Category Archives: Infectious disease

Tetanus

UK schedule is for 3 tetanus containing vaccines in first year of life, followed by extra dose of 6 in 1 at 18 months (new from July 2025). First real booster is pre-school (3 years 4 months). Second booster is at 10 years after 1st course, routine is for Td/IPV at 14.

Incubation period is 4-21 days.

Tetanus prone wounds

  • Puncture in soil contaminated environment
  • Wounds containing foreign bodies
  • Compound fractures
  • Wounds/burns with systemic sepsis
  • Some animal bites/scratches

Not exclusive. Animal bites/scratches depends on whether there would have been soil in the mouth/claw…

High risk wounds on the other hand include heavy contamination with soil/manure, wounds/burns with extensive devitalised tissue, delayed surgical intervention beyond 6 hours even if not high risk initially.

Management of Wounds

If within 5 years of last vaccine (and complete primary course) – so up to 8 years old, likely good antibody levels so no booster required. If more than 5 years since immunisation, then giving booster vaccine is as effective as giving Tetanus immunoglobulin (TIG) so save it for high risk wounds only.

Avian influenza

UK-PAS meeting (David Goldfarb from University of British Columbia – PID and micro.)

H5N1 first appeared in 1997 in China but no more cases until early 2000s.

2017 report lots of young children, high mortality (53%). Unrecognised cases never admitted?

New clade 2.3.4.4b in 2021 – crossing over to mammals in Americas. Last year some mild cases related to cows.

Death in Louisiana H5N1 2025 (not the clade in dairy farms), related to poultry (underlying health issues and over 65 years). H5N1 circulating in wild and farmed birds in Scotland, H5N5 back in wild birds.

HPS guidance here.

Case

2024 – 13yr old mild asthma, obesity (117kg), presented with conjunctivitis and fever. Then vomiting and dyspnoea, quickly transferred to PICU. LLL pneumonia. No risk factors.

Biofire resp panel used for PICU – includes pan influenza A antigens, so positive but H1/3 negative. Then did reflexive Xpert assay, which is quantitative.  Relatively strong so referred to reference lab.

Genomics done within 4 days. Showed close to “cackling goose” strains. Also identified mutations associated with increased binding (not seen before in H5) so infectivity increased.

At same time Louisana case with same gene type and mutations.

Infection control tricky – new genes! Other studies have suggested incubation up to 13 days. Maintained airborne precautions until 2 negative samples (lower resp samples continued to be positive for 15 days, tracheal just 2 days…)

Note potential exposure to lab staff – discuss!

Ashraf Znait (PICU fellow) – intubated for hypoxia despite BipAP. Echo showed good function on intoropes. Started ECMO at 6 hours after intubation. Double cannulas (IJ and femoral) required to achieve sats of 80%. Dual lumen cannula. Required CRRT for fluid overload and anuria but high pressure with combination so switched to separate femoral dialysis catheter.

SIRS and haemodynamic instability persisted, decided against steroids (higher mortality in influenza cases 2019 – Recovery trial in UK currently?) so plasmapheresis.

D10 off inotropes. D15 before decannulated. D21 extubated.

Mode of acquisition never explained! No immunological problem found.

Ellie MacBain (PID fellow)  – case series from 2012 found 75% increased risk of death with delayed oseltamivir treatment. IL6 and IFNgamma, resp sample viral load higher in fatal cases.

Oseltamivir resistance has been described in avian cases of this clade. WHO suggests higher doses (eg 150mg BD), combination therapy, or prolonged treatment.

This case had PCR positive serum with cycle threshold (CT) suggestive of true viraemia. Added amantadine, baloxavir, unable to procure IV zanamavir. From different classes of antiviral in any case.

Never positive bacterial cultures! On/off antibiotics throughout.

Ashley Roberts (Prof PID) – treatment doses used for oseltamivir prophylaxis, for 7-10 days.

Rabies

Incubation period can be more than 1yr!

Nasty viral infection that travels slowly through the nervous system until it reaches the brain. Around 30 people have survived but often with severe disability.

A 15yr old girl from Milwaukee survived with only mild neurological sequelae (reported in 2005) after treatment with induced coma (midazolam, barbiturates, ketamine) and antivirals (amantadine and ribavirin). The aim was to maintain burst suppression until rabies antibodies in the CSF started to increase (day 8). Extubated on day 27. Since then this approach has been tried multiple times, with poorly reported outcomes – has been criticised for lack of evidence of benefit but also for poor evidence for underlying therapeutic principles [Alan Jackson, neurologist at University of Calgary].

Any warm blooded animal is a potential risk, including bats, monkeys and rodents as well as cats, dogs and foxes. Animals behaving abnormally represent a higher risk of infection (but normal appearance and behaviour do not exclude rabies) – unprovoked bites obviously suggest abnormal behaviour, and carry greater risk than provoked bites.

Domestic dogs or cats behaving normally at 15 days after an exposure would not have been infectious at the time of the exposure.

The risk of infection depends on:

  • country of exposure – see below
  • category of exposure – see below – higher risk with broken skin, including single or multiple transdermal bites, severe lacerations, or where mucous membranes or an existing skin lesion have been contaminated by the animal’s saliva or other body fluid (intact skin is a barrier against infection).
  • site (on body) of exposure
  • whether the patient is immunosuppressed or has any allergies
  • any previous rabies vaccinations or immunoglobulin treatment

For more on bites, see PHS bat bites page and PHS other animal bites page.

Country and category of exposure

Determine “combined country or animal risk” – Rabies risks by country – GOV.UK

Determine category of exposure – grade 1-3, with 1 being no physical contact with saliva, 3 being direct contact. Slightly different rules for bats!

