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Book cover for Oxford Handbook of Emergency Medicine (4 edn) Oxford Handbook of Emergency Medicine (4 edn)
Disclaimer
Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always … More Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up to date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-pregnant adult who is not breastfeeding.

Incubation periods 220

Notifiable infectious diseases 221

Childhood infectious diseases 222

Meningitis 224

Gastroenteritis/food poisoning 226

Fish poisoning 229

Infestations 230

Tuberculosis 232

Anthrax 233

Streptococcal infections 234

Staphylococcal infections 235

Tetanus 236

Gas gangrene 237

Botulism 237

Sexually transmitted diseases 238

Hepatitis 239

Leptospirosis (Weil's disease) 239

Herpes virus infections 240

Infectious mononucleosis (glandular fever) 241

Human immunodeficiency virus (HIV) 242

Presentation of HIV +ve patients 244

Imported infectious diseases 246

Malaria 247

Typhoid and paratyphoid (enteric fever) 248

Dengue 248

Poliomyelitis 249

Rabies 249

Viral haemorrhagic fevers 250

Severe acute respiratory syndrome 251

Influenza pandemics, avian flu, and swine flu 252

Staphylococcal enteritis

1–6 hours

Salmonella enteritis

6–48 hours (usually 12–24 hours)

Bacillary dysentery (Shigella)

1–7 days (usually 1–3 days)

Botulism

12–96 hours (usually 18–36 hours)

Cholera

12 hours–6 days (usually 1–3 days)

Dengue

4–7 days

Diphtheria

2–5 days

Gas gangrene

6 hours–4 days

Legionnaires’ disease

2–10 days (usually 7 days)

Meningococcaemia

1–7 days (usually 3 days)

Scarlet fever

1–4 days

Yellow fever

3–6 days

Staphylococcal enteritis

1–6 hours

Salmonella enteritis

6–48 hours (usually 12–24 hours)

Bacillary dysentery (Shigella)

1–7 days (usually 1–3 days)

Botulism

12–96 hours (usually 18–36 hours)

Cholera

12 hours–6 days (usually 1–3 days)

Dengue

4–7 days

Diphtheria

2–5 days

Gas gangrene

6 hours–4 days

Legionnaires’ disease

2–10 days (usually 7 days)

Meningococcaemia

1–7 days (usually 3 days)

Scarlet fever

1–4 days

Yellow fever

3–6 days

Brucellosis

7–21 days (occasionally some months)

Chickenpox

10–20 days (usually about 14 days)

Lassa fever

6–21 days

Leptospirosis

2–26 days (usually 7–12 days)

Malaria (falciparum)

7–14 days (occasionally longer)

Malaria (vivax, malariae, ovale)

12–40 days (occasionally >1 year)

Measles

10–18 days (rash usually 14–18 days)

Mumps

14–18 days

Pertussis (whooping cough)

5–14 days (usually 7–10 days)

Poliomyelitis

3–21 days (usually 7–10 days)

Rubella

14–21 days

Tetanus

1 day–3 months (usually 4–14 days)

Typhoid

3–60 days (usually 7–14 days)

Typhus

7–14 days

Brucellosis

7–21 days (occasionally some months)

Chickenpox

10–20 days (usually about 14 days)

Lassa fever

6–21 days

Leptospirosis

2–26 days (usually 7–12 days)

Malaria (falciparum)

7–14 days (occasionally longer)

Malaria (vivax, malariae, ovale)

12–40 days (occasionally >1 year)

Measles

10–18 days (rash usually 14–18 days)

Mumps

14–18 days

Pertussis (whooping cough)

5–14 days (usually 7–10 days)

Poliomyelitis

3–21 days (usually 7–10 days)

Rubella

14–21 days

Tetanus

1 day–3 months (usually 4–14 days)

Typhoid

3–60 days (usually 7–14 days)

Typhus

7–14 days

Amoebiasis

2 weeks–many months

Hepatitis A

2–6 weeks (usually 4 weeks)

Hepatitis B, hepatitis C

6 weeks–6 months

HIV

2 weeks–3 months (anti-HIV appears)

Infectious mononucleosis

4–7 weeks

Rabies

4 days–2 years (usually 3–12 weeks)

Syphilis

10 days–10 weeks (usually 3 weeks)

Amoebiasis

2 weeks–many months

Hepatitis A

2–6 weeks (usually 4 weeks)

Hepatitis B, hepatitis C

6 weeks–6 months

HIV

2 weeks–3 months (anti-HIV appears)

Infectious mononucleosis

4–7 weeks

Rabies

4 days–2 years (usually 3–12 weeks)

Syphilis

10 days–10 weeks (usually 3 weeks)

Chickenpox

3 days before rash until last vesicle crusts

Hepatitis A

2 weeks before until 1 week after jaundice starts

Measles

4 days before rash until 5 days after rash appears

Mumps

3 days before to 1 week after salivary swelling

Pertussis

3 days before to 3 weeks after start of symptoms

(5 days if on appropriate antibiotic)

Rubella

1 week before to 1 week after onset of rash

Scarlet fever

10–21 days from onset of rash (1 day if on penicillin)

Chickenpox

3 days before rash until last vesicle crusts

Hepatitis A

2 weeks before until 1 week after jaundice starts

Measles

4 days before rash until 5 days after rash appears

Mumps

3 days before to 1 week after salivary swelling

Pertussis

3 days before to 3 weeks after start of symptoms

(5 days if on appropriate antibiotic)

Rubella

1 week before to 1 week after onset of rash

Scarlet fever

10–21 days from onset of rash (1 day if on penicillin)

In Britain certain infectious diseases are ‘notifiable’. A doctor who knows or suspects that a patient has one of these diseases is obliged to notify the local Health Protection department. Use the special notification form if available. Telephone the consultant in Communicable Disease Control if investigation or control of an outbreak may be needed.

HIV and AIDS are not notifiable diseases, but may be reported in strict confidence in the same way.

Anthrax

Botulism

Brucellosis

Cholera

Diphtheria

Encephalitis (acute)*

Erysipelas**

Food poisoning*

Haemolytic uraemic syndrome (HUS)

Haemophilus influenzae type b (Hib)**

Infectious bloody diarrhoea (E. coli O157 infection**)

Infectious hepatitis (acute)*

Invasive group A streptococcal disease and scarlet fever*

Legionnaires’ disease*

Leprosy*

Malaria*

Measles

Meningitis (acute)*

Meningococcal septicaemia*/meningococcal disease**

Mumps

Necrotizing fasciitis**

Paratyphoid

Pertussis (whooping cough)

Plague

Poliomyelitis

Rabies

Rubella

Severe acute respiratory syndrome (SARS)

Smallpox

Tetanus

Tuberculosis

Tularaemia**

Typhoid

Typhus*

Viral haemorrhagic fever (VHF)

West Nile fever**

Yellow fever

Unimmunized children are at risk of infections which would be prevented by the standard immunization schedule. Always ask about vaccination status in any febrile, unwell child. The common infectious diseases of childhood can be very serious in children with immune deficiency or those on immunosuppressant drugs. Refer such children for specialist advice if they develop an infectious disease or have been in contact with one. Children with cystic fibrosis can become very ill with measles, whooping cough or chickenpox—refer these also. Neonates rarely develop the common exanthems of childhood, but require referral if these occur. Chickenpox can be particularly serious in this age group.

A virus infection spread by airborne droplets.

=10–18 days. Infectious from just before the onset of symptoms until 5 days after the rash appears.

(lasting ≈3 days) are fever, malaise, coryza, conjunctivitis and cough. Koplik's spots (small white spots like grains of salt) appear inside the cheeks. 1–2 days later a red maculopapular rash starts behind the ears, and spreads to the face and down the body.

is symptomatic unless there are complications (eg otitis media or bacterial pneumonia). Febrile convulsions may occur. Encephalitis is rare, but can be fatal. Hospital admission is rarely needed unless the child is very ill or has pre-existing disease. In the tropics many malnourished children die from measles, but in the UK the mortality is very low.

Mumps is a virus infection spread by saliva and respiratory droplets. Infectivity is greatest at the onset of symptoms, but many sub-clinical cases also spread infection.

 = 14–18 days.

are fever with pain and swelling in one or both parotid glands. Aseptic meningitis may occur. Orchitis affects 10–15% of post-pubertal males, but rarely causes sterility. The pain of orchitis may be relieved by analgesia and a short course of steroids. Orchitis is uncommon before puberty, so consider torsion of the testis if a child presents with testicular pain and swelling (graphic  p.700).

Rubella is usually a mild disease, but infection during pregnancy may cause severe congenital disorders, particularly eye defects, heart defects and deafness. Guidance on the management of, and exposure to, rubella in pregnancy is available from the Health Protection Agency based in London (www.hpa.org.uk/infections). The virus is spread mainly by the airborne route, with an incubation period of 2–3 weeks and infectivity from 1 week before symptoms until 1 week after the rash appears. A macular rash occurs on the face and trunk, with mild fever, occipital lymphadenopathy and sometimes transient arthralgia. Rare complications are encephalitis and thrombocytopenia.

is generally symptomatic. The clinical diagnosis of rubella is unreliable: similar rashes may occur with enterovirus and parvovirus infections. If there is concern about rubella infection in pregnancy take blood for viral antibody levels and arrange urgent follow-up by the GP or obstetrician.

see graphic  p.684.

