and soft-tissue infections;
(2) Necrotizing fasciitis — rapidly spreading subcutaneous infection involving skin down to fascia and muscle, causing necrosis, severe pain, and systemic illness requiring ICU; IV antibiotics alone are insufficient — urgent surgical debridement is essential; IVIG may also be given;
(3) Necrotizing haemorrhagic pneumonia following an influenza-like illness — carries high mortality;
(4) In children, the pro-coagulant state frequently results in venous thrombosis.

What are the main clinical manifestations of Herpes Simplex Virus (HSV) infections in children?

HSV infections are mostly asymptomatic, but several important clinical forms exist:
(1) Gingivostomatitis — most common primary HSV illness in children (ages 10 months–3 years); painful vesicular ulceration of lips, gums, tongue, and hard palate with high fever; may require IV fluids and aciclovir;
(2) Eczema herpeticum — widespread vesicular lesions on eczematous skin; can lead to secondary bacterial infection and septicaemia; treat with IV aciclovir;
(3) Herpetic whitlows — painful erythematous pustules on fingers from autoinoculation;
(4) Eye disease — blepharitis, conjunctivitis, and potentially dendritic corneal ulceration leading to scarring/vision loss; requires urgent ophthalmologic assessment;
(5) CNS disease — aseptic meningitis or encephalitis;
(6) Neonatal HSV — focal, encephalitic, or disseminated; high morbidity and mortality;
(7) Disseminated infection in immunocompromised — pneumonia, oesophagitis, proctitis, multi-organ involvement.

Treatment for severe forms: aciclovir (a viral DNA polymerase inhibitor).

What are the clinical features and complications of Chickenpox (primary VZV infection)?

Chickenpox spreads by respiratory droplets with an incubation period of 10–23 days (median 14).

Clinical features:
fever followed by an itchy rash appearing in crops over 3–5 days, with 50–500 lesions starting on the head/trunk and progressing to the peripheries. Lesions progress from papules → vesicles with surrounding erythema → pustules → crusts simultaneously, and may occur on the palate.
Scratching can cause scarring or secondary infection.

Complications:
(1) Secondary bacterial superinfection (Staph/Strep) — may cause toxic shock syndrome or necrotizing fasciitis; suspect if fever recurs after initially settling;
(2) CNS: cerebellitis (most characteristic — child becomes ataxic ~1 week after rash, usually resolves within a month), generalized encephalitis, and aseptic meningitis;
(3) Purpura fulminans — widespread blood clotting in small vessels (microvasculature) due to antibodies cross-reacting with protein C or S, increasing clotting risk;
(4) In immunocompromised hosts: haemorrhagic lesions, pneumonitis, progressive disseminated infection (up to 20% mortality).

Key warning: never admit a chickenpox contact to a ward with immunocompromised children.

How is Chickenpox treated and prevented, especially in high-risk patients?

Treatment for most healthy children is supportive.
Oral aciclovir has highly variable absorption and is NOT recommended in the UK.
For immunocompromised children: IV aciclovir initially, switchable to oral valaciclovir if no organ dissemination has occurred.
Prevention in high-risk immunocompromised individuals (with deficient T-cell function): human varicella zoster immunoglobulin (VZIG) is recommended after contact with chickenpox; protection is not absolute and depends on how soon after contact it is given.
A live attenuated varicella vaccine is available and used routinely in some countries (not in the UK routinely, but can be given to siblings of at-risk children). Human varicella zoster immunoglobulin is also recommended for maternal chickenpox shortly before or after delivery.

What is Shingles (herpes zoster), how does it differ in children vs. adults, and what associations should trigger concern?

Shingles is caused by reactivation of latent VZV in sensory nerve ganglia, producing a vesicular eruption in a dermatomal distribution, most commonly in the thoracic region (though any dermatome can be affected). It is uncommon in children.

Key differences from adults:
children rarely suffer from post-herpetic neuralgia.
Shingles in childhood is more common in those who had primary VZV infection in the first year of life.
Clinical concern: recurrent shingles or multidermatomal shingles is strongly associated with underlying immunocompromise (e.g., HIV infection) and suggests a primary or secondary T-cell immune defect.
In immunocompromised individuals, reactivated VZV can disseminate to cause severe systemic disease.

