7- Infectious diseases (Rashes) (5/5) Flashcards

1
Q

kawasaki background

A
  • A systemic, medium-sized vessel vasculitis
  • Typically affects children <5
  • No clear cause or trigger
  • Key complication: coronary artery aneurysm
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2
Q

Risk factors of kawasaki

A
  • More common in Asian children (particularly Japanese and Korean)
  • More common in boys
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3
Q

how to remember presentation of kawasaki

A

CRASH AND BURN

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4
Q

crash and burn for kawasaki

A
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5
Q

description of kawasaki presentation

A
  • Persistent high fever (above 39 degrees) for more than - - 5 days (Pyrexia of unknown origin)
  • Children will be unhappy and unwell

Key skin finding:
- Widespread erythematous maculopapular rash
- Desquamation (skin peeling) on the palms and soles e.g. fingers peeling

Other features
- Strawberry tongue
- Cracked lips
- Cervical lymphadenopathy
- Bilateral conjunctivitis

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6
Q

investigations for kawasaki

A
  • Full blood count can show anaemia, leukocytosis and thrombocytosis
  • Liver function tests can show hypoalbuminemia and elevated liver enzymes
  • Inflammatory markers (particularly ESR) are raised
  • Urinalysis can show raised white blood cells without infection
  • Echocardiogram can demonstrate coronary artery pathology
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7
Q

why echocardiogram for kawasaki

A

can demonstrate coronary artery pathology

  • Key complication: coronary artery aneurysm
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8
Q

Management of kawasaki

A

First line:
- High dose aspirin to reduce the risk of thrombosis
- IV immunoglobulins (ig) to reduce risk of CAAA
- Close follow up with echocardiograms to monitor for evidence of CAA

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9
Q

kawasaki disease course

A

Disease Course
There are three phases to Kawasaki disease:

  • Acute phase: The child is most unwell with the fever, rash and lymphadenopathy. This lasts 1 – 2 weeks.
  • Subacute phase: The acute symptoms settle, the desquamation and arthralgia occur and there is a risk of coronary artery aneurysms forming. This lasts 2 – 4 weeks.
  • Convalescent stage: The remaining symptoms settle, the blood tests slowly return to normal and the coronary aneurysms may regress. This last 2 – 4 weeks.
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10
Q

scarlet fever background

A
  • Diffuse erythematous eruption occurring in association with pharyngitis.
  • Requires prior exposure to Group A streptococcus (S. pyogenes) (1-2 days earlier).
  • Occur as delayed-type skin reaction to pyogenic exotoxin (erythrogenic toxin) produced by organism.
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11
Q

Typical presentation of scarlet fever

A
  • Initially appears on neck and chest, then spreads to the rest of the body.
  • Texture of rash (feels like sandpaper) more important than appearance to confirm diagnosis.
  • Most marked in skin folds; linear petechial character in antecubital fossa/axilla/groin (Pastia’s lines).
  • Can last more than 1 week; as rash fades skin around fingertips, toes and groin may peel.
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12
Q

complication of scarlet fever

A

can predispose to rheumatic fever

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13
Q

management of scarlet fever

A
  • Same as pharyngitis- Penicillin V for 10 days
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14
Q

scarlet fever vs strep A pharyingitis

A

Bacteria called group A Streptococcus (group A strep) cause scarlet fever.

These bacteria are also the cause of strep throat.

The bacteria sometimes make a toxin (poison), which causes a rash — the “scarlet” of scarlet fever.

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15
Q

Roseola (roseola infantum or sixth disease) background

A
  • Illness of young children – peak prevalence between 7 and 13 months
  • Caused by respiratory droplet spread of human herpesvirus 6 variant B (HHV-6).
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16
Q

Typical presentation of roseaola infantum

A
  • Characterised by 3-5 days of high fever (may exceed 40○C) that resolves abruptly and is followed by a rash.
  • Cervical, post auricular and suboccipital lymphadenopathy are common.
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17
Q

roseola infantum rash

A
  • Blanching macular or maculopapular rash; Starts on neck and trunk; spreads to face and extremities.
  • Typically persists for 2-4 days; may come and go within a few hours.
  • Often misinterpreted as drug allergy as child often receiving antibiotics for fever.
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18
Q

Management roseola infantum

A

Benign, self-limiting illness. Clinical diagnosis, does not need any investigations.

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19
Q

Slapped cheek disease (erythema infectiosum or fifth disease) backgroun

A
  • Parvovirus B19
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20
Q

Typical presentation of slapped cheek

Infection during pregnancy can lead to miscarriage, intrauterine death, non-immune hydrops.

A
  1. Erythema infectiosum
    Illness begins with non-specific prodrome: fever, coryza, headache, myalgia, nausea and diarrhoea. Two to five days later classical erythematous malar appears with relative circumoral pallor.
    Facial rash followed several days later by lacelike or reticulated rash on truck and extremities.
  2. Arthropathy (arthralgia and/or arthritis). Minority of cases (10%) with/without rash. More common in adults, particularly women. Symmetrical in small joints of hands and feet. Does not cause joint destruction.
    Usually resolves in 3 weeks.
  3. Transient aplastic crisis
    Temporary suspension of erythropoiesis.
    Leads to severe anaemia and complications.
    Occurs in individuals with: haematological disorders e.g. sickle cell disease, hereditary spherocytosis.
    reduced red cell production e.g. iron deficiency anaemia.
  4. Neurological manifestations
    Central – encephalitis; peripheral – Guillain-Barre.
  5. Foetal infection
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21
Q

Hand foot and mouth disease background

A
  • a common, mild self-limiting infection
  • commonly affecting young (<5 years old) children
  • an enterovirus infection caused most commonly by Coxsackie A16.
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22
Q

Typical presentation hands foot and mouth disease

A

a clinical syndrome characterised by oral exanthem and a macular, maculopapular or vesicular rash on the hands and feet - one of the most recognizable exanthems in children/adults.

Symptoms:
Small vesicle and ulcers in and around mouth, palate and pharynx - can be painful. Lesions on palms and soles: evolve from flat, pink patches to elongated grey blisters.
peel off within a week and and leave no scars. Red macules and papules on buttocks; sometimes arms, occasionally genatalia.

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23
Q

Mumps
Background

A

Viral infection (paramyxovirus) spread by respiratory droplets
- Incubation: 14-25 days
- Usually self limiting conditions that last around a week
- Supportive management
- Involves treating complications
- Vaccination history essential
o MMR offers 80% protection for mumps

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24
Q

mumps presentation

A

rash not classic
Presentation
- Prodrome: flu-like symptoms
- Parotid swelling (unilateral or bilateral) and
o Fever
o Muscle aches
o Lethargy
o Reduced appetite
o Headache
o Dry mouth
- Symptoms of complications
o Abdominal pain (pancreatitis)
o Testicular pain and swelling (orchitis)
o Confusion, neck stiffness and headache (meningitis or encephalitis)

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25
Q

mumps investgations

A

Investigation
- PCR testing on saliva swab
- Antibody testing of blood or saliva

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26
Q

Management of mumps

A

Notifiable disease – notify public health of any suspected and confirmed cases
- Management is supportive- self limiting
o Rest
o Fluids
o Analgesia
- Stay off school for 5 days after symptom onset

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27
Q

complications of mumps

A

Complications
- Pancreatitis
- Orchitis- infertility
- Meningitis
- Sensorineural hearing loss

28
Q

Measles
background

A

Background
- RNA morbillivirus from the paramyxovirus family
- One of the most contagious infectious diseases
- Transmission: airborne via respiratory droplets
- Incubation period of 10 days
- Person is infectious from when their symptoms start (around 4 days before rash)

29
Q

measles presentation

A

Rash for at least 3 days

  • First seen on forehead, neck and spreads to the trunk and limbs
  • Leaves behind a brownish discolouration

**Fever >40 degrees **for at least one day and at least one of the following
Prodrome (2-4 days)
- Fever
- Cough
- Runny nose
-Conjunctivitis

Other symptoms
- Diarrhoea
- Koplik spots
- Swelling around the eyes and photophobia

30
Q

koplik spots

A

Pathognomonic for measles– appear on buccal mucosa -> opposite second molar teeth
Small red spots each with a bluish-white speck (like a grain of rcie)

31
Q

investigations for measles

A

Investigations
- Salivary swabs for measles-specific immunoglobulin M (IgM)
- RNA detection in salivary swabs

32
Q

measles management

A

Notifiable disease – notify public health of any suspected and confirmed cases
- Management is supportive- self limiting
o Rest
o Fluids
o Analgesia
- Stay off school for at least four days from when rash appeared

33
Q

Complications of measles

A

Complications
- Bronchopneumonia
- Encephalitis
- Visual impairment esp if Vit A def
- Miscarriage and congenital malformation

34
Q

rubella background
x

A
  • Viral RNA infection (rubivirus)
  • Transmission: airborne via respiratory droplets
  • Incubation period 14-21 days (patients infectious up to seven days before and four days after symptoms appear
  • Mainly seen in spring and early summer
  • Rare now due to MMR
35
Q

presentation of rubella

A

Prodromal phase (may be absent in children)
- Lassitude
- Low grade fever
- Headache
- Mild conjunctivitis
- Anorexia
- Rhinorrhoea