Meningitis may be bacterial, viral, or occasionally fungal. Bacterial causes of meningitis include meningococci, pneumococci, Haemophilus influenzae, Listeria, and tuberculosis (TB). Other bacteria may also cause meningitis in neonates, the elderly, and immunosuppressed patients.

Some patients with meningitis have the classic features of headache, neck stiffness, photophobia, fever and drowsiness. However, the clinical diagnosis of meningitis may be very difficult in early cases. Neonates may present with anorexia, apnoea, or fits. Meningitis may start as a ‘flu-like’ illness, especially in the immunosuppressed or elderly. Consider meningitis in any febrile patient with headache, neurological signs, neck stiffness, or ↓ conscious level.

is caused by Neisseria meningitidis. It can result in septicaemia, coma, and death within a few hours of the first symptoms. Skin rashes occur in 50% of patients, often starting as a maculopapular rash before the characteristic petechial rash develops. There may be DIC and adrenal haemorrhage (Waterhouse–Friderichsen). Meningococcal septicaemia (graphic  p.666) may occur without meningitis.

Resuscitate if necessary, give oxygen and obtain venous access.

Start antibiotics immediately (without waiting for investigations) if the patient is shocked or deteriorating or there is any suspicion of meningococcal infection (especially a petechial or purpuric rash): give IV ceftriaxone or cefotaxime (adult 2g; child 80mg/kg). Chloramphenicol is an alternative if there is a history of anaphylaxis to cephalosporins (see BNF). In adults >55 years add ampicillin 2g qds to cover Listeria. Give vancomycin ± rifampicin if penicillin-resistant pneumococcal infection is suspected. Give IV dexamethasone (0.15mg/kg, max 10mg, qds for 4 days) starting with or just before the first dose of antibiotics, especially if pneumococcal meningitis is suspected.

are FBC, U&E, glucose, clotting screen, ABG, CRP, blood cultures, EDTA sample for PCR, and clotted blood for serology. LP is needed if meningitis is suspected, unless there is a coagulopathy or ↑ ICP: do CT scan if there is suspicion of i ICP (confusion/coma, hypertension, bradycardia or papilloedema) or focal neurological signs.

IV fluids.

Pressure area care.

Monitor conscious level, T°, BP, ECG, SpO2, and fluid balance.

Get expert help promptly and organize ICU care.

For the latest advice and algorithms see www.meningitis.org and www.nice.org.uk/guidance/CG102/quickrefguide

For meningitis and LP in children see graphic  p.666.

While intubating a patient with suspected meningococcal infection wear a suitable mask (eg FFP3) and a face shield to reduce the risk of infection.

Meningococcal infection is spread by droplets from the nose of an infected carrier, who may be well. Notify the consultant in Communicable Disease Control (graphic  p.221) immediately about any suspected meningococcal infection and obtain advice about antibiotic prophylaxis. Prophylactic antibiotics (rifampicin, ciprofloxacin or ceftriaxone) are needed for the patient's family and close contacts. Hospital and ambulance staff do not need prophylaxis unless they have given mouth to mouth ventilation or intubated the patient without using protective equipment.

is given 12 hourly for 2 days (5mg/kg for child aged <1 year; 10mg/kg at 1–12 years; 600mg at age >12 years. It makes the urine orange or brown, discolours soft contact lenses, and ↓ effectiveness of OCP for ≈4 weeks (see BNF)—give appropriate warnings and record this in the notes.

is given as a single oral dose of 500mg (adults), 250mg (child 5–12 years) or 125mg (child 2–5 years), although it is not licensed for chemoprophylaxis of meningitis.

is given as a single IM dose of 250mg (adults and children >12 years) or 125mg (children <12 years).

Tell contacts of meningococcal patients to report to a doctor at once if they develop symptoms.

Often gradual onset, with malaise, anorexia, vomiting, headache and eventually signs of meningitis. Cranial nerve palsies, spastic paraplegia and coma can occur. Meningitis may be part of miliary TB (graphic  p.232), which may be apparent on chest X-ray. Ophthalmoscopy may show choroidal tubercles and papilloedema, which is found more commonly than in other forms of meningitis. Refer for specialist investigation and treatment.

Viral causes of meningitis include coxsackie, mumps, and echoviruses. Viral meningitis produces similar clinical features to bacterial infection, but the illness is often less severe. The initial management is the same as for suspected bacterial meningitis. Refer for admission and investigation.

Fungal meningitis is usually part of disseminated infection in immunosuppressed patients, (eg those with AIDS (graphic  p.242), lymphoma, or on steroid therapy). Cryptococcus neoformans is the commonest organism. Symptoms usually develop slowly, as with TB meningitis. There may be papilloedema and focal neurological signs. Admit for specialist investigation and treatment.

is the usual presenting symptom of gastroenteritis, but it may also occur in many other conditions as diverse as otitis media, appendicitis and ulcerative colitis. Antibiotics often cause diarrhoea. Constipation may present as diarrhoea if there is overflow around an obstructing stool. A rectal tumour may present similarly.

may seek advice about diarrhoea when in fact the stools are normal. Breast-fed babies almost always have loose stools, which may be yellow or green and very frequent, often after every feed. However, gastroenteritis is very rare in fully breast-fed babies. In children aged >6 months, normal stool frequency ranges from 1 stool on alternate days to 3 stools daily.

may be caused by many types of bacteria and viruses, and also by some toxins and poisons. Many episodes of gastroenteritis result from contaminated food, usually meat, milk or egg products, which have been cooked inadequately or left in warm conditions. The specific cause is often not identified. Some infections are spread by faecal contamination of water (eg cryptosporidiosis from sheep faeces). Rotavirus infection (common in children) may be transmitted by the respiratory route. Severe illness with bloody diarrhoea, haemolysis and renal failure may result from infection with verocytotoxin producing E. coli (VTEC O157).

are unnecessary in most cases of gastroenteritis, but obtain them if the patient has been abroad, is severely ill, has prolonged symptoms, comes from an institution or works as a food-handler.

is a notifiable disease (graphic  p.221). Immediate notification by telephone is mandatory if an outbreak is suspected. The food eaten, symptoms and incubation period may suggest the organism or toxin involved (see Table 5.1). Carbon monoxide poisoning (graphic  p.208) may cause malaise and vomiting in several members of a family and be misdiagnosed as food poisoning.

Table 5.1
Food poisoning characteristics
CauseIncubationFoodSymptoms*

Staph. aureus

1–6 hours

Meat, milk

D, V, P, shock

Bacillus cereus

1–16 hours

Rice

D, V, P

Salmonella

6–48 hours

Meat, eggs

D, V, P

Escherichia coli

1–2 days

Any food

D, V, P

E. coli VTEC 0157

1–2 days

Meat, milk

D, V, P

Campylobacter

1–3 days

Meat, milk

Fever, P, D

Shigella

1–3 days

Any food

Bloody D, V, fever

Vibrio parahaem

2–3 days

Seafood

Watery D

Cholera

12hr–6 days

Water, seafood

D (watery), shock

Rotavirus

1–7 days

D, V, fever, cough

Botulism

12–96 hours

Preserved food

V, paralysis

Histamine fish poisoning (scombrotoxin)

<1 hour

Fish

Flushing, headache, D, V, P (graphic  p.229)

Ciguatera fish poisoning

1–6 hours (rarely 30 hours)

Fish from tropical coral reef

D, V, P, paraesthesiae, muscle weakness (graphic  p.229)

Paralytic shellfish poisoning

30 min–10 hours

Shellfish

Dizziness, paraesthesiae, weakness, respiratory failure (graphic  p.229)

Chemicals

<2 hours

Food, water

Various

Mushrooms

<24 hours

Mushrooms

D, V, P, hallucinations (graphic  p.212)

CauseIncubationFoodSymptoms*

Staph. aureus

1–6 hours

Meat, milk

D, V, P, shock

Bacillus cereus

1–16 hours

Rice

D, V, P

Salmonella

6–48 hours

Meat, eggs

D, V, P

Escherichia coli

1–2 days

Any food

D, V, P

E. coli VTEC 0157

1–2 days

Meat, milk

D, V, P

Campylobacter

1–3 days

Meat, milk

Fever, P, D

Shigella

1–3 days

Any food

Bloody D, V, fever

Vibrio parahaem

2–3 days

Seafood

Watery D

Cholera

12hr–6 days

Water, seafood

D (watery), shock

Rotavirus

1–7 days

D, V, fever, cough

Botulism

12–96 hours

Preserved food

V, paralysis

Histamine fish poisoning (scombrotoxin)

<1 hour

Fish

Flushing, headache, D, V, P (graphic  p.229)

Ciguatera fish poisoning

1–6 hours (rarely 30 hours)

Fish from tropical coral reef

D, V, P, paraesthesiae, muscle weakness (graphic  p.229)

Paralytic shellfish poisoning

30 min–10 hours

Shellfish

Dizziness, paraesthesiae, weakness, respiratory failure (graphic  p.229)

Chemicals

<2 hours

Food, water

Various

Mushrooms

<24 hours

Mushrooms

D, V, P, hallucinations (graphic  p.212)

*

D = diarrhoea, V = vomiting, P = abdominal pain.