What are the clinical features, diagnosis, and management of Infectious Mononucleosis (EBV / glandular fever)?

EBV causes infectious mononucleosis; transmission is primarily by oral contact. Most infections are subclinical.
Symptomatic disease (mainly older children/adolescents) features:
fever, malaise, severe tonsillitis/pharyngitis (may compromise breathing),
prominent cervical lymphadenopathy, petechiae on the soft palate, splenomegaly (50%), hepatomegaly (10%), maculopapular rash (5%), and jaundice.

Diagnosis:
atypical lymphocytes (large T cells) on blood film; positive monospot test (detects heterophile antibodies — may be negative in young children or early infection); seroconversion with VCA IgM/IgG and EBNA antibodies.

Treatment: mainly symptomatic; corticosteroids if airway is compromised; penicillin if GAS is co-isolated.
Critical warning: NEVER give ampicillin or amoxicillin — they cause a florid maculopapular rash in EBV-infected patients.
Symptoms persist 1–3 months; fatigue is prominent in adolescents.
EBV is also linked to Burkitt lymphoma, nasopharyngeal carcinoma, and lymphoproliferative disease in immunocompromised hosts.

What is CMV infection and what are its manifestations in different host groups?

CMV is transmitted via saliva, genital secretions, or breastmilk (rarely via blood products, organ transplants, or transplacentally).
In normal hosts, it causes mild or subclinical infection, or a mononucleosis-like syndrome.
Unlike EBV, pharyngitis and lymphadenopathy are less prominent; patients may have atypical lymphocytes on blood film but are heterophile antibody (monospot) negative.

In immunocompromised hosts (e.g., transplant recipients, HIV patients), CMV is a major pathogen causing: retinitis, pneumonitis, bone marrow failure, encephalitis, hepatitis, oesophagitis, and enterocolitis.

Transplant recipients are closely monitored by blood PCR; CMV-negative blood products are used;
ganciclovir prophylaxis is given; and CMV-positive organs into CMV-negative recipients are avoided where possible.

Treatment: IV ganciclovir, oral valganciclovir, foscarnet, or cidofovir (all can cause serious side effects).
Congenital CMV infection may be present at birth or manifest at an older age.

What is Roseola Infantum (Exanthem Subitum) and what causes it, and what are its diagnostic pitfalls?

Roseola infantum is classically caused by Human Herpesvirus 6 (HHV-6), or less commonly HHV-7.
Most children are infected by age 2 via oral secretions of a family member.
Clinical features:
high fever with malaise lasting a few days, followed by a generalized macular rash appearing as the fever wanes (first on the trunk, then spreading to the face and extremities).
Many children have a febrile illness without rash; many have subclinical infection.
Diagnostic pitfalls:
(1) Frequently misdiagnosed as measles or rubella — these are rare in the UK and must be confirmed by PCR/serology if suspected;
(2) During the febrile stage, antibiotics are often prescribed, and when the rash appears, it is mistakenly attributed to a drug allergy.
Rare complications: aseptic meningitis, encephalitis, hepatitis, and mononucleosis-like syndrome.

What is Human Parvovirus B19 and what are its different clinical syndromes, including in vulnerable populations?

HPV-B19 causes erythema infectiosum (fifth disease / "slapped cheek syndrome").
It infects erythroblastoid red cell precursors in the bone marrow.

Transmission: respiratory secretions, vertical (mother to fetus), and blood products.
Clinical syndromes:
(1) Asymptomatic infection — most common
(2) Erythema infectiosum — viraemic phase of fever, malaise, headache, myalgia, followed ~1 week later by a slapped-cheek rash on the face, progressing to a maculopapular "lace-like" rash on the trunk and limbs; arthralgia/arthritis more common in adults;
(3) Aplastic crisis — most serious complication; occurs in children with chronic haemolytic anaemias (sickle cell disease, thalassaemia) or immunocompromised children who cannot produce neutralizing antibodies — they cannot compensate for the temporary cessation of red cell production;
(4) Fetal hydrops — maternal infection transmitted to the fetus may cause severe fetal anaemia and death, though most infected fetuses recover.

What are enteroviruses and what clinical syndromes do they cause in children?

