Viral exanthems 2

Question 1

What is typhoid fever?

Answer 1

tropical infection caused by Salmonella typhi or paratyphi (usually less severe)
Worsening fever, headaches, cough, abdo pain, anorexia, malaise and myalgia
GI symptoms may not appear until second week
Splenomegaly, bradycardia, rose coloured spots on the trunk

Question 2

What is the management for typhoid fever?

Answer 2

a 3rd generation cephalosporin or azithromycin is usually effective

Question 3

How does malaria present?

Answer 3

Fever (often not cyclical), diarrhoea, vomiting, flulike symptoms.
Whilst typically the onset is 7-10 days after inoculation, infections can present months later, depending on the species
thick blood films examination
Treated with quinine or artemisinin-based formulations

Question 4

What are the investigations for kawasaki disease?

Answer 4

Raised CRP
Raised WBC
Raised platelet count (2nd week) 
Raised ESR
Raised LFTs
Low albumin 
Anaemia 
Echocardiogram

Question 5

What are the complications of Kawasaki disease?

Answer 5

Coronary artery aneurysms, myocarditis, pericarditis and sudden death

Question 6

What are the features of a petechial rash in N. meningitidis?

Answer 6

common and develops in 50-80% of patients
involves the axillae, flanks, wrists and ankles
they are usually located in the centre of light coloured macules, these are non- blanching and a sign of vasculitis

Question 7

What are the signs in meningitis?

Answer 7

Brudzinski: flexion of the neck with the child supine causing flexion of the knees and hips
Kernig: with the child lying supine and with the hips and knees flexed there is back pain on extension of the knee
Opisthotonus is arching of the back with increased ICP

Question 8

What is the classical clinical presentation of meningitis?

Answer 8

Headache
o	Fever
o	Vomiting
o	Photophobia
o	Lethargy
o	Neck stiffness
o	Rash >50%
o	Seizures 20%
o	Early non-specific symptoms

Question 9

What is septicaemia?

Answer 9

results from the activation and continued stimulation of the immune system by pro- inflammatory cytokines  caused by endotoxin
o	Capillary leak
o	Coagulopathy
o	Metabolic derangement
o	Myocardial failure

Question 10

What is the typical presentation of septicaemia?

Answer 10

Fever
o	Rash- may initially be erythematous and may change to petechiae and purpura
o	Vomiting
o	Headache
o	Myalgia
o	Abdominal pain
o	Tachycardia/tachypnoea
o	Hypotension
o	Cool extremities
o	Initially normal conscious level

Question 11

What are the investigations for meningococcal sepsis?

Answer 11

FBC & differential count
o Blood glucose & gas for acidosis
o Coagulation screen & CRP
o U&E and LFTs
o Culture- blood, throat swab, urine, stool
o Rapid antigen test for meningitis organsism blood, CSF or urine
o LP for CSF unless contraindicated
o Serum for comparison of convalescent titres
o PCR for possible organisms- blood & CSF
o Consider CT/MRI head and EEG

Question 12

What are the nervous system complications of meningococcaemia?

Answer 12

Hearing loss 
Local vasculitis 
Local cerebral infarction 
Subdural effusion 
Hydrocephalus 
Cerebral abscess
Occupying lesion

Question 13

What are the other complications of meningococcaemia?

Answer 13

DIC
o	Thrombocytopenia
o	Septic arthritis
o	Pericarditis
o	Bacterial endocarditis
o	Gangrene

Question 14

What are the clinical features of malaria?

Answer 14

o	Fever often not cyclical
o	Diarrhoea
o	Vomiting
o	Flu-like symptoms
o	Jaundice
o	Anaemia
o	Thrombocytopenia
Whilst typically the onset is 7-10 days after inoculation infections can present many months later

Question 15

What is cerebral malaria?

Answer 15

Rapidly developing encephalopathy which only occurs in 20-50% of people who develop malaria it occurs when parasites adhere to the cerebral microvasculature causing blockage this loads to a shortage of oxygen to this site and therefore numerous complications around half these patients have elevated ICP and seizures

Question 16

How is malaria diagnosed?

Answer 16

by examination of a thick film-species (falciparum, vivax, ovale or malariae) is confirmed on a thin film- repeated blood films may be necessary

Question 17

What is the management for malaria

Answer 17

Quinine is required in most cases of Plasmodium falciparum seen in the UK- because of the emergence of chloroquine-resistant strains worldwide
Prophylaxis reduces, but does not eliminate the risk of infection- prevention of mosquito bites with repellents and bed nets is also important

Question 18

What are the secondary causes of immunodeficiency>

Answer 18

	Intercurrent bacterial or viral infection
	Malignancy
	Malnutrition
	HIV infection
	Immunosuppressive therapy
	Splenectomy
	Nephrotic syndrome

Question 19

What are T cell defects?

Answer 19

Severe and/or unusual viral and fungal infections and failure to thrive in the first months of life e.g. severe bronchiolitis, diarrhoea, oral thrush and PCP
SCID
HIV
Wiskott Aldrich-a triad with thrombocytopenia and eczema (X-linked)
DiGeorge
Duncan- inability to make a normal response to EBV and child either succumbs to infection or develops secondary lymphoma
Ataxia telangiectasia- defect in DNA repair, also increased risk of lymphoma there is cerebellar ataxia and developmental delay

Question 20

What are b-cell defects?

Answer 20

In the first 2 years there are severe bacterial infections especially of the ear, sinus’, skin and pulmonary
system there is often diarrhoea and failure to thrive
X-linked agammaglobulinaemia-abnormal tyrosine kinase gene, eseential for B-cell maturation
Common variable immunodeficiency (CVID) B cell deficiency, high risk of autoimmune disorders and malignancy
Hyper IgM syndrome- B cells produce IgM but prevented from switching to IgG and IgA
Selective IgA deficiency- most common primary immune defect usually asymptomatic or recurrent ear, sinus and pulmonary infections

Question 21

What are neutrophil defects?

Answer 21

• Recurrent bacterial infections- abscesses (skin, lymph nodes, lung, liver, spleen, bone), poor wound healing, perianal disease and periodontal infections invasive fungal infections such as aspergillosis
Diarrhoea and failure to thrive granulomas from chronic inflammation
Chronic granulomatous disease- most are x-linked recessive, some autosomal recessive defect in phagocytosis as fail to produce superoxide after ingestion of micro-organism

Question 22

What are leucocyte function defects?

Answer 22

Delayed separation of umbilical cord, delayed wound healing, chronic skin ulcers and dee-seating infection
o Leucocyte adhesion deficiency (LAD) deficiency of neutrophil surface adhesion molecules leads to inability of neutrophils to migrate to sites of infection/inflammation

Question 23

What are complement defects?

Answer 23

• Recurrent bacterial infections, SLE like illness, recurrent meningococcal infections with deficiency of the terminal complement components
o Early complement component deficiency
o Terminal complement component deficiency
o Mannose-binding lectin (MBL) deficiency

Question 24

What is the management for immunodeficiencies?

Answer 24

• Antimicrobial prophylaxis- for T-cell and neutrophil defects give cotrimoxazole to prevent pneumocystis jiroveci infection and itraconazole or fluconazole to prevent other fungal infections for B-cell defects give antibiotic prophylaxis (e.g. azithromycin) to prevent recurrent bacterial infections
Antibiotic treatment
Screen for end organ disease
Immunoglobulin replacement therapy
Bone marrow transplantation- used for SCID or granulomatous disease
Gene therapy- SCID
• Gene therapy for certain forms of SCID but