Record the duration of symptoms and the frequency and description of stools and vomit. Document other symptoms (eg abdominal pain, fever), food and fluid ingested and drugs taken. Enquire about affected contacts, foreign travel and occupation (especially relevant if a food-handler).

Look for abdominal tenderness, fever and other signs of infection. Record the patient's weight and compare this with any previous records. Assess the degree of dehydration—this is traditionally classified as mild (<5%), moderate (5–10%), or severe (>10%), as outlined opposite.

Thirst.

↓ urinary output (in a baby <4 wet nappies in 24hr).

Dry mouth.

Sunken fontanelle in infants.

Sunken eyes.

Tachypnoea due to metabolic acidosis.

Tachycardia.

↓ skin turgor on pinching the skin.

Drowsiness/irritability.

Most cases are self-limiting, but careful attention is needed to ensure adequate fluid replacement and also to prevent cross-infection (graphic  p.32).

is needed if the patient looks seriously ill, dehydration is >5%, there is a high fever or the family are unlikely to cope with the patient at home. Babies aged <3 months may be difficult to assess and can deteriorate rapidly—refer for admission. Severely dehydrated (>10%) children need immediate IV fluids, initially 0.9% saline (10–20mL/kg over 5min, repeated as necessary).

is effective in most patients with gastro-enteritis (<5% dehydration). Standard ORT products (eg Dioralyte®) contain glucose, sodium, potassium, chloride and citrate (details in BNF). Glucose is important to enhance absorption of sodium and water.

Usual dose of ORT: infant 1–1½ times usual feed volume. child 200mL after each loose stool. adults 200–400mL after each loose stool.

Extra ORT can be given if the patient is still thirsty. Frequent small sips are usually tolerated better than a large drink. Check that the patient (or parent/carer) can understand the instructions supplied with the ORT sachets or effervescent tablets and can measure the necessary amounts of clean water.

after 24hr (or earlier if diarrhoea has settled or the patient is hungry). Give further ORT if the diarrhoea continues. A child with acute diarrhoea requires daily review (usually by the GP), but should be seen earlier if he becomes more ill (especially if drowsy or pyrexial), or if vomiting and/or diarrhoea worsens. Home-made salt and sugar mixtures may be dangerously inaccurate for ORT, but if nothing else is available, one could use salt 2.5mL (half a 5mL spoonful) and sugar 20mL (4 × 5mL spoonfuls) in 1 pint (500mL) of cooled boiled water.

other than ORT are rarely needed in gastroenteritis. In adults an anti-emetic (prochlorperazine 12.5mg IM or 3mg buccal) may be helpful, but in children prochlorperazine often causes troublesome side effects. However, oral ondansetron (0.1–0.15mg/kg, max 8mg) reduces vomiting and the need for IV fluids and admission. Prolonged vomiting requires investigation and hospital admission.

(eg kaolin, codeine phosphate, loperamide) are contraindicated in children and rarely needed in adults: they may aggravate nausea and vomiting and occasionally cause ileus.

are only needed in special circumstances. Most episodes of gastroenteritis are brief and many are caused by viruses and not helped by antibiotics. Patients with amoebiasis, giardiasis, Campylobacter or Shigella infections may need antibiotics: refer to an Infectious Diseases unit for treatment and follow-up. Antibiotics are occasionally useful in traveller's diarrhoea before a long journey or an important meeting: trimethoprim (200mg bd PO for 5 days) or ciprofloxacin (500mg bd PO for 2 days: see the BNF or data sheet about side effects and warnings).

Also known as scombroid fish poisoning or scombrotoxin poisoning, this is caused by ingesting toxins in fish such as tuna, mackerel, and other dark-meat fish, which have been stored improperly. If the fish is not cooled rapidly after it is caught, an enzyme in bacteria converts histidine into histamine and other toxins, which are heat-stable and so are unaffected by cooking. The patient may notice that the fish tastes metallic, bitter, or peppery and the flesh looks honeycombed. Symptoms start within a few minutes to 2 hours, with flushing of the face and upper body, headache, nausea, vomiting, abdominal pain, diarrhoea, dizziness and palpitations. Urticaria and bronchospasm are less common. The symptoms usually settle within 6 hours without treatment, but resolve more quickly with antihistamines (eg chlorphenamine 10mg IV in adults, 250 micrograms/kg in children). In severe cases cimetidine and, rarely, adrenaline might be needed, with oxygen, IV fluids and bronchodilators.

The patient should be told that histamine fish poisoning is caused by improper fish handling and storage. It is not an allergic reaction and so the patient would not have to avoid eating fish in future.

This is caused by a neurotoxin called ciguatoxin which is produced by a dinoflagellate (a unicellular plankton) associated with coral reefs. Fish imported from the tropics may cause ciguatera poisoning in the UK and elsewhere. Symptoms usually start 1–6 hours after ingestion with nausea, vomiting, watery diarrhoea and abdominal pain, followed by neurological symptoms, including paraesthesiae of the lips, tongue and feet, ataxia and muscle weakness. A classic feature is paradoxical temperature reversal (cold objects feel hot and hot objects feel cold). Alcohol makes these symptoms worse. Bradycardia and hypotension may occur. Treatment is symptomatic and supportive. Gastro-intestinal symptoms usually settle within 1 day, but paraesthesiae may persist for weeks or months.

This can be caused by eating molluscs such as mussels, clams, cockles and scallops which concentrate a neurotoxin called saxitoxin produced by dinoflagellate plankton. This plankton proliferates when sea temperatures rise in summer and may make the sea look red (‘red tide’). Symptoms start 30 minutes to 10 hours after ingestion, with dizziness, ataxia, paraesthesiae and muscle weakness, which may progress to respiratory failure. Treatment is supportive, with assisted ventilation if necessary. Complete recovery is usual within 24 hours.

The most common helminthic infection seen in the UK is the threadworm Enterobius vermicularis. This causes anal itching, especially at night. Sometimes intact worms (length 5–13mm, diameter 0.1–0.5mm) are seen in the faeces. Unwashed fingers transmit ova from the perianal skin to the mouth. Personal hygiene is important in treatment and in prevention of reinfection (hand-washing and nail-scrubbing before each meal and after every visit to the toilet). A bath immediately after getting up removes ova laid overnight. All members of the family require treatment with mebendazole or piperazine (see BNF).

include roundworms, hookworms and tapeworms. Obtain advice from departments of Infectious Diseases or Tropical Medicine (see graphic  p.246).

Humans may be infected by the body louse (Pediculosis humanis corporis), head louse (Pediculosis humanis capitis), or the ‘crab’/pubic louse (Phthirus pubis).

are common in school children. Infection is not related to lack of hygiene or the length of hair. Adult lice are 3–4mm long, vary in colour from white to grey-black and attach themselves firmly to the scalp at the base of hairs. The egg cases (‘nits’) are white and 1–2mm in diameter, glued firmly to the base of hairs and moving outwards as the hair grows. Head lice cause intense itching, which may suggest the diagnosis. Secondary infection may result in impetigo. Head lice are usually treated with malathion, phenothrin or simeticone, repeated after 7 days (see BNF). Drug-resistant lice occur in some areas. Wet combing to remove head lice takes time and is possibly less effective than drug treatment.

is related to poor hygiene and infrequent washing of clothes. Body lice are found in the seams of clothing, and sometimes in body hair. Treatment is with malathion. Clothes can be disinfected by boiling or by machine laundering and ironing. Body lice may transmit ricketsial diseases (louse-borne typhus) and other infections.

are usually transmitted sexually. They cause itching in pubic hair areas. Occasionally, children become infested on eyelashes or eyebrows. Treat with permethrin or malathion (see BNF). Sexual partners or other family members may also need treatment. There may be other co-existing sexually transmitted diseases.

There are many different types of flea. They cause itchy bites with linear erythematous papules. Treat with calamine lotion and an oral antihistamine (eg chlorphenamine) if itching is severe. A long-acting insecticide is needed in the house, especially in cracks in the floor and under furniture. All household cats and dogs must be treated for fleas. Fleas can transmit many infections, including plague, typhus and Q fever.

Scabies is caused by infestation with a mite, Sarcoptes scabiei, which is about 0.2–0.4mm long and burrows into the skin. It is most often found in the finger webs and on the flexor aspect of the wrists. After 4–6 weeks, intense itching occurs, especially at night or after a hot shower. Burrows (3–15mm long) may be apparent, especially on palpation of affected skin. Genital lesions are reddish and nodular. Secondary bacterial infection may occur. Scabies can be confirmed by microscopy of scrapings from suspected lesions. Treat with permethrin or malathion (see BNF). Treat all members of the household at once. Calamine lotion and an oral antihistamine may help to relieve itching.

