Exanthemata Flashcards
What is exanthemata?
-To bloom/ break out
-Used to describe an acute onset, widespread skin rash
-Often associated with fever
=Usually in children
-Not necessarily infectious: allergens, toxins etc may trigger a similar phenomenon
Examples of contemporary exanthemata
-Measles
-Scarlet fever
-Rubella
-Parvovirus B19 (slapped cheek/ 5th disease)
-Roseola infantum (6th disease)
Causative organism of measles
-Measles morbillivirus
=Single-stranded, -ve sense RNA: Paramyxovirus family
Causative organism of scarlet fever
-Streptococcus pyogenes, ONLY BACTERIA
=Streptococcus: Beta-haemolytic, Lancefield group A
=Necrotising fasciitis
Causative organism of rubella
-Rubella virus
=Single-stranded, +ve sense RNA: Togavirus family
Causative organism of parvovirus B19
-Parvovirus B19
=Single-stranded, DNA: Parvovirus family
Causative organism of roseola infantum
-Human herpes virus 6
=Double-stranded DNA: Herpesvirus family
Clinical course of measles
-Spread by droplets and contaminated surfaces
-Incubation period of 7-18 days
-Initial prodrome of fevers for 2-4 days
=With evolving coryza, conjunctivitis and Koplik’s spots
-Rash
Appearance of measles rash
-Typically cranio-caudal spread (head to tail, upper back more affected than lower)
-Small macules/papules, becoming confluent (maculopapular rash)
-Blanching (initially)
-As it resolves there it can become non-blanching and the overlying skin may
desquamate
Describe Koplik Spots
-Small, bluish-white,
firm lesions on the
buccal mucosa
-Useful in diagnosis
as precedes rash
by 24-48 hours
-However: present
only in a minority
(48%) of cases and
may be confused
for other forms of
oral ulcerations
Clinical significance of measles
-Extremely high “attack rate” i.e. the chance of a non-immune, exposed person contracting measles is very high (15 mins in same room). R number 15
-Severe complications may occur with associated mortality
=Pulmonary measles
=Encephalitis, including subacute sclerosing panencephalitis (SSPE)
-Case fatality of around 1:1000 – higher in immunocompromised and malnourished
-Must be notified to Public Health
-Vaccine preventable
=MMR contains live vaccine, which is not suitable for immunocompromised patients
Clinical course of scarlet fever
-Begins with pharyngeal infection with fever, cervical lymphadenopathy, and headache
-Florid rash appears 1-2 days after onset of sore
throat
Appearance of scarlet fever rash
-Starts on face – circumoral sparing
-Blanching rash with elevations around hair follicles
-Capillary haemorrhage in skin folds – Pastia’s lines
-Strawberry tongue
-Rash is followed by desquamation
Two immunologically mediated complications of scarlet fever
-Post-streptococcal glomerulonephritis (may follow pharyngeal or skin infection)
-Rheumatic fever
Describe rheumatic fever
-Multi-system autoimmune disorder occurring 3 weeks after pharyngeal
streptococcal infection
-Pancarditis (peri-, myo- and endocarditis)
-Arthritis (large joints, migratory)
Consequence of rheumatic fever
-May lead to valvular insufficiency
-Vulnerable to infective endocarditis in the future
Clinical course of rubella
-Spread by droplets and contaminated surfaces
-Prodromal fever, and characteristic posterior auricular lymphadenopathy
-Rash appears after 2-3 days
=Typically macular
=May be itchy
=Lasts 2-3 days
=No desquamation or skin staining (cf. measles)
-Associated with small petechiae of the palate (Forchheimer’s Sign)
What is the Forchheimer’s sign?
Posterior auricular lymphadenopathy
Who is most affected by congenital rubella syndrome?
-The clinical significance of Rubella infection is not in children, but pregnant
women
-Risk depends on stage of pregnancy
=< 10 weeks 90%
=11-12 weeks 30%
=13-20 weeks <10%
=>20 weeks very low risk
-Features in the affected child may be transient, permanent or developmental
Transient features of congenital rubella syndrome
-Hepatitis and jaundice, rash
-Thrombocytopenia
-Anaemia
-Lymphadenopathy
Permanent features of congenital rubella syndrome
-Classic triad: Patent ductus arteriosus, cataracts and sensorineural deafness (occurs in c. 50% of affected babies)
-Other cardiac defects (e.g. PA stenosis), ophthalmic (e.g. retinopathy, corneal defects, glaucoma) or neurological (e.g. microcephaly)
Developmental features of congenital rubella syndrome
-Increased risk of insulin dependent diabetes (20% by 35y)
-Thyroid disease
-Progressive hearing or visual loss
Clinical course of parvovirus B19
-Fever then rash
=Initially on face followed 1-2 days later by generalised rash with characteristic lacy
appearance
-Can precipitate arthritis especially in adults
-Infect red cell precursor
What does parvovirus B19 cause?
-Aplastic crisis in patients with pre-existing haemolytic anaemia (e.g. sickle cell)
-Chronic infection and anaemia in immunocompromised (e.g. HIV)
-Foetal anaemia (hydrops fetalis) in ~5% of maternal infections (risk highest in first trimester)
Appearance of the parvovirus B19 rash
-Popular rash affecting cheeks (blanching, not itchy or painful)
-Maculopapular rash symmetrically affecting feet (and hands)- painful, significant oedema, non-blanching
-Papular Purpuric gloves and socks (rare manifestations)
Describe Monkeypox
-Clinical syndrome caused by monkeypox virus
=Double stranded DNA virus of the poxviridae family
=Related to other pox viruses: vaccinia (smallpox), variola (used as smallpox vaccine)
-Historically only sporadic cases outside Africa, and limited transmission events
between humans
=Current outbreak: 35,000 cases, 6 fatalities (as of Aug 2022)
=Current epidemiology is mainly men who have sex with men
=Transmission can be abated by vaccination with smallpox vaccine