Human enteroviruses (coxsackieviruses, echoviruses, polioviruses) are common childhood pathogens transmitted primarily by faecal-oral and respiratory droplet routes; infections peak in summer and autumn.
Over 90% of infections are asymptomatic or cause a non-specific febrile illness, sometimes with a blanching rash or fine petechiae over the trunk.

If the rash is non-blanching, admission for observation and parenteral antibiotics (e.g., ceftriaxone) until negative blood cultures are needed.

Clinical syndromes:
(1) Hand, foot, and mouth disease — painful vesicular lesions on hands, feet, mouth, tongue, and buttocks; mild systemic features;
(2) Herpangina — vesicular/ulcerated lesions on the soft palate and uvula; anorexia, painful swallowing, fever; severe cases need IV fluids;
(3) Viral meningitis/encephalitis — enteroviruses are the most common cause of viral meningitis in high-income countries; long-term sequelae are rare;
(4) Pleurodynia (Bornholm disease) — fever, pleuritic chest pain, muscle tenderness;
(5) Myocarditis and pericarditis;
(6) Eczema coxsackium — vesicular/bullous eruption in eczematous children; resolves spontaneously, no treatment;
(7) Neonatal enteroviral sepsis syndrome — rare, severe, mimics bacterial sepsis, multiorgan failure; no effective antivirals; IVIG use controversial;
(8) Enterovirus D68 — mild respiratory illness or rarely severe respiratory illness/acute flaccid myelitis.

What are the clinical features and complications of Measles?

Measles spreads by droplets (highly infectious).
Incubation: ~10–14 days.
Prodrome: fever, cough, coryza (runny nose), and conjunctivitis.
Pathognomonic sign: Koplik spots — white spots on the buccal mucosa against a bright red background; pathognomonic but difficult to see; appear just before the rash.
Rash: maculopapular, spreading downward from behind the ears to the whole body; becomes blotchy and confluent; may desquamate in the second week.

Serious complications:
(1) Pneumonia — secondary bacterial or giant-cell pneumonia in immunocompromised;
(2) Encephalitis — ~1 in 5000 cases, a few days after onset; mortality 15%; long-term sequelae (seizures, deafness, hemiplegia, severe learning difficulties) in up to 40% of survivors;
(3) Subacute Sclerosing Panencephalitis (SSPE) — rare (1 in 100,000); manifests on average 7 years after infection; mostly in those infected before age 2; caused by a persistent variant of measles virus in the CNS; progressive neurological decline to dementia and death; diagnosed by high measles antibody in blood/CSF and EEG changes;
(4) In low-income countries: malnutrition and vitamin A deficiency worsen outcomes; give vitamin A and supportive care; ribavirin may be used in immunocompromised patients.

What is Mumps and what are its clinical features and complications?

Mumps is caused by a paramyxovirus spread by droplet infection.
Its incidence has declined dramatically due to the MMR vaccine, but outbreaks still occur in unvaccinated populations.

Incubation: 15–24 days.
Clinical features: fever, malaise, and parotitis (uncomfortable parotid gland swelling, initially may be unilateral then bilateral);
up to 30% of cases are subclinical.
Children may complain of earache or pain on eating/drinking.
Plasma amylase is often elevated; if associated with abdominal pain, consider pancreatic involvement.
Infectivity lasts up to 7 days after onset of parotid swelling.
The illness is generally mild and self-limiting.

Complications:
(1) Viral meningitis/encephalitis — lymphocytes in CSF in ~50%, meningeal signs in ~10%, encephalitis in ~1 in 5000;
(2) Orchitis — most feared complication, but uncommon in prepubertal males; usually unilateral; rarely causes infertility despite evidence of reduced sperm count;
(3) Hearing loss — usually unilateral and transient;
(4) Rarely: oophoritis, mastitis, arthritis.

What is Rubella (German measles) and why is it especially important in pregnancy?

Rubella is a mild viral disease in childhood caused by a togavirus. Incubation: 15–20 days.
Spread: respiratory route.
Prodrome: mild low-grade fever or none.
Rash: maculopapular, appearing first on the face and spreading centrifugally over the whole body; fades in 3–5 days.
Prominent lymphadenopathy, particularly of the suboccipital and postauricular nodes.
Rare childhood complications: arthritis, encephalitis, thrombocytopenia, myocarditis.
Clinical differentiation from other viral infections (including enteroviruses) is unreliable.

Critical importance in pregnancy:
Rubella during pregnancy can cause severe congenital rubella syndrome — cataracts, heart defects, deafness, and developmental delay.
If there is any risk of exposure of a non-immune pregnant woman, diagnosis must be confirmed serologically.
There is no effective antiviral treatment. Prevention is by immunization (MMR vaccine), with 80% coverage needed for herd immunity.

What is Kawasaki Disease, how is it diagnosed, and why is early treatment critical?

Kawasaki disease is a systemic vasculitis of unknown aetiology, mainly affecting children aged 6 months to 4 years (peak at end of first year).
It is more common in Japanese and Black-Caribbean children.

Diagnosis is entirely clinical — no diagnostic test exists:
fever for ≥5 days PLUS at least 4 of 5 features:
(1) Bilateral non-purulent conjunctival injection;
(2) Erythema/cracking of lips, strawberry tongue, and/or erythema of oral mucosa;
(3) Cervical lymphadenopathy (>1.5 cm, usually unilateral);
(4) Maculopapular rash, diffuse erythroderma, or erythema multiforme-like rash;
(5) Erythema and oedema of hands/feet in acute phase and/or desquamation around nails in subacute phase.

Affected children are strikingly irritable with a high, difficult-to-control fever.
CRP, ESR, and WBC are elevated; platelets rise in the second week. "Incomplete" disease may occur, especially in infants — maintain high suspicion in persistently febrile infants without all features (higher risk of delayed diagnosis and coronary aneurysms).
Coronary arteries are affected in ~1/3 of children within 6 weeks — aneurysms detectable on echocardiography.
Untreated aneurysms can cause myocardial ischaemia and sudden death.

Treatment: IV immunoglobulin (ideally within 10 days) + low-dose aspirin;
resistant cases: second IVIG, corticosteroids, or infliximab.
Children with coronary aneurysms require long-term aspirin and lifelong follow-up.

What is Paediatric Multisystem Inflammatory Syndrome (PIMS) associated with SARS-CoV-2, and how does it present and differ from Kawasaki disease?

PIMS (also called MIS-C) is a severe systemic inflammatory response occurring in a small number of children following SARS-CoV-2 infection.
It is thought to result from an abnormal immune response to the virus.
Features: persistent fever, evidence of inflammation (neutrophilia, lymphopenia, high CRP), and single or multi-organ failure.
Gastrointestinal symptoms, rash, and conjunctivitis are common.
Cardiac involvement includes myocarditis, coronary artery abnormalities, valve involvement, and pericardial effusion.
Some children develop severe inflammatory shock requiring ICU.

Key differences from Kawasaki disease:
PIMS tends to affect older children or adolescents (classic Kawasaki disease peaks under age 4).
Features may overlap with Kawasaki disease, bacterial sepsis, or toxic shock syndrome.
Children are often SARS-CoV-2 PCR negative but serology positive. Antibiotics are started until infection is ruled out.
Treatment: IVIG, low-dose aspirin, and corticosteroids.
The full spectrum and optimal treatment remain incompletely understood.

What are the clinical features, diagnosis, and diagnostic challenges of Tuberculosis (TB) in children?

TB is caused by M. tuberculosis, spread almost invariably by the respiratory route from a household contact (children are generally not infectious themselves as their disease is paucibacillary).
Distinction: latent TB (asymptomatic, positive immune tests) vs. active TB disease.

Clinical features:
often non-specific — prolonged fever, malaise, anorexia, weight loss;
focal signs such as lymph node swelling in TB lymphadenitis. ~75% of active TB is pulmonary;
extrapulmonary includes TB lymphadenitis, osteoarticular TB, genitourinary TB, and TB meningitis.