Ticks may be acquired from domestic animals or while walking through undergrowth or exploring caves. Ticks may be removed with tweezers or curved forceps. They can carry several diseases, including Lyme disease (see below), tick-borne encephalitis, typhus, and Rocky Mountain spotted fever. Tick paralysis occurs in North America and Australia, with progressive paralysis which is often misdiagnosed as poliomyelitis. However, the risk of infection from tick bites is low in most areas, and so routine prophylaxis with antibiotics is not recommended.

(Lyme borreliosis) is caused by a tick-borne spirochaete, Borrelia burgdorferi, and occurs in the UK, most of Europe, the USA, and parts of Asia and Australia. Most cases occur in the summer and early autumn, and are transmitted by ticks from deer or sheep. The initial tick bite may go unnoticed. Clinical illness develops after about 7–14 days (range 2–30 days) with an expanding red area around the site of the bite (erythema migrans). The second clinical stage of the disease occurs some weeks or months later, with fever, muscle and joint pains, and sometimes facial palsy or other cranial nerve or peripheral nerve palsies. Meningitis, encephalitis and arthritis may develop. Myocarditis and heart block occur occasionally. Refer to an Infectious Diseases specialist for confirmation and treatment if Lyme disease is suspected.

The Mycobacterium genus is characterized by acid-fast staining (ie it is not decolourized by acid after staining with hot carbol fuchsin).

Infection with Mycobacterium tuberculosis is common throughout the world. There is growing concern about the re-emergence of TB in the UK and other countries. Many cases of TB occur in the lower socio-economic groups, ethnic minorities and the immunocompromised.

The incidence of TB ↑ with age.

TB can involve almost any organ of the body.

is usually pulmonary and often asymptomatic.

may present with malaise, weight loss and night sweats, with localized symptoms depending on the organs involved.

may result in cough, haemoptysis, pneumonia and pleural effusion (graphic  p.103).

with blood-borne infection of many organs, develops over 1–2 weeks with fever, weight loss, malaise and breathlessness: CXR may show multiple small opacities throughout the lung fields, and choroidal tubercles may be visible in the optic fundi.

causes headaches and vomiting, sometimes with neck stiffness, cranial nerve palsies and papilloedema (see graphic  p.224).

usually affects the spine, with collapse of adjacent vertebrae and a paravertebral abscess.

Patients may present with swollen lymph nodes from tuberculous lymphadenitis or with sinuses or cold abscesses from bone or soft tissue infection: microscopy of the discharge will show acid-fast bacilli.

Refer patients with suspected TB to an appropriate specialist for assessment and treatment. Isolation is required for patients with untreated pulmonary TB. Notify the local Health Protection department (graphic  p.221).

Anthrax is caused by the bacterium Bacillus anthracis which affects cows and other herbivorous animals, especially in warm climates. The bacterium forms spores, which may remain infective for years. Most human cases of anthrax are cutaneous anthrax caused by direct skin contact with infected tissues and occur in people working with animal products such as imported hides. Less common, but more serious, are inhalation anthrax caused by inhalation of anthrax spores, and intestinal anthrax which is a rare form of food poisoning caused by under-cooked infected meat. Anthrax spores released deliberately in terrorist attacks could cause cutaneous anthrax or inhalation anthrax, which is often fatal.

starts 2–7 days after infection, with a red papule which develops into an ulcer with a black leathery eschar, surrounded by non-pitting oedema. The lesion is painless but may itch. Small satellite lesions may surround the original lesion. Malaise and fever may occur, with septicaemia in 10–20% of cases. Penicillin ↓ risk of complications from cutaneous anthrax. Clinical diagnosis is confirmed by microscopy and culture of the pustule.

starts within 48 hours of exposure (rarely up to 6 weeks) with a flu-like illness, followed by breathlessness, cyanosis, stridor and sweating, often with subcutaneous oedema of the chest and neck. CXR and CT show mediastinal widening from lymphadenopathy and pleural effusions. Shock, septicaemia and meningitis are common and usually fatal, despite antibiotics and intensive treatment.

Airborne transmission of anthrax from one person to another does not occur, but cutaneous anthrax could result from direct contact with anthrax lesions. Obtain expert advice immediately if anthrax is suspected. It is a notifiable disease (graphic  p.221). Post-exposure antibiotics can prevent anthrax if started early enough. Press enquiries must be anticipated after any case of anthrax, especially if anthrax has been released deliberately. Further information is available from: www.hpa.org.uk/infections.

After a serious anthrax outbreak in heroin users in Scotland in 2010, Health Protection Scotland (www.hps.scot.nhs.uk) advised doctors to suspect anthrax in a drug user presenting with any of the following:

Severe soft tissue infection and/or signs of severe sepsis/meningitis.

Clinical features of inhalational anthrax.

Respiratory symptoms + features of meningitis or intracranial bleeding.

GI symptoms (eg pain, bleeding, nausea, vomiting, diarrhoea, ascites).

Get expert help early to advise on management (microbiology, hospital infection control team, Public Health, ICU, surgeons). Start IV antibiotics according to advice (eg combination of ciprofloxacin, clindamycin + penicillin, or if there is soft tissue infection: ciprofloxacin, clindamycin, penicillin, flucloxacillin + metronidazole). Experts will advise on whether to use anthrax immune globulin.

Streptococcus pyogenes and other streptococci may reside in the pharynx without symptoms, but can cause sore throats (graphic  p.554), soft tissue infections (graphic  pp.413 and 528), scarlet fever, and occasionally endocarditis and septicaemia. Later, non-suppurative sequelae of streptococcal infections include erythema nodosum, rheumatic fever (graphic  p.496) and glomerulonephritis. Streptococci and Staphylococci may cause necrotizing fasciitis, impetigo, and toxic shock.

Some streptococcal infections are associated with scarlet fever. A diffuse blanching scarlet rash often involves the neck, chest, axillae and groin. Occlusion of sweat glands makes the skin feel rough, like sandpaper. During the first 1–2 days of illness there is a ‘white strawberry tongue’, with red papillae protruding through white furry material. After a few days the white fur separates, leaving a shiny ‘raspberry tongue’. 10–14 days after onset of the rash, skin may peel from palms and soles. Treat with penicillin or erythromycin for 14 days. Complete recovery is usual.

Endocarditis may develop on previously normal heart valves, as well as on diseased or prosthetic valves. The commonest organism is Strep. viridans, but many others have been implicated. Many acute cases present with heart failure and involve Staphylococcus aureus. Injecting drug users are liable to staphylococcal infection of the tricuspid valve, with fever and pneumonia from septic PE.

Fever and changing murmurs suggest endocarditis. Emboli may cause strokes. Ask about weight loss, malaise, night sweats. Look for clubbing, splinter haemorrhages, splenomegaly, anaemia, microscopic haematuria.

On suspicion of endocarditis, admit immediately for investigation (blood cultures, echocardiography) and treatment.

Treat these bacterial skin infections as described in graphic  p.528.

This is a rare and severe bacterial infection of soft tissues. It can occur with or without obvious trauma and may follow illicit IM heroin injection (‘muscle popping’). Strep. pyogenes is often involved, sometimes with Staph. aureus or other bacteria. Often there are both aerobic and anaerobic organisms. Infection involves fascia and subcutaneous tissues, with gas formation and development of gangrene. Infection may spread to adjacent muscles, causing myonecrosis or pyogenic myositis. Similar infections may involve the abdomen and groin (Fournier's gangrene).

may be vague, with very severe pain, but little to find on examination: the affected area may be tender, sometimes with slight erythema and swelling. The patient is usually pyrexial. Infection can spread rapidly and cause marked soft tissue swelling with discolouration, bruising, haemorrhagic blisters, or overlying skin necrosis. Toxic shock may develop and the mortality rate is high. X-rays may show gas in the soft tissues but may be normal.

involves resuscitation with IV fluids and antibiotics (penicillin and clindamycin), urgent surgery to debride the affected area and excise necrotic tissues, and intensive care.

Staphylococcus aureus is involved in many infections of wounds, soft tissues (graphic  p.413), joints and bones (graphic  p.494 and 705). Staphylococci may also cause impetigo, scalded skin syndrome, food poisoning, toxic shock syndrome, endocarditis, pneumonia, septicaemia and meningitis.

A highly infectious superficial skin infection caused by staphylococci or streptococci. It may involve normal skin or complicate a pre-existing condition, such as eczema or scabies. Lesions often start around the mouth and nose, spreading rapidly on the face and to other parts of the body. Irregular golden-yellow crusted lesions occur, particularly in streptococcal infections. Staphylococci may cause bullous impetigo, with bullae containing pus which rupture and dry to form crusts. Treat with topical fusidic acid or mupirocin (usually for 7 days, max. 10 days) and give oral flucloxacillin or erythromycin if lesions are widespread or there is cellulitis or pyrexia.