Combine the 2 according to the risk matrix –

Green get nothing, obviously, amber get rapid vaccine schedule (days 0, 3, 7, 21) – modified if fully immunised already or immunosuppressed. Red get rapid vaccine schedule plus Human Rabies Immunoglobulin.

Atypical mycobacterial infection

Classically a cold abscess, usually in the neck. Ingested soil?

Overlying skin can become discoloured, and ultimately fistulation may occur. Child is usually systemically well.

Blood tests are normal. Mantoux testing can be positive due to cross reaction with BCG. Fine needle aspiration may be most appropriate.

Drug treatment needs to be prolonged and recurrence is common.

Surgery can be tricky.

Monkeypox

=mpox (considered less stigmatising?).

Emerging infection particularly in men who have sex with men. Reached the UK in 2022.

New variant (Clade I) has high mortality, started in Central Africa (Congo, Central African Republic, Burundi, Uganda), now in Kenya, first case now reported in Europe (Sweden, 2024). Grade 3 human pathogen (along with Yersinia pestis, O157, TB, anthrax…).

Viral haemorrhagic fever found in these areas too, of course…

Incubation period is 5-21 days. High risk would be household contact, mucosal (with bodily fluids) or broken skin, inhalation without PPE if cleaning room or changing bedding. Medium risk would be intact skin with bodily fluids or face to face within 1m considered medium risk – do not need to isolate but should be offered post-exposure prophylaxis. See PHS matrix.

Besides blistering rash, can cause fever, sore throat, lymphadenopathy, myalgia.

Swab blistering lesion, or if none then throat. MSS (molecular sampling solution, as used for flu etc) ideally otherwise extra transport precautions required. Mark sample “suspected HCID”, notify lab in advance – needs to arrive for 9am!!!

Cases are asked to self isolate at home.

PPE – as for viral haemorrhagic fever. https://learn.nes.nhs.scot/58193/high-consequence-infectious-diseases-hcid

Post-exposure prophylaxis with MVA-BN vaccine (Imvanex®) offered within 14 days. Pregnant and children under 5 considered at risk.

Smallpox vaccine was considered effective.

UTI prevention

For lower tract:

  • Cranberry juice still not definitely proven.
  • Methenamine tablets found to be equivalent to trimethoprim prophylaxis – licensed for adults only but BNFc gives dose for children. Needs acidic urine to work so don’t use citrates at same time.
  • D-mannose some evidence – from health food shops! Capsules I think, prob no dose for children.
  • Citrates?
  • NICE CKS specifically advises AGAINST use of these non-drug products, with exception of methenamine! Prob because self initiated short course trimethoprim superior?

Pyrexia of Unknown Origin

A technical term, not just a fever without obvious source! Essentially presence of confirmed fever for 8 days or more in a child in whom a careful thorough history and physical examination, and preliminary laboratory data fail to reveal a probable cause.

Long list of possible causes, long lists of possible tests – do thorough history and repeated examinations, then follow the clues!

In kids, infection is the commonest cause. But can be connective tissue disorder, or malignancy.

Beware factitious fever – admission sensible.

If possible, stop all drugs. Antipyretics may obscure the pattern of fever, and can occasionally be its cause (drug fever is one cause).

Unless the child is critically ill, try not to give antibiotics. If the diagnosis remains obscure, go back and take the history again, examine the child (fully) again, send the specimens again!

Special points in history/examination

  • Travel – malaria can present 6-12 months later. Typhoid.
  • Ethnicity – tuberculosis
  • Outdoor activities – rats/ticks as vectors of infectious diseases
  • Animal contact – cows/sheep (brucellosis), cats (cat scratch)
  • Mouth ulcers (IBD, Behcets, PFAPA)
  • Periodicity – see Periodic fever
  • Sinus tenderness, nasal congestion (sinusitis)
  • Bone/spine tenderness – discitis, vertebral osteomyelitis

Tests

  • 3 sets of blood cultures, different sites, different times (at least a few hours apart), off antibiotics – standard for endocarditis
  • ASOT
  • EBV, CMV
  • LDH, CK
  • ANA/RF
  • Urine/stool culture
  • Swab everything!
[Rosie Hague, Current peds 2001]

PFAPA

=periodic fever, aphthous stomatitis, pharyngitis, adenitis.

Fever every 4-6 weeks (periodic). Neutrophil count normal, cf cyclical neutropenia.

Besides mouth ulcers, sore throat and cervical lymphadenopathy, headache, musty smell (!), abdo pain.

Affected children continue to grow normally, are well between attacks, and do not suffer long-term sequelae.

Treatment with steroids or with cimetidine has been effective, and some children have had no further attacks following tonsillectomy (which suggests some relationship with strep infection but not clear).

Periodic fever

Infectious causes
Mycobacteria (TB and non-tuberculous disease)
Borrelia
Leptospira
Streptobacillus moniliformis (rat bite fever)
Hepatitis B
Orbivirus
Rickettsea (typhus)
Entamoeba histolytica
Others
Cyclical neutropoenia
PFAPA
Behcet’s
Hyper IgD (HIDS)
Familial Mediterranean fever
Familial Hibernian fever/TRAPS
Cryopyrin disorder

Periodic fevers are defined as uniform periods of fever that recur regularly in individuals who are healthy between attacks. Parents may organize life eg holidays around expected attacks and don’t have any concerns otherwise cf child with recurrent respiratory and gastrointestinal infections after starting nursery who “always has something”.

Recurrent bacterial infections esp recurrent/chronic pneumonia or otitis media may indicate a humoral immune defectSimilarly, recurrent documented viral or fungal infections may indicate a cell mediated immune defect.