Primary complex (Ghon complex) = lung lesion + regional lymph nodes.
Reactivation may cause localized or miliary (disseminated) TB.
Diagnosis challenges:
Children usually swallow sputum, so gastric washings on 3 consecutive mornings are used with acid-fast bacilli stains (Ziehl-Neelsen/auramine) and mycobacterial cultures.
Tuberculin Skin Test (TST/Mantoux):
induration ≥5mm is positive per NICE guidelines regardless of BCG status.
IGRAs (Interferon-Gamma Release Assays): blood-based tests assessing T-cell response to M.
A negative IGRA does not reliably exclude TB;
HIV coinfection causes false-negative TST and IGRA results; chest X-ray and tissue diagnosis become more important.

What is the treatment of active TB in children and how is latent TB managed?

Active TB treatment:
initial quadruple therapy —
rifampicin + isoniazid + pyrazinamide + ethambutol — for 2 months, then reduced to rifampicin + isoniazid alone for a further 4 months (total 6 months for uncomplicated pulmonary TB or TB lymphadenitis).

Longer courses required for osteoarticular TB, TB meningitis, or disseminated disease.

In tuberculous meningitis, dexamethasone is given initially to reduce long-term sequelae.
Compliance is crucial — support with DOTS (directly observed therapy) or VOTS (video observed therapy).

In adolescents, pyridoxine is given weekly to prevent isoniazid-associated peripheral neuropathy (does not occur in young children).

Latent TB (positive TST/IGRA, no active disease):
treat with rifampicin + isoniazid for 3 months or isoniazid alone for 6 months to prevent future conversion to active disease.
BCG vaccine reduces TB incidence but is not fully protective;
in the UK, BCG is given at birth only to high-risk groups.
BCG is a live vaccine and must NOT be given to HIV-positive or immunocompromised children.
Children under 2 years with close contact with a sputum smear-positive TB case should receive prophylactic anti-TB antibiotics.

What is the approach to a febrile child returning from the tropics and what are the key infections to consider?

Most febrile returning travellers have a non-tropical infection (e.g., common viral illness), but serious tropical infections must be excluded.
Key history: all places visited, duration, immunization status, malaria prophylaxis, food/water exposure, insect exposure, and infectious contacts.

Key tropical infections:
(1) Malaria — primarily Plasmodium falciparum;
causes fever (often not cyclical), diarrhoea, vomiting, flu-like symptoms, jaundice, anaemia, thrombocytopenia;
children are especially susceptible to severe anaemia and cerebral malaria;
diagnosis by thick blood films (repeated if needed) ± rapid diagnostic tests; treat P. falciparum with quinine or artemisinin-based formulations;
(2) Typhoid (Salmonella typhi/paratyphi) —
worsening fever, headaches, cough, abdominal pain, anorexia, malaise;
GI symptoms may appear in second week; splenomegaly, bradycardia, rose-coloured spots;
serious complications: GI perforation, myocarditis, hepatitis, nephritis;
treat with third-generation cephalosporin or azithromycin (multidrug-resistant strains increasing from Indian subcontinent);
(3) Viral haemorrhagic fevers (Lassa, Marburg, Ebola, Crimean-Congo) — rare, highly contagious, high mortality; strict isolation within 21-day incubation period;
(4) Dengue — fine erythematous rash, myalgia, arthralgia, high fever; dengue haemorrhagic fever occurs on re-infection with different strain;
(5) Zika virus — fetal microcephaly risk in pregnancy;
(6) Chikungunya — fever, arthralgia, arthritis.

What is HIV infection in children — how is it transmitted, diagnosed, and what are the clinical features?

The major route of HIV in children is mother-to-child transmission (intrauterine, intrapartum, or via breastfeeding).
HIV can also be transmitted iatrogenically (infected blood products, contaminated needles) or through sexual abuse.

Diagnosis:
children >18 months: HIV antibody test.
Children <18 months: antibody test is unreliable due to passively acquired maternal IgG; use HIV DNA PCR or viral load assay.
Clinical features vary with degree of immunocompromise:
Mild — lymphadenopathy or parotid enlargement;
Moderate — recurrent bacterial infections, candidiasis, chronic diarrhoea, lymphocytic interstitial pneumonitis (LIP);
Severe AIDS — PCP (Pneumocystis jirovecii pneumonia), severe growth faltering, encephalopathy, and malignancy.

Without treatment, ~20% of infected infants rapidly progress to AIDS in the first year of life. Always suspect HIV in children with an unusual constellation of symptoms, persistent lymphadenopathy, hepatosplenomegaly, recurrent fever, parotid swelling, or serious/unusual/recurrent infections.

