Category Archives: Infectious disease

Scarlet Fever

Has Victorian connotations as fatal epidemics of Scarlet fever swept through slums in the pre-antibiotic era.

Group A streptococcus pyogenes is still carried in up to 20% of young children’s throats. Disease peaks in winter and spring (cool conditions, and more time indoors?). Spread easily through saliva.

Scarlet fever (scarlatina is usually used for mild cases) is when an exotoxin is produced, that causes fever and rash. Characteristic features are:

  • Strawberry tongue – progresses from white coated, to red, beefy tongue as coating lifts.
  • Perioral pallor
  • Fiery, widespread rash – rough “sandpaper” feel characteristic
  • Pastia’s lines – lines of petechiae in creases esp wrists, elbows
  • Palatal petechiae (“Forchheimer spots”) – not specific, also measles. 
  • As rash fades, desquamation can occur, particularly on fingers/toes. Should only happen once in lifetime, as antibodies form to toxin!?

No longer notifiable in Scotland, cf England/Wales.

Complications can still be severe of course, as with any group A strep disease:

Benefit of antibiotic treatment just ½ day symptoms! But without treatment would need to exclude from nursery/school for 14 days!!! Else after 24hrs antibiotics.

No resistance to penicillin and low MIC so preferred, although 10 day course needed for clearance from throat, as opposed to clinical improvement. Other antibiotics eg clindamycin may be chosen however if invasive disease.



Incubation period is 8-14 days. Starts with a prodrome of cough, coryza, conjunctivitis and fever lasting 2-6 days. Then the rash appears: brick red, maculopapular, starts behind ears, spreads from face on to trunk and then everywhere including palms/soles. Discrete spots may then coalesce. With time the rash may darken (“stain”) and may desquamate. The child is typically irritable – compare other common childhood rashes.

Koplik’s spots are pathognomic but easily missed as they appear early in the illness, disappearing within a few days of the rash starting. They are grey or white spots on the buccal mucosa opposite the 2nd molars.

Case definition is rash 3+ days, fever, cough, conjunctivitis or coryza plus diagnostic lab result. Diagnosis is by throat swab (or urine) for PCR. Send blood for IgG/M too.


  • Check vulnerable contacts eg unvaccinated, immunosuppressed but also infants and pregnant women. There is not an explicit definition for close contact. Ideally vaccination should be offered within 3 days.
    • Pregnant vaccinated women should be fine, if in doubt do rapid antibody levels, give HNIG (Human Normal Immunoglobulin, NOT MMR) if necessary, repeat serology at 3/52.
    • Infants under 6/12 should get HNIG, unless mother has had natural measles (or born before 1970!). Else MMR, unless 6-8/12 old and a household contact or high risk.
  • Respiratory protective equipment should be worn when caring for confirmed or suspected cases viz FFP3 respirator.

[HPN Scottish Guidance Dec 2013]


Measles now endemic again in England and many European countries, with cases increasing year on year with only a slight reversal during lockdown. Before vaccines, pretty much inevitable part of childhood.

Andrew Wakefield in 1998 didn’t help – no immediate problem with his false paper (due to herd immunity), first death not until 2006, at which point rate 13x higher than pre-Wakefield. Vaccine hesitancy continues to be one of the biggest global health challenges of our time.

Measles after MMR occurs 7-14 days post-vaccination. Very rare after booster. Tends to be mild fever, rash and conjunctivitis.

Porto Outbreak

March-April 2018, 96 confirmed cases in a hospital in Porto, Portugal. Mostly vaccinated Health care workers!!!

Atypical presentations – mac-pap rash only, low fever.

Chances of an “escape variant” not covered by vaccine almost zero.

Paediatric multi inflammatory syndrome associated with COVID19 (PIMS-TS)

Condition seen in context of SARS-Cov2 infection, with similarities to Kawasaki syndrome.

Neutrophilia (most), lymphopenia, single or multiorgan dysfunction.  Possibly Kawasaki criteria. Exclude other infectious cause including shock syndromes and myocarditis (but don’t delay seeking advice).

Abnormal fibrinogen, d-dimer, ferritin, hypoalbuminaemia. Other features eg coagulopathy variable.

PCR for SARS-Cov2 often negative, but antibody positive.

WHO refer to PIMS-TS as Multisystem Inflammatory Syndrome in Children (MIS-C), case definition is similar but requires at least 3 days of fever and either evidence of COVID-19 on PCR or serology or a likely contact with COVID-19.

In England, PICU admission related to age 15-17yrs, female, black/Asian. Length of PICU stay generally short, some require ECMO, majority survive. [Ward, MedRxIv 2021]


Infection with T solium can be asymptomatic, or lead to subcutaneous lumps, or enter the central nervous system.

In tissues, can cause muscle pseudohypertrophy, can enter the eye, can cause conduction defects.

In the brain, acute encephalitis, pseudotumour with raised intracranial pressure, dementia/psychosis, chronic meningitis and neuropathies, spinal cord compression.

