Category Archives: Infectious disease

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

Infectious disease

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]



Eosinophilia

Allergy, General paediatrics, Immunology, Infectious disease

Usually just a marker of atopy, so common with asthma, hay fever, eczema. Mild generally accepted as 0.5–1.5×109/L, moderate 1.5–5, and severe >5. Persistent would be over 2 weeks.

But beware rare things eg HyperIgE syndrome. Any evidence of organ impairment? Also seen with malignancy, PFAPA, Familial Mediterranean Fever. With the rheumatological conditions, eosinophilia is often severe (>5) but with malignancy, usually mild…

And helminth infection, viz

  • Fever and hepatosplenomegaly
  • Liver/lung/brain cysts
  • Uveitis/macular oedema
  • Anaemia with abdominal pain or wheeze
[Turkish study and protocol, not v useful European Journal of Pediatrics (2023); from Florence – https://doi.org/10.1111/apa.17266]

Cysticercosis

General paediatrics, Infectious disease

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).

Helminths

General paediatrics, Infectious disease

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.

Cestodes

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.

Trematodes

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.

Macrolides

General paediatrics, Infectious disease,

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

Schistosomiasis

General paediatrics, Infectious disease

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.   

Campylobacter

Gastro, General paediatrics, Infectious disease

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

Common, General paediatrics, Infectious disease

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.

Diagnosis

Blood film characteristically shows atypical lymphocytosis. Monospot test (for “heterophile” antibodies, against horse blood cells, characteristic of EBV) only 70-90% sensitive, even worse under 4yrs of age. May also be negative if done too early. Also prone to false positives although this is rare (lymphoma, hepatitis).

Serology is a bit complicated – anti VCA (viral capsid antigen) IgM comes up first, IgG follows after 2-4 weeks then persists for life. Anti EA (early antigen) IgG is an unusual one which comes up quickly and then disappears after 3-6 months. EBNA (ENV nuclear antigen) only comes up after a few months. There are false negatives (usually because illness resolves before any antibodies appear) and false positives.

If important to know, do PCR.

Mild hepatitis and cholestasis pretty common. So can be confused with autoimmune hepatitis, especially since both can give positive IM tests.

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

Severe illness in boys suggests XLP.

Management

Supportive.

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]

Meningococcal disease

Emergency medicine, General paediatrics, Infectious disease

Gram negative diplococci, causing meningitis and septicaemia. Sometimes bone/joint infection. Neisseria (not meningitidis) responsible for ophthalmia neonatorum.

Main serogroups:

  • A – responsible for epidemics of meningitis across “Meningitis belt” of Sub-Saharan Africa, until Men A monovalent vaccine introduced in 2010 (still epidemics, but due to other serotypes). Hajj also triggers outbreaks.
  • B – 4 component vaccine introduced in 2015 to deal with B being the most common cause of invasive meningococcal disease since introduction of MenC vaccine. Based on vaccine developed for New Zealand epidemic.
  • C – used to be most common cause of invasive meningococcal disease in UK until vaccine introduced. So successful that early dose was dropped from routine schedule, although later resurgence in older children and young people, so teenage booster and university catch up programme introduced.

Clinically, notorious for rapidly evolving, often fatal septicaemia with non blanching rash and limb ischaemia. Curiously, meningococcal meningitis, on the other hand, is the most benign of the various causes of bacterial meningitis. Can be mixed picture, ranging from a few petechial spots only with an otherwise typical meningitis presentation, or else meningococcal septicaemia with neck stiffness, where presence of meningitis is actually a good prognostic sign.

Exquisitely sensitive to antibiotics. Meningitis epidemics in Africa treated with single IM dose ceftriaxone!!! Nasal carriage is the reason for spread, so prophylaxis for close contacts important.

Uveitis

Clinical, General paediatrics, Immunology, Infectious disease, Rheumatology

The Uvea is the term for the whole eye (uvea=peeled grape). Whereas conjunctivitis looks like a red eye, it’s only really the surface that is inflamed. With uveitis, all the different tissues of the eye are inflamed. Acutely, might not look that different to conjunctivitis but painful, whereas latter usually just itchy. Anterior chamber starts to fill up with inflammatory cells so vision starts to deteriorate. An irregular pupil due to synechiae can eventually be seen, with hypopyon. Cataracts and scarring can follow.

Chronic on the other hand can be subclinical but potential for visual loss so screening important in associated conditions.

Usually idiopathic, otherwise:

  • Juvenile idiopathic arthritis – about 10% of patients with non-oligoarthritis, and 30% of ANA positive oligo so pretty common
  • HLA-B27 – with or without other B27 conditions such as Ankylosing spondylitis
  • Behcet’s disease (so do HLA B51)
  • Crohns disease and other IBD
  • Granulomatosis with polyangitis (ex-Wegeners)
  • Sarcoidosis (so do chitotriosidase)
  • Tubulointerstitial nephritis and uveitis (TINU) syndrome

Some infections can cause it: