Infectious diseases Flashcards
Macular/maculopapular viral rashes
Roseola infantum
Slapped cheek
Measles
Rubella
Macular/maculopapular bacterial rashes
Scarlet fever
Rheumatic fever
Typhoid fever
Lyme’s disease
Macular/maculopapular rash other causes
Kawasaki’s disease
Juvenile RA
Vesicular, bullous or pustular viral rashes
Herpes simplex
Varicella
Hand-foot-and-mouth
Vesicular, bullous or pustular bacterial rashes
Boils
Impetigo
Staphylococcal scalded skin
Vesicular, bullous or pustular rashes other causes
Erythema multiforme
TEN
SJS
Petechial/purpuric viral rashes
Enterovirus
Adenovirus
Petechial/purpuric bacterial rashes
Meningococcal
Infective endocarditis
Petechial/purpuric rashes other causes
HSP
Thrombocytopenia
Vasculitis
Cellulitis
Bacterial infection that affects the dermis and the deeper subcutaneous tissues
Clinical diagnosis
Cellulitis clinical features
Commonly occurs on shins → usually unilateral
Erythema → well-demarcated margins
Swelling
Systemic upset - fever, malaise & nausea
Cellulitis classification
Eron classification
I - no signs of systemic toxicity & no uncontrolled co-morbidities
II - person is either systemically unwell/systemically unwell but a co-morbidity that may complicate resolution of infection
III - significant systemic upset/unstable co-morbidities/limb-threatening infection due to vascular compromise
IV - sepsis syndrome/severe life-threatening infection
Cellulitis admission criteria
Eron class III/class IV cellulitis
Severe or rapidly deteriorating cellulitis
Very young (< 1 year) or frail
Immunocompromised
Significant lymphoedema
Facial cellulitis/periorbital cellulitis
Cellulitis mx
Guided by Eron classification
I - oral flucloxacillin, clarithromycin/erythromycin/doxycycline for penicillin allergic
II - admission may not be required if facilities are available in the community & can be monitored closely
III-IV - admit, IV co-amoxiclav/clindamycin/cefuroxime/ceftriaxone
Epiglottitis
Acute, life threatening condition, most commonly caused by an infection
Epiglottis = flap of cartilage behind the tongue, designed to protect the larynx during swallowing
Epiglottitis pathophysiology
H. influenzae and strep pneumoniae may locally invade the epiglottis → inflammation
Inflammation starts on the lingual surface of the epiglottis before spreading to other laryngeal structures → aryepiglottic folds, the arytenoids and supraglottic larynx
Children are at a higher risk of acute airway obstruction as epiglottis is much more floppy, broader, longer & angled more obliquely to the trachea
Epiglottitis risk factors
Children not receiving the HiB vaccine
Male gender
Immunosuppression
Epiglottitis clinical features
4 D’s - dyspnoea, dysphagia, drooling & dysphonia
Symptoms < 12 hours & typically no cough
High grade fever, sore throat, dehydration & signs of partial airway obstruction
Stridor is a late sign
Some children may adopt a tripod position → patient leans forward on outstretched arms with neck extended & tongue out
Epiglottitis ix
Shouldn’t be examined → high risk of airway obstruction
Throat swabs - bacterial and viral
Blood tests - FBC, cultures & CRP
Lateral neck x-ray
- thumb-print sign
- thickened aryepiglottic folds
- increased opacity of the larynx and vocal cards
CT/MRI only if not responding to the initial treatment
Epiglottitis mx
Secure the airway
Oxygen
Nebulised adrenaline
IV antibiotics - cefotaxime/ceftriaxone
IV steroids
IVI - resus and maintenance
Epiglottitis complications
Mediastinitis - infection spreads to retropharyngeal space
Deep neck space infection
Pneumonia
Meningitis
Sepsis/bacteraemia
Neonatal HSV aetiology
Can occur when the baby comes into contact with primary vesicles in the maternal genital tract during delivery
Risk is low with recurrent herpes infection