Staph. aureus may produce an exotoxin causing separation of the outer layers of the epidermis, large sections of which slide off with minimal pressure, leaving large raw areas resembling a severe scald. Drug allergies can cause similar lesions. Most cases of scalded skin syndrome (toxic epidermal necrolysis, Lyell's syndrome) occur in children. Admit for nursing and medical care.

This is caused by exotoxins from Staph. aureus or (less commonly) Strep. pyogenes. Some cases during menstruation are related to tampons, other cases occur after surgical operations, burns, other trauma, or local infections. There is high fever, a generalized erythematous rash, confusion, diarrhoea, muscle pains, hypotension, and renal failure. Subsequently, scales of skin separate from hands and feet. Death may occur from multiple organ failure. Treat for septic shock with IV fluids and anti-staphylococcal antibiotics. Remove tampons and send for culture. Refer to ICU. Involve a surgeon if an associated abscess requires drainage.

Occurs particularly in debilitated or immune-compromised patients and in injecting drug users. There may be endocarditis with metastatic infection of lungs, bone or soft tissues and gangrene due to emboli or arterial thrombosis. Signs of meningitis and DIC may suggest meningococcal septicaemia (graphic  p.224) and the rash may be similar.

MRSA causes particular concern because of antibiotic resistance and is carried by many asymptomatic people (patients and staff). Transmission is minimized by hand washing (graphic  p.32) and other infection control measures. An information leaflet about MRSA for patients is available at www.hpa.org.uk/infections/topics_az/staphylo/mrsa_leaflet.htm.

An acute and often fatal disease, common in much of Asia, Africa, and South America, especially in neonates. Now rare in developed countries: 30–40 cases/year in UK, many involving the elderly. Injecting drug users (eg those ‘skin popping’) are also at particular risk. Spores of the Gram +ve organism Clostridium tetani (common in soil and animal faeces) contaminate a wound, which may be trivial. The spores germinate in anaerobic conditions, producing tetanospasmin, an exotoxin which blocks inhibitory neurones in the CNS and causes muscle spasm and rigidity.

is usually 4–14 days, but may be 1 day to 3 months. In 20% of cases there is no known wound. Tetanus occasionally occurs after surgery or IM injections.

Stiffness of masseter muscles causes difficulty in opening the mouth (trismus, lockjaw). Muscle stiffness may spread to all facial and skeletal muscles and muscles of swallowing. Characteristically, the eyes are partly closed, the lips pursed and stretched (risus sardonicus). Spasm of chest muscles may restrict breathing. There may be abdominal rigidity, stiffness of limbs and forced extension of the back (opisthotonus). In severe cases, prolonged muscle spasms affect breathing and swallowing. Pyrexia is common. Autonomic disturbances cause profuse sweating, tachycardia and hypertension, alternating with bradycardia and hypotension. Cardiac arrhythmias and arrest may occur.

Dystonic reaction to metoclopramide or phenothiazines, strychnine poisoning, quinsy, dental abscess, meningitis, rabies. Procyclidine relieves muscle spasms from drug-induced dystonia, but will not affect tetanus; diazepam may relieve dystonia or tetanic spasms.

Obtain senior medical and anaesthetic help. Monitor breathing, ECG and BP. Refer to ICU. Control spasms with diazepam. Paralyse and ventilate if breathing becomes inadequate. Clean and debride wounds. Give penicillin and metronidazole and human tetanus immune globulin.

Depends on severity of disease and quality of care. Short incubation (<4 days) and rapid progression suggest severe disease with a high mortality. With expert intensive care, the mortality in adults is <10%, but neonatal tetanus is often fatal.

Tetanus is eminently preventable by immunization and by proper care of wounds (graphic  p.406, graphic  p.410).

This is a rapidly spreading infection of muscle caused by toxin-producing Clostridial bacteria (anaerobic Gram +ve bacilli), usually C. perfringens. It is fatal if untreated. It may involve wounds of the buttocks, amputations for vascular disease or severe muscle injuries (eg gunshot wounds). Occasionally gas gangrene of the perineum occurs without trauma.

is usually <4 days (sometimes a few hours). Sudden severe pain occurs at the wound site. Generalized toxicity develops, with tachycardia, sweating and fever. Swelling and skin discolouration occur around the wound, with a serous ooze, marked tenderness and sometimes haemorrhagic vesicles and crepitus. Shock and renal failure develop, with death often within 2 days of the first symptoms.

depends on clinical features. Severe pain necessitates wound inspection (remove or window any plaster of paris (POP). Obtain immediate senior surgical advice if gas gangrene is suspected. The wound discharge may contain Gram +ve bacilli. X-rays may show soft tissue gas, but its absence does not exclude gas gangrene.

IV antibiotics (penicillin and clindamycin), immediate surgical removal of all infected tissue, and intensive care. Hyperbaric O2 and gas gangrene antitoxin are rarely available and of no proven benefit.

The exotoxin of Clostridium botulinum paralyses autonomic and motor nerves by blocking acetylcholine release at neuromuscular junctions and nerve synapses. Infection occurs from eating tinned or preserved food contaminated with C. botulinum spores: cases have involved sausage, tinned salmon, hazelnut yoghurt and other foods. Rarely, C. botulinum infects wounds or colonizes the gut. Injecting drug users may develop botulism after IM or SC injections of contaminated drugs.

is 12–72hr. Initial symptoms may be GI (nausea, vomiting, abdominal discomfort, dryness of the mouth) or neurological (dizziness, blurred vision, diplopia). Later problems include dysarthria, dysphagia, muscle weakness or paralysis, constipation and urinary retention, respiratory failure, and sudden death. Susceptibility varies: some people who eat contaminated food develop no symptoms or suffer only mild fatigue.

result from involvement of autonomic and motor nerves: dry mouth, cranial nerve palsies (ptosis, squint, fixed pupils, weakness of tongue), limb weakness with flacid muscles. Consciousness and sensation are preserved. Hypotension and ileus may occur. Fever is unusual.

are Guillain–Barré syndrome, myasthenia, brainstem stroke, diphtheria, poisoning (anticholinergics or organophosphates), paralytic rabies. Botulism may be misdiagnosed as staphylococcal food poisoning, paralytic shellfish poisoning, CO or mushroom poisoning.

Get senior help. Assess breathing, ventilate if necessary and admit to ICU. Botulinum antitoxin reduces mortality and morbidity: see BNF and TOXBASE (graphic  p.181). Inform Public Health: others who have eaten contaminated food may need urgent treatment. Anticipate media enquiries and the arrival of worried people with tins of suspicious food.

The commonest sexually transmitted disease (STD) is non-specific genital infection. Other common diseases include chlamydia, gonorrhoea, genital herpes, trichomoniasis, genital warts, pediculosis pubis, HIV, and syphilis. Many patients have more than one disease. Suspicion of STD necessitates prompt referral to a genitourinary (GU) medicine clinic for proper diagnosis, treatment and follow-up of the patient and contacts. Some GU departments provide an on-call service. Only prescribe antibiotics for suspected STDs on the advice of a GU specialist.

Most genital ulcers/erosions are either multiple and painful or single and painless. In the UK, multiple genital ulcers are most often due to herpes simplex; other causes are Behçet's disease and (rarely) chancroid or scabies. Multiple painful sores may occur with gonorrhoea, candida, or other conditions. Painless genital ulceration should suggest syphilis (primary chancre is a single ulcer, secondary syphilis often multiple: both are highly infectious and incidence has ↑ recently). Other causes of painless ulcers include carcinoma and trauma (possibly self-inflicted).

In men, dysuria and urethral discharge are the commonest presenting symptoms of an STD. However, 5–10% of men with gonococcal or non-gonococcal urethritis have no symptoms. Urethritis may result from physical trauma, foreign bodies or attempts at self-treatment with intraurethral chemicals.

Gonorrhoea usually has a shorter incubation period (3–5 days) than non-gonococcal urethritis (eg chlamydia 7–14 days), but do not rely on a clinical diagnosis: refer to a GU clinic for diagnosis, management and follow-up. If no GU advice is available and treatment cannot wait for attendance at a GU clinic, give doxycycline 200mg PO stat and then 100mg PO daily (or tetracycline 500mg PO qds). If possible, make a glass slide of the discharge, dried in air, for the patient to take to the clinic. He should be told not to pass urine for 4 hours before the appointment, in order to allow serial urine samples to be taken.

is a rare complication of non-gonococcal urethritis. There is arthritis (mainly of knees, ankles and feet) and sometimes conjunctivitis, rashes and cardiac and neurological problems.

Gonorrhoea may infect the urethra, cervix, rectum, pharynx or conjunctiva. Men usually have dysuria and urethral discharge, with rectal discharge and tenesmus in homosexuals. Women are often asymptomatic, but may have dysuria and vaginal discharge.

include prostatitis, epididymitis, salpingitis, Bartholin's abscess; rarely septicaemia with arthritis, fever, rash (maculopapular initially, then pustular) and endocarditis.