Rash develops (may be absent in young children)
- Initially pink discrete macules that coalesce, starting behind the ears and on the face, spreading to the trunk and then the extremities

other symtpoms
- Cervical, suboccipital and postauricular lymphadenopathy
- Forchheimers sign- petechiae on soft palate

36
Q

investigations for rubella

A
  • Serological or PCR testing
  • FBC may show low WBC and increased lymphocytes and thrombocytopenia
37
Q

management of rubella

A
  • Supportive
  • Keep child away from school for four days after rash appears
  • Analgesia and antipyretics
  • Ask about contact with pregnant women
38
Q

complications of rubella

A
  • Maternal rubella
    o Early pregnancy infection can cause congenital rubella syndrome
  • Guillain-Barre syndrome
  • Rubella encephalopathy
39
Q

chicken pox background

A
  • Varicella zoster virus (VZV)
  • 1 of 8 herpes virus- chickenpox and shingles
  • Highly contagious
  • More severe in adults and immunocompromised
  • incubation period of 14-16 days
  • infective 24h before and until rash crusts
40
Q

Presentation of chicken pox

A
  • Prodrome: fever, malaise, pharyngitis.
  • Rash appears within 24 hours; usually pruritic. Occurs in crops; different stages on body.
  • New lesions stop after 4 days.
  • Most lesions have crusted by 6 days.
41
Q

complications of chicken pox

A
  1. Soft tissue infection.
  2. Acute cerebellar ataxia.
    * Days to weeks after infection.
    * Benign with full recovery.
  3. Diffuse encephalitis.
  4. Reye’s syndrome.
  5. Pneumonia.
  6. Hepatitis.
42
Q

management of chickenpox

A

There is no specific treatment for chickenpox, but there are pharmacy remedies that can alleviate symptoms. These include paracetamol to relieve fever, and calamine lotion and cooling gels to ease itching. In most children, the blisters crust up and fall off naturally within one to two weeks.

DO NOT GIVE IBUPROFEN- can result in necrotising fasciitis, a skin infection.

42
Q

management of chickenpox

A

There is no specific treatment for chickenpox, but there are pharmacy remedies that can alleviate symptoms. These include paracetamol to relieve fever, and calamine lotion and cooling gels to ease itching. In most children, the blisters crust up and fall off naturally within one to two weeks.

DO NOT GIVE IBUPROFEN- can result in necrotising fasciitis, a skin infection.

43
Q

Herpes simplex virus (HSV)
Background

A
  • Worldwide herpes virus is estimated to infect 66% of the population; more low- and middle-income.
  • Transmitted by contact of herpetic lesions, saliva or skin containing HSV-1 virus.
  • Clinical manifestation depends on site of disease and whether primary or latent infection.
44
Q

pathophysiology of primary vs secondary infections with HSV

A
45
Q

presentation of primary HSV

A

Typical presentation

Primary: Abrupt onset; fever, irritability, unable to eat/drink.
Gingivitis (swollen, erythematous, bleeding gums. Vesicular lesions on tongue, buccal mucosa, palate. Extend to lips and face; can coalesce and ulcerate. Tender submandibular and cervical adenopathy.

46
Q

presentation of secondary HSV

A

Reactivation after trauma/dental procedure. Mild prodrome.
Localised pain, burning, tingling, itching; then lesion. Vesicular lesion commonly on vermilion border.

47
Q

Impetigo background

A
  • Contagious superficial bacterial infection (most common 2-5 years)
  • Cause
    o Streptoccus pyogenes
    o Staphylococcus aureus
  • Usually occurs in warm, humid conditions
  • Risk factors
    o Poverty
    o Crowding
    o Poor hygiene
    o Underlying scabies
48
Q

presentation of imetigo

A

Types:

Non-bullous impetigo

  • Most common.
  • Papules, vesicles, pustules that break down to form golden, adherent crusts.
  • Multiple lesions may develop but tend to remain localised.
  • Most commonly seen on face or extremities.

Bullous impetigo

  • Seen primarily in young children.
  • Vesicles enlarge to form flaccid bullae with clear yellow fluid.
  • Fewer lesions; trunk more commonly affected.
49
Q

Complications of impetigo

A
  • Post-streptococcal glomerulonephritis
  • Rheumatic fever.
50
Q

erythema multiform background

A
  • Immune mediated and self limiting
  • Mucocutaneous condition characterised by target lesions. Erosions or bullae involving
    –>Oral
    –> Genital
    –> Ocular mucosa
  • Typically induced by infection e.g. herpes
  • Other triggers
    o Medication
    o Immunisation
    o Autoimmune disease
    o Malignnay
  • Evolves over 3-5 days and resolves in 14 days
  • Skin lesions don’t scar
  • Can cause visual impairment
51
Q

presentation of erythema multiform

A

Skin rash
- Target lesions are the hallmark of the disease; begin as round, erythematous papules.
- Skin lesions appear symmetrically initially on dorsum of hands and feet.
- Spread centrally – to involve face, neck, palms, soles, flexures ± trunk.