How is HIV infection in children treated and what are the key management principles?

Combination antiretroviral therapy (ART) — three or four drugs — should be started in ALL HIV-infected children regardless of CD4 count once diagnosis is confirmed.
Cotrimoxazole prophylaxis against PCP is given to all HIV-infected infants and older children with low CD4 counts.
Other management principles:
Immunization — follow routine schedule EXCEPT BCG must NOT be given (live vaccine, risk of dissemination);
MMR can be given to HIV-positive children on ART;
additionally consider influenza, hepatitis A and B, and VZV vaccines.

Co-infection alert: all individuals with TB should be tested for HIV and vice versa (overlapping epidemiology).
Lymphoid interstitial pneumonitis can mimic TB on chest X-ray in ~20% of HIV-infected children — do not misdiagnose.
In advanced HIV immunocompromise, both TST and IGRA can be false negative, making TB diagnosis even harder.
Prevention of mother-to-child transmission: ART for the mother during pregnancy and labour, ART prophylaxis for the newborn, elective Caesarean section, and avoidance of breastfeeding (in high-income settings) dramatically reduce transmission rates.

What is Lyme Disease, how does it progress through stages, and how is it diagnosed and treated?

Lyme disease is caused by Borrelia burgdorferi,
transmitted by the bite of the Ixodes tick in forested areas of Europe and North America.
Clinical stages:
(1) Early localized —
erythema migrans: a characteristic red, expanding ring-shaped rash at the site of the tick bite appearing days to weeks after the bite, often with fever, malaise, and myalgia;
(2) Late disseminated disease (weeks to months later):
Neurological — fluctuating fatigue, meningoencephalitis, and peripheral/central/autonomic neuropathies;
Cardiac — myocarditis and heart block;
Joints — brief migratory arthralgia to acute asymmetric monoarthritis/oligoarthritis of large joints; recurrent arthritis is common; chronic erosive joint disease in ~10% months to years later.

Diagnosis: clinical + epidemiological features + serology (seroconversion occurs 4–6 weeks after tick attachment — serology will be negative in early erythema migrans).
Isolation of organism is not routinely undertaken.
Treatment: early uncomplicated Lyme disease: doxycycline (≥8 years) or amoxicillin (<8 years); carditis or neurological disease: IV ceftriaxone. Follow NICE guidelines.

What are primary immunodeficiencies (PIDs), how do they present clinically, and what are the main categories and management options?

Primary immunodeficiencies are rare genetically determined defects in immune system development or function (>250 recognized disorders).
They should be suspected with SPUR infections: Severe, Persistent, Unusual, or Recurrent.
Additional clues: family history of consanguinity or unexplained deaths in boys, faltering growth, chronic diarrhoea, and severe early-onset eczema.

Main categories and examples:
(1) T-cell defects —
severe viral/fungal infections; examples:
SCID (fatal without treatment), DiGeorge syndrome (cardiac defects, absent thymus, hypocalcaemia, chromosome 22q11.2 deletion), Wiskott-Aldrich syndrome (immunodeficiency + thrombocytopenia + eczema; X-linked), Ataxia-telangiectasia;
(2) B-cell (antibody) defects — recurrent bacterial infections after maternal antibodies wane (beyond infancy);
examples: X-linked (Bruton) agammaglobulinaemia (abnormal tyrosine kinase, absent B-cell maturation), CVID, Hyper-IgM syndrome,
Selective IgA deficiency (most common PID, often asymptomatic);
(3) Neutrophil defects — recurrent abscesses and invasive fungal infections; example: Chronic Granulomatous Disease (CGD — neutrophils fail to produce superoxide);
(4) Complement defects — recurrent meningococcal/pneumococcal/Hib infections;
(5) Leukocyte adhesion deficiency (LAD) —
delayed cord separation, poor wound healing, deep-seated infections.

Management: antimicrobial prophylaxis (cotrimoxazole for T-cell/neutrophil defects; prophylactic antibiotics for B-cell defects), immunoglobulin replacement therapy (IV or SC), bone marrow transplantation (e.g., for SCID and CGD), and evolving gene therapy