Hepatitis A occurs throughout the world, but is particularly common in the tropics and subtropics. It is transmitted by contamination of food or water with infected faeces or urine. Many infections are asymptomatic. The incubation period is 2–6 weeks (usually ≈4 weeks). Fever, malaise, anorexia and nausea may last for 2–7 days before jaundice develops. Jaundice is more common in adults than in children and is associated with dark urine, pale stools and tender hepatomegaly.

is symptomatic, but alcohol should be avoided. Infectivity is greatest before jaundice develops, so isolation is of little value. Arrange follow-up by a specialist or GP. Complete recovery is usual. Hepatitis A vaccine should be considered for close contacts (see BNF).

Hepatitis B is transmitted by infected blood (eg shared needles in drug abusers, tattooing, needlestick injury) and by sexual intercourse. The incubation period is 6 weeks to 6 months. The symptoms are similar to hepatitis A, often with arthralgia and skin rashes. Most patients with hepatitis B recover completely. A few patients develop liver failure or chronic hepatitis, with a risk of primary liver cancer. Refer to a specialist for follow-up. Asymptomatic carriers of hepatitis B virus are common (≈0.1% of the population in the UK, but ≈20% in parts of Africa and Asia). Because of the high risk of infection, all health care workers should be immunized against hepatitis B and use ‘standard precautions’ (graphic  p.32) when handling all blood samples and ‘sharps’. The management of needlestick injury is described on graphic  p.418.

are spread in the same way as hepatitis B, and may cause hepatic failure or chronic liver disease. No immunization is available.

is similar to hepatitis A, but has a high mortality in pregnancy. Refer to a specialist for follow-up.

Leptospirosis, caused by the spirochaete Leptospira interrogans and other Leptospira species, is spread by contact with infected rat's urine, often in rivers, canals or sewers. The leptospires enter the body through small breaks in the skin or via mucous membranes of the eyes or nose. About 10 days after exposure (range 2–26 days) the illness starts with fever, severe muscle pains, headache, sore throat, nausea and vomiting. Conjunctival reddening is common. A haemorrhagic rash, jaundice, renal failure and pulmonary haemorrhage may occur (Weil's disease).

Refer to an Infectious Diseases unit. Treatment is with penicillin or doxycycline with supportive care and haemodialysis if necessary. Prophylactic doxycycline is reasonable for people who fall into waterways likely to be contaminated with leptospires.

results from primary infection with varicella zoster virus, which then remains dormant in the dorsal root ganglia. Reactivation of the virus causes shingles. Chickenpox is usually a mild disease of childhood. An itchy vesicular rash appears, most densely on the trunk and face, but decreasing peripherally. The lesions appear in crops and crust over in 3–4 days. Fever, malaise and muscle aches may occur in adults. Infectivity starts 3 days before the rash appears and lasts until the last lesion has crusted.

Treat symptomatically, eg calamine lotion for itching and paracetamol for fever. Occasionally, antibiotics are needed for secondary bacterial skin infection (usually Staph. or Strep.). Pneumonia is rare and in children is usually staphylococcal, but in adults may be caused by chickenpox virus. Chickenpox may be severe in neonates and in patients with cystic fibrosis or immune deficiency, who need specialist assessment and treatment with aciclovir and/or varicella-zoster immune globulin. Consider aciclovir also for adults and older adolescents (see BNF).

often occurs in the elderly and may affect any dermatome, most often thoracic. The pain of shingles may cause diagnostic difficulty until the rash appears, usually after 1–4 days. Erythema is followed by vesicles and then crusting of lesions in a unilateral distribution over 1 dermatome or 2 adjacent dermatomes. Ophthalmic shingles may affect the eye via the long ciliary nerves: skin lesions on the side of the tip of the nose imply a high risk of eye involvement. Oral lesions occur in maxillary and mandibular shingles. Infection of the geniculate ganglion causes a facial palsy with lesions in the pinna of the ear and on the side of the tongue and hard palate (Ramsay–Hunt syndrome). In severe shingles there may be weakness of muscles supplied by nerves of the same spinal root.

(aciclovir, famciclovir, or valaciclovir) ↓ risk of post-herpetic pain if given early (within 72hr of start of rash). Dose: aciclovir 800mg 5 times daily for 7 days. In renal failure antiviral drugs may cause severe toxicity, so use much smaller or less frequent doses. Patients with immune deficiency or ophthalmic zoster need immediate specialist referral and antiviral treatment. Give analgesia. Antibiotics may be required for secondary infection.

Primary herpes simplex infection causes painful vesicles and ulceration of the mouth or genitalia (graphic  p.238). The virus may be inoculated into skin by trauma (herpes gladiatorum, scrumpox) or by contamination of fingers causing herpetic paronychia (whitlow). Infection of the cornea may cause dendritic ulcers (graphic  p.543). Herpes simplex meningitis and encephalitisND are uncommon, but may be fatal, especially in immunodeficient patients.

The herpes simplex virus persists in sensory ganglia and may be reactivated by stimuli such as sun, cold, trauma, or viral infections. Recurrence of cold sores of the lips is often preceded by tingling: aciclovir cream or tablets may prevent the development of vesicles. Secondary bacterial infection may require antibiotics. Do not incise a suspected whitlow. Cover it with a dressing and advise care to avoid spreading infection to the lips or eyes.

Infection with the Epstein–Barr virus is common in children and young adults and is spread by saliva or droplets. Infection often occurs without clinical disease. In glandular fever there is malaise, fever, a sore throat, and cervical lymphadenopathy. The throat may be very red and in 25% of cases there is also infection with a β-haemolytic streptococcus. In severe cases there is marked oedema of the throat with tonsillar swelling and a membranous exudate (‘anginose’ infectious mononucleosis) with difficulty in swallowing and breathing. A rash is uncommon unless ampicillin or amoxicillin are given, causing a widespread erythematous maculopapular rash (which does not signify allergy to penicillins in general).

of infectious mononucleosis include respiratory obstruction, ruptured spleen (spontaneously or after minor trauma), thrombocytopenia, jaundice, meningitis, encephalitis, facial palsy, and acute polyneuritis (occasionally causing respiratory failure).

FBC and blood film (for atypical lymphocytes), Monospot test or Paul–Bunnell test (which may be –ve initially).

includes cytomegalovirus and toxoplasmosis.

is unnecessary in most patients. Severe or complicated cases need specialist assessment and follow-up. In anginose infectious mononucleosis, a short course of high dose oral steroids gives rapid relief of symptoms (prednisolone 80mg on day 1; 15mg tds on days 2–3; 10mg tds on days 4–5; 5mg tds on days 6–7). Steroids are also helpful in patients with neurological complications. Concurrent β-haemolytic streptococcal infection requires erythromycin (500mg qds), which would also treat the rare unrecognized case of diphtheria.

First reports of acquired immune deficiency syndrome (AIDS) involved homosexuals in the USA in 1981. HIV (previously called HTLV-III, LAV, or ARV) was identified as the causative agent in Paris in 1983.

HIV is an RNA retrovirus. Retroviruses are characterized by having the enzyme reverse transcriptase. This allows viral RNA to be transcribed (copied) into DNA and incorporated into host cells, which then make a new virus. This mechanism has proved difficult to overcome: no ‘cure’ or ‘vaccine’ is yet available.

Glycoproteins on the surface of HIV bind to specific receptors on target cells. The cellular receptor for HIV is the CD4 molecule. CD4 receptors are found on a variety of cells, particularly helper/inducer T lymphocytes (‘CD4 cells’), but also monocytes and macrophages. CD4 cells normally play a crucial role in co-ordinating the immune response: as HIV infection progresses and CD4 cell counts ↓, the patient develops profound cellular immunodeficiency. Although other complex mechanisms are also involved, CD4 cell counts provide a useful index of disease stage and progress.

HIV has been found in many body fluids, but is mostly transmitted via blood, semen, cervical secretions and, perhaps, breast milk. It may be acquired by:

Sexual intercourse (vaginal or anal), with ↑ risk of transmission where individuals already have a genital mucosal breach (eg co-existent STD).

Risk of transmission from HIV +ve pregnant mother to baby is ≈15%.

Transfusion of unscreened blood/blood products (screening started in 1985 in the UK).

Contaminated needles shared amongst IV drug abusers. Needlestick injuries from an HIV positive source carry a risk of ≈0.3%.

Antibodies to HIV provide evidence of infection and form the basis of current blood tests, but these antibodies may not appear until 3 months after exposure. HIV testing is not appropriate in the ED, but reserved for clinics where informed consent and counselling are available. Refer patients requesting HIV tests to local Infectious Diseases/GU clinics or advisory organizations, eg Terrence Higgins Trust (tel. 0808 802 1221), or the NHS Sexual Health Helpline (24hr freephone 0800 567 123).

HIV infection progresses through phases, which form the basis of the two commonly used classification systems (World Health Organization (WHO) and CDC systems).