Prodrome probably due to triggering infection.

Mucosal involvement:
- Lesions develop as blisters, then break into shallow erosions with overlying white pseudo-membrane.
- Favour oral membranes (70%) but may also present as urogenital and more rarely ocular lesions.
- Mucous membrane lesions can be painful and limit oral intake.
- May precede or follow oral lesions.

52
Q

management of erythema multiform

A

reatment of symptomatic mild cases:

Itch — oral antihistamines and/or topical steroids for itch or discomfort associated with cutaneous lesions
Pain — for mild mucosal involvement, oral washes containing antiseptic or local anaesthetic.
Other treatments are dependent on cause:

Precipitating infections — treat appropriately (note treatment of HSV does not significantly alter the course of single episode erythema multiforme)
Offending medications — cease and avoid in future.
Severe mucosal disease:

May require hospital admission for support of oral intake
Although evidence is limited, prednisone has been suggested to reduce the severity and duration of symptoms in these cases.
Recurrent disease:

At least 6 months of continuous oral antiviral therapy (typically acyclovir/aciclovir), even if a clear cause has not been identified

53
Q

immune thrombocytopenic pupura (ITP)

A

Background
- Acquired immune mediated disorder
- Characterised by isolated thrombocytopaenia (100x109/L) without identifiable cause

54
Q

pathophysiology of ITP

A
  • Increased platelet destruction -most patients have platelet membrane auto-antibodies
  • Antibody coated platelets are rapidly cleared by macrophages
  • May be triggered by viral URTI in preceding month (60%)
55
Q

presentation of ITP

A
56
Q

investigations for ITP

A

History
- Type, severity and duration of bleeding
- Presence of systemic symptoms (fever, anorexia, bone pain, weight loss)- would be indicative of other causes
- Recent URTI
- Family history of bleeding disorders
- Considered non-accidental injury in younger children
Examination: normal except evidence of bleeding manifestations
Bloods: FBC to look at platelets

57
Q

management of ITP

A

Management:
* Reassurance that most can live comfortably and safely with low platelet counts.
* No IM injections; no NSAIDs, avoid contact sports (including PE until platelets >30).

Prognosis
- 75% resolve within 3 months
- 5-15% become persistent or chronic

58
Q

3 manifestations of meningococcal infection

A
  • Bacterial meningitis – bacteria infecting the meninges.
  • Meningitis with accompanying meningococcaemia – bacteria multiplying in the bloodstream.
  • Meningococcaemia without clinical evidence of meningitis.
59
Q

presentation of meningococcal septicaemia

A

Presentation
Non-blanching rash (may not be present in early stages) with:

  • Fever.
  • Nausea and vomiting.
  • Lethargy.
  • Muscle ache; joint pain.
  • Rapid breathing/breathlessness
  • Cold hands and feet
  • Pale/mottled skin
  • Confusion
  • Leg pain
  • Very sleepy
60
Q

meningococcal septicaemia: rash

A

The rash: petechiae -> purpura fulminans
1) Petechiae:

  • Appears as petechiae (1-2mm) initially on trunk and lower limbs.
  • Can coalesce into purpura and ecchymoses.
  • Petechiae correlate with degree of thrombocytopaenia; indicator of potential bleeding complications secondary to DIC.

2) Purpura fulminans:
* Cutaneous haemorrhage and necrosis due to vascular thrombosis and DIC.

61
Q

Cellulitis and erysipelas
background

A
  • Erysipelas is superficial skin infection whereas
  • Cellulitis involves deeper subcutaneous tissues (dermis and subcutaneous tissue)
62
Q

Cause of cellulitis

A
  • Strep. pyogenes or Staph. Aureus
  • Occasionally Haemophilus influenzae.
63
Q

presentation of cellulitis

A

Presentation
- Starts small, may look shiny
- Not itchy
- Tender, warm, spreading, sharply marginated erythema +/– oedema.
- May also have ascending red streaks of lymphangitis
- Regional lymphadenopathy, fever, malaise.
- Deeper infection may co-exist, e.g. osteomyelitis.

64
Q

investigations for cellulitis

A

Investigations
- Swab skin and blood culture.

65
Q

management of cellulitis

A

If erysipelas alone, IV penicillin (erythromycin if penicillin-allergic).

Cellulitis:
raise affected part (e.g. limb);
Combination of IV penicillin and flucloxacillin.
Consider cefotaxime instead of penicillin if child aged <5yrs and not immunized against Haemophilus.