Finding T solium in the stool has low sensitivity/specificity. CSF may show eosinophils but may be normal. Imaging shows rings or blobs, can look like TB. Can be calcified, doesn’t necessarily mean dead!

Treat with albendazole or praziquantel. Immune reactions to treatment can be severe (raised ICP).


So nematodes (round worms), cestodes (tapeworms), trematodes (flukes). Do not multiply in human hosts cf parasitic protozoa. Multiply through reinfection though! Most have life cycle in other hosts.


Mostly intestinal tapeworms, not that important, but Taenia solium eggs cause cysticercosis.

Hydatid cysts (larval stage of Echinococcus granulosus) are life threatening. Adult stage found only in dogs.


Complex life cycles involving snails. Cysts are ingested, with exception of schistosomiasis, where larvae (cercariae) penetrate skin. Migration within the body is a feature, where they end up causes problems even if it’s a dead end for the organism.


Erythromycin, clarithromycin, azithromycin.

Bacteriostatic not bacteriocidal, but doesn’t necessarily mean inferior.

Broad spectrum, including things that aren’t even bacterial! eg Bordetella pertussis, syphilis.

Diarrhoea and vomiting as main side effects, not an allergy as such. True allergy is virtually unheard of! Other important issues:

  • Risk of pyloric stenosis in neonates
  • Prolong QT, so beware other things that also prolong QT including electrolyte disturbance


Egg in freshwater taken up by snails.  Cercariae released into water and penetrate skin.  With this first infection, urticaria, discrete raised lesions 1-3cm and immune response (to dying larvae, rather than living!).  These then migrate into lungs, so acute schistosomiasis causing immune complex deposition, lymphadenopathy, eosinophilia, pulmonary infiltrates. 

Larvae mature in liver.  Adult worms migrate to mesenteric vessels of bowel, where eggs are laid.  Chronic blood loss from gut lesions. Hepatomegaly, splenomegaly, eventually varices if fibrotic. 

Worms can live 3-10 years.  Immunity only really develops where lots of dead worms, not necessarily high worm burden!  Eggs only start appearing 8 weeks after infection, and multiple samples required (intermittent excretion, perhaps every few days). 

Serology only really useful in travellers as persists? Praziquantel often causes abdo pain, rash, headache.  Only acts on adult worms.   


Common cause of bloody diarrhoea. As with other causes of bloody diarrhea, often associated with fever and abdominal cramps.

Usually self resolving within a week. Antibiotics help if symptoms severe enough.

Excretion continues for a number of weeks, although risk of spreading infection after diarrhoea has settled of course much less, assuming decent hygiene.

Chronic excretion can occur with continuous symptoms rarely, certainly in immunosuppressed patients. Asymptomatic carriers exist, although seems to be more common in developing countries (so malnutrition probably a factor) and reinfection can also occur, of course.

About 1 in 1000 cases develop Guillain Barre syndrome after the infection. Inflammatory bowel disease seems more common after campylobacter infection?

Epstein Barr virus

One of the Herpes virus family, and like other herpesviruses (herpes, varicella) becomes latent in the body after infection, in the case of EBV in B-lymphocytes. Immune system has developed specific strategies over the course of human evolution to control it – hence specific immunodeficiencies such as Duncan’s syndrome where EBV appears to be the only infection that becomes problematic (even catastrophic).

Associated with a number of tumours, including non-Hodgkin’s lymphoma, Burkitt Lymphoma (especially in Africa), nasopharyngeal carcinoma.

In most children, a mild febrile illness, with lymphadenopathy (“glandular fever” or infectious mononucleosis), sore throat (can be severe). Failure to improve with antibiotics is a clue! Peak age for severe presentations is teenagers – “kissing disease” (sexually transmitted!? Edinburgh students study found lower rates if routine barrier methods used). Prolonged incubation period of 30-50 days!

Classically rash triggered by amoxicillin (which is why amoxicillin isn’t recommended for sore throats, but rash can be seen with penicillin too) – maculopapular, sometimes petechial and/or urticarial, which is rather more suggestive.

On examination, hepatosplenomegaly can be seen.

Blood film characteristically shows atypical lymphocytosis. Monospot test (for heterophile antibodies) 70-90% sensitive so has false negatives as well as false positives so may need to proceed to PCR if important to know.

Mild hepatitis and cholestasis pretty common.

Rarer features are dacrocystitis, pneumonia, myocarditis, low platelets and neutrophils, interstitial nephritis, encephalitis. Haemophagocytic syndrome. 20x higher risk of Guillain Barre syndrome after EBV



Splenic rupture after EBV has been reported but is very rare. Advice usually given to avoid contact sports. In ultrasound studies, peak spleen size is typically noted within the first 2 weeks of illness, but may extend to 3.5 weeks. The majority of spleen injuries occur within the first 21 days of illness and are exceedingly rare at >28 days, so one month avoidance probably sufficient.

A minority develop chronic fatigue type symptoms.

[Sports health 2014]