Acute infection is often sub-clinical, but 2–6 weeks after exposure there may be a non-specific febrile illness with lethargy, myalgia, sore throat, lymphadenopathy, and often a maculopapular rash on the face and trunk. This illness usually resolves after 1–2 weeks but sometimes persists for longer. A long asymptomatic period (≈10 years) follows the initial illness.

Some patients develop persistent generalized lymphadenopathy (PGL), with lymphadenopathy (>1cm) at two non-inguinal sites for 3 months. Patients become symptomatic as their immunity ↓, developing unusual infections and tumours. Many are ‘AIDS-defining diseases’ (see below). The label ‘AIDS’ has significant psychological connotations. Most patients with AIDS survive >2 years.

Anti-retroviral drugs (AZT and other drugs) delay the onset of AIDS in asymptomatic patients and ↑ length of survival. ‘HAART’ (highly active antiretroviral therapy) is a regime combining 3 or more anti-HIV drugs.

Many HIV +ve patients attending the ED are aware of their HIV status. Some patients, however, present with HIV-related illness, without knowing (or admitting) that they are HIV +ve. Presentation of any of the diseases listed below should arouse particular suspicion.

Group I Acute infection

Group II Asymptomatic

Group III Persistent generalized lymphadenopathy

Group IV Symptomatic infection with subgroups:

  A—constitutional disease (fever, diarrhoea, weight loss)

  B—neurological disease (dementia, peripheral neuropathy)

  C—secondary infectious diseases

  D—secondary cancers (lymphomas, Kaposi's sarcoma)

  E—other conditions

Pneumocystis jiroveci pneumonia (previously called P. carinii).

Kaposi's sarcoma.

Tracheobronchial or oesophageal candidiasis.

Cerebral toxoplasmosis.

Pulmonary TB.

Cytomegalovirus retinitis.

Cerebral lymphoma.

Recurrent Salmonella septicaemia.

Disseminated histoplasmosis.

Invasive cervical carcinoma.

Disseminated coccidioidomycosis.

Cryptococcosis.

Cryptosporidiosis.

Progressive multifocal leucoencephalopathy.

Oesophageal or bronchial herpes simplex.

CD4 counts provide an indication of disease progession: many HIV +ve patients know what their last count was. In the USA, CD4 counts <200/mm3 may also be used to define AIDS.

Many patients with symptomatic HIV infection bypass the ED and liaise directly with the specialist unit caring for them. Assessment of HIV +ve patients is difficult in the ED, where advanced infections may present with relatively few signs and little past history is available. Similarly, interpretation of investigations is difficult without knowledge of previous results. It is therefore reasonable to have a low threshold for specialist referral. HIV +ve patients may present with a variety of complications:

As CD4 counts ↓, pneumonia due to Pneumocystis jiroveci (previously Pneumocystis cariniii) becomes more likely and it is a common indicator diagnosis of AIDS. A non-productive cough occurs with dyspnoea and fever. CXR may show bilateral interstitial mid-zone shadowing, but may be normal. Obtain blood and sputum cultures, rehydrate with IV fluids as necessary and refer urgently for IV co-trimoxazole or pentamidine ± steroids. Occasionally, Pneumocystis infection may present with fulminant respiratory failure needing emergency tracheal intubation and IPPV. Other common infections include Aspergillus, Cryptococcus and TB. Injecting drug users are at increased risk of bacterial infection, especially Haemophilus influenzae and Strep. pneumoniae.

meningitis may present with headache, fever and sometimes ↓ conscious level. Neck stiffness and photophobia are rare. Obtain a CT scan to exclude space-occupying lesions before LP and CSF examination. Cerebral toxoplasmosis may present similarly, often with focal signs or fits. Neurological problems may also be caused by cerebral lymphoma, progressive leucoencephalopathy (focal deficits secondary to papovaviruses), CMV encephalitis (retinopathy is usually present—see below) and HIV-associated delirium or dementia.

The most significant eye problem is Cytomegalovirus (CMV) retinitis, occurring in 15% of patients. This presents with blurred vision, blind spots, ‘floaters’ or flashing lights, and ↓ VA. Characteristic retinal changes are irregular yellow-white lesions and perivascular haemorrhages that have been called ‘pizza pie’. Retinal detachment may occur. Refer urgently for ophthalmological assessment and treatment with ganciclovir or foscarnet.

Oral candidiasis, seborrhoeic dermatitis, and oral hairy leukoplakia (white ridges on lateral border of tongue) are often seen before AIDS develops. As immunity ↓, patients may develop herpes simplex, herpes zoster and molluscum contagiosum. Gum bleeding and dental problems are common: the former may be due to thrombocytopenia. Kaposi's sarcoma is seen in skin and mucous membranes, particularly in homosexuals with AIDS. It is rarely life-threatening, but requires specialist evaluation and treatment.

Nausea, vomiting, diarrhoea and weight loss are common complaints and can be due to drug therapy. Dysphagia may result from oesophageal candidiasis, herpes simplex, CMV, or Kaposi's sarcoma, all of which require specialist investigation and treatment.

can cause a serious illness, characterized by abdominal pain, diarrhoea and fever. Obtain plain X-rays if the recognized complication of toxic dilatation is suspected. Other frequently implicated infective causes of diarrhoea include cryptosporidium, Giardia, microsporidium and Salmonella. Send stool specimens (including for Clostridium difficile) and treat severe diarrhoea by IV rehydration and correction of electrolyte imbalance before referral.

are likely to complicate the picture in injecting drug users, many of whom are infected with hepatitis B and C.

Many patients will present with symptoms due to drug therapy. This may not be initially apparent: the safest approach is to exclude tumours and opportunistic infection first.

ED staff are often concerned about the possibility of acquiring HIV from patients. The need to perform invasive emergency procedures on ‘high risk’ patients makes these concerns understandable. Additionally, apparently ‘low risk’ patients may also pose a threat. Therefore treat every patient as if he is ‘high risk’. The risk to ED staff is largely in the form of needlestick injury (although the risk of acquiring HIV following needlestick from a HIV +ve source can be ↓ by post-exposure prophylaxis—see graphic  p.418). Safe practice is reflected in the recommended standard precautions (see graphic  p.32)—follow these in all patients. Pregnant staff should not treat patients with AIDS (because of concern about CMV and herpes simplex virus).

Despite vigorous attempts to educate the general public, HIV and AIDS remain taboo subjects amongst many in society. It is imperative to treat all patients, including those who are HIV +ve, with sensitivity and compassion. Touching and shaking hands with HIV +ve patients is perfectly safe, and may help to reassure them that the discrimination and irrational treatment they may have received outside hospital does not extend into the ED. In view of prevailing attitudes towards HIV, patient confidentiality is of the utmost importance. Remember that family and friends accompanying the patient may be unaware of his HIV status.

The risk to patients from ED staff infected with HIV is minimal, but remains a theoretical possibility. Staff who believe that they may be HIV +ve must obtain and follow occupational health advice.

See graphic  p.418.

Patients may present to the ED with infectious diseases acquired abroad. It is essential to ask where a patient has been, especially in the 6 weeks before the onset of symptoms. The most common imported diseases are bowel infections causing diarrhoea (graphic  p.226). Less common, but very important diseases include malaria (graphic  p.247), typhoid (graphic  p.248), Legionnaires’ disease (graphic  p.110) and hepatitis (graphic  p.239). Rabies (graphic  p.249) and viral haemorrhagic fevers, such as Lassa fever (graphic  p.250) are very rare in the UK.

Occasionally, tropical diseases are acquired in Britain from bites by infected insects carried by plane (eg ‘airport malaria’).

Advice about tropical diseases is available from departments of Infectious Diseases or Tropical Medicine:

Birmingham (Heartlands Hospital). www.heartofengland.nhs.uk Telephone 0121 424 2000.

Liverpool (School of Tropical Medicine). www.liv.ac.uk/lstm Telephone 0151 705 3100.

London (Hospital for Tropical Diseases) www.thehtd.org/Emergencies.aspx Telephone 0845 155 5000.

Oxford (Churchill Hospital) Telephone 01865 741 841.

Glasgow (Brownlee Centre for Infectious and Communicable Diseases, Gartnavel General Hospital) Telephone 0141 211 3000.

A public access website provided by the NHS which gives information for people travelling abroad from the UK is www.fitfortravel.scot.nhs.uk

Think of and check for malaria (graphic  p.247) in any febrile patient who has been in a malarious area. Consider Lassa fever (graphic  p.250) in someone who has been in West Africa in the previous 3 weeks. Typhoid (graphic  p.248) often presents as a septicaemic illness with constipation, rather than diarrhoea. TB (graphic  p.232) and brucellosis may cause fever and sweating at night.

FBC, thick and thin blood films for malaria, U&E, blood glucose, blood culture, urine stick testing, microscopy and culture, CXR.

Further investigations may include LFTs and viral titres.

Barrier nurse in a cubicle (use a negative pressure room if available). Wear gown, gloves, goggles and mask. Record vaccination and prophylaxis history, with countries and areas visited, and dates of travel and onset of symptoms. Look particularly for confusion, dehydration, jaundice, rashes, chest signs, liver and spleen enlargement and tenderness, lymphadenopathy, neck stiffness, photophobia. Seek expert advice at once if the patient is very ill or there is concern about typhoid or Lassa fever or other viral haemorrhagic fevers. Refer to an Infectious Diseases specialist.

Malaria is very common in the tropics and subtropical regions, and is a parasitic infection transmitted by mosquitoes. The five species which cause malaria in humans are Plasmodium falciparum, P. vivax, P. malariae, P. ovale, and P. knowlesi. Falciparum (‘malignant tertian’) malaria is the most important, since it may be rapidly fatal and drug-resistant strains are common. Serious complications are unusual in the other types of malaria, but they may cause febrile convulsions in children.

occurs in travellers from malarious areas, especially P. vivax from the Indian subcontinent and P. falciparum from Africa, South-East Asia, and Central and South America. Malaria often develops despite antimalarial tablets, because of drug resistance or incorrect dosage. Check for malaria in any febrile illness within 2 months of visiting a malarious area. Common misdiagnoses are influenza and viral hepatitis.

The incubation period is usually 7–14 days for P. falciparum and 12–40 days for other types of malaria, but occasionally it is much longer (>1 year), especially in P. malariae and P. vivax infections. There is malaise, fatigue, fever and headache followed by paroxysms lasting 8–12hr of rigors, vomiting and then severe sweating. The fever may be periodic (classically 48hr in P. ovale or P. vivax, and 72hr in P. malariae). Haemolytic anaemia, jaundice and splenomegaly may occur, but lymphadenopathy is not a feature. P. falciparum may cause cerebral malaria with coma, fits and focal neurological signs. Diarrhoea, cardiac failure, pulmonary oedema and shock may occur. Deterioration can be rapid.

Consider Lassa fever (graphic  p.250) in recent visitors to West Africa. In any ill patient who has been in a malarious area send blood for thin and thick film examination for malaria. Repeated blood films may be needed. Also arrange FBC (since malaria may cause anaemia, thrombocytopenia and neutropenia), blood glucose (hypoglycaemia may be severe), U&E (renal failure is possible), and test the urine for blood (‘black water fever’).

Careful monitoring is needed ± ICU. Obtain expert advice from a tropical disease specialist (graphic  p.246), especially if the patient is severely ill or has come from south-east Asia, where there is widespread drug resistance.

Give quinine, orally or IV depending on the severity of illness: oral quinine sulphate 600mg (adult) or 10mg/kg (child) every 8hr for 7 days, followed by doxycycline 200mg od for 7 days, clindamycin 450mg tds for 5 days or Fansidar® 3 tablets. Alternative oral drugs are Malarone® (proguanil with atovaquone) or Riamet® (artemether with lumefantrine): for details see BNF. For algorithm1 see www.britishinfectionsociety.org.

The usual treatment is chloroquine (see BNF). A course of primaquine is also needed to prevent relapse in vivax and ovale infections, but glucose-6-phosphate dehydrogenase levels should be checked before primaquine is used, since it may cause haemolysis in G6PD deficient patients. In the UK refer to an Infectious Diseases unit for treatment and follow-up.

These fevers, caused by Salmonella typhi and S. paratyphi A, B, or C, occur throughout the world, especially where hygiene is inadequate. They are spread by contamination of food or water by urine or faeces from a patient or an asymptomatic carrier. Typhoid may occur despite immunization. Typhoid and malaria are the first diseases to consider if fever develops soon after a visit to the tropics. The incubation period is usually 7–14 days, but may range from 3–60 days.

Headache, fever, and a dry cough, with abdominal discomfort and anorexia. Constipation is common, but diarrhoea may occur, especially in children. Confusion and hallucinations may develop.

This may be normal except for fever. There may be a relative bradycardia (ie less than the usual 15 beats/min ↑ in pulse rate per °C of fever). Splenomegaly and abdominal tenderness occur, but there is no lymphadenopathy. ‘Rose spots’ are pink macular spots on the lower chest or upper abdomen which blanch on pressure. There may be signs of pneumonia or dehydration. Intestinal perforation or haemorrhage occur occasionally.

FBC (mild anaemia is common, WBC usually normal), blood films for malaria, U&E, LFTs, blood cultures, CXR (for signs of TB or pneumonia).

Isolate and barrier nurse. Admit suspected cases to an Infectious Diseases unit and notify the local consultant in Communicable Disease Control. The usual drug treatment is with ciprofloxacin or cefotaxime but other antibiotics may be needed for drug-resistant infections.

Dengue is a mosquito-borne viral infection which is common in southern Asia, the western Pacific, central Africa and central and south America. Most infections are asymptomatic. Symptoms start after an incubation period of 4–7 days with fever, malaise, nausea and vomiting, headache, severe muscle and bone pains (‘break bone fever’). Some patients have a transient macular rash, petechiae, lymphadenopathy, hepatomegaly, ↓ WCC and platelets and ↑ liver enzymes.

Most patients recover after 3–7 days with symptomatic treatment. A few develop dengue shock syndrome (DSS) with hypotension, pleural effusions, ascites, ↓ plasma protein and bleeding problems. Abdominal pain may be severe. Treatment is supportive, with careful fluid balance management and IV fluids in DSS. With expert care most patients with severe dengue eventually make a full recovery.

Paralytic poliomyelitis is rare in developed countries where vaccination is routine. Fever is followed by signs of meningitis, pain and spasm in limb muscles. Respiratory failure may be fatal.

if necessary and refer to ICU.

The differential diagnosis includes Guillain–Barré syndrome (graphic  p.142) and organophosphate poisoning (graphic  p.206).

Rabies is a viral infection of mammals that occurs in most parts of the world, including much of the Arctic, as well as tropical and temperate regions. At present it is not endemic in the UK, Norway, Sweden, Iceland, Australasia, or Japan. Human and animal rabies is most common in the Indian subcontinent, China, Thailand, the Philippines, and parts of South America. Most human infections result from dog bites, but rabies can be transmitted by many other domesticated or wild animals, such as cats and foxes. Rabies virus in an animal's saliva may cause infection by contamination of a bite or scratch or by absorption through mucous membranes of the eye, mouth or nose. Rarely, infection occurs from inhalation of the virus in bat-infested caves.

Prevention of rabies after a bite is described on graphic  p.415.

Advice about post-exposure treatment and suspected cases of rabies is available in the UK from the Health Protection Agency. For details see www.hpa.org.uk/Topics/InfectiousDiseases/InfectionsAZ/Rabies

The incubation period of rabies is usually 3–12 weeks, but can vary from a few days to >2 years.

The first symptoms are itching, tingling or pain at the site of the bite wound. Headache, fever, and malaise occur, with spreading paralysis and episodes of confusion, hallucination and agitation. Hydrophobia is characteristic: attempts at drinking cause spasm of muscles involved in breathing and swallowing and also profound terror. In ≈20% of cases there is ‘dumb rabies’ with increasing paralysis but no episodes of spasm or hyperactivity. Rabies is almost always fatal, even with ICU treatment.

If rabies is suspected, barrier nurse the patient in a quiet room with the minimum of staff, who must wear gowns, gloves, eye protection and masks. Obtain advice immediately from a specialist in Infectious Diseases. Anticipate press enquiries. Record the names of all staff involved, so that they can be offered rabies immunization.

Lassa fever occurs in many rural parts of West Africa. It is a viral infection acquired from infected blood or secretions, transmitted by inadvertent innoculation (eg needlestick injuries) or contamination of mucous membranes or broken skin. In Africa it is transmitted by multimammate rats. The incubation period is up to 3 weeks. There is a high mortality.

are non-specific with fever, malaise, headache, sore throat, retrosternal chest pain and backache. Periorbital oedema, swelling of the neck and conjunctival injection are common. Suspect Lassa fever in any pyrexial patient who has been in rural West Africa (south of the Sahara) in the previous 3 weeks. However, malaria and typhoid are much more common and need urgent diagnosis and treatment.

If Lassa fever is possible, barrier nurse the patient in a cubicle by staff wearing gloves, gowns, goggles and masks. Take special care to avoid needlestick injuries, which may cause fatal infection. Before taking any blood samples, discuss the case with a tropical diseases specialist and the local consultant in Communicable Disease Control. Start treatment immediately for falciparum malaria (graphic  p.247). Warn the laboratory about Lassa fever and send blood for examination for malaria. The patient will be admitted to an isolation bed, possibly in a high security Infectious Diseases unit.

These are viral haemorrhagic fevers which occur in West and Central Africa (Zaire, Uganda, Kenya and Sudan), and have similar clinical features and a high mortality. Transmission is usually by infected blood, but the viruses may be acquired from monkeys or apes. The incubation period is usually 4–10 days. Illness starts suddenly with severe headache, high fever, and generalized