Neonatal HSV clinical features
Vesicular lesions on the skin
Eye involvement
Oral mucosa involvement, without internal organ involvement
Disseminated features - seizures, encephalitis, hepatitis, sepsis
Features commonly appear in first week of birth but manifestation can be as late as fourth week of life
Neonatal HSV ix
Identifying presence of virus in the newborn - PCR, virus culture, DFA testing
MRI brain - cases of suspected encephalitis
Neonatal mx
Parenteral acyclovir with intensive supportive therapy for severe cases
Elective c-section/intrapartum IV acyclovir may be advised if active primary herpes lesions are present on mother at term OR primary outbreak within 6 weeks of labour
8 weeks vaccine
- 6 in 1 vaccine (diphtheria, tetanus, pertussis, polio, haemophilus influenza type B (Hib) and hepatitis B)
- meningococcal type B
- rotavirus (oral vaccine)
12 weeks vaccine
- 6 in 1 vaccine
- pneumococcal
- rotavirus
16 weeks vaccine
- 6 in 1 vaccine
- meningococcal type B
1 year vaccine
- 2 in 1 (haemophilus influenza type B and meningococcal type C)
- pneumococcal
- MMR vaccine
- meningococcal type B
Yearly from age 2-8 vaccine
influenza vaccine (nasal vaccine)
3 years 4 months vaccine
- 4 in 1 (diphtheria, tetanus, pertussis and polio)
- MMR vaccine
12-13 years vaccine
HPV vaccine
14 years vaccine
- 3 in 1 (tetanus, diphtheria and polio)
- meningococcal groups A, C, W & Y
Malaria
Disease caused by Plasmodium protozoa which is spread by the female Anopheles mosquito
Malaria protective factors
Sickle-cell trait
G6PD deficiency
HLA-B53
Absence of Duffy antigens
Features of severe malaria
Schizonts on a blood film
Parasitaemia > 2%
Hypoglycaemia
Acidosis
Temperature > 39
Severe anaemia
Complications
Malaria complications
Cerebral malaria - seizures, coma
Acute renal failure - blackwater fever, secondary to intravascular haemolysis
ARDS
Hypoglycaemia
DIC
Uncomplicated falciparum malaria management
Artemisinin-based combination therapies as first-line
E.g. artesunate + amodiaquine
Severe falciparum malaria management
Parasite count > 2% → parenteral mx irrespective of clinical state
IV artesunate
Parasite count > 10%, exchange transfusion should be considered
Non-falciparum features
General features of malaria - fever headache, splenomegaly
Plasmodium vivax/ovale - cyclical fever every 48 hours, plasmodium malariae - cyclical fever every 72 hours
Plasmodium malariae - associated with nephrotic syndrome
Non-falciparum management
Artemisinin-based combination therapy or chloroquine
ACTs avoided in pregnant women
Patients with ovale/vivax - given primaquine following acute mx with chloroquine to destroy liver hypnozoites & prevent relapse
Measles clinical features
Prodromal phase - irritable, conjunctivitis, fever
Koplik spots - typically develop before the rash, white (’grain of salt’) on the buccal mucosa
Rash - starts behind ears then to the whole body, discrete maculopapular rash becoming blotchy & confluent
- desquamation that typically spares the palms & soles may occurs after a week
Diarrhoea (10%)
Measles ix
Measles-specific IgM and IgG serology (ELISA)
- most sensitive 3-14 days after onset of the rash
Measles RNA detection by PCR
- best for swabs taken 1-3 days after rash onset
Measles mx
Mainly supportive
Vitamin A in children < 2 years
Admission may be considered in immunosuppressed/pregnant patient
Notifiable disease → inform public health
Measles complications
Otitis media
Pneumonia
Encephalitis
Subacute sclerosing panencephalitis - 5-10 years after illness
Febrile convulsions
Keratoconjunctivitis, corneal ulceration
Diarrhoea
Increased risk of appendicitis
Myocarditis
Measles mx of contacts
Child not immunised against measles comes into contact → MMR should be offered
- given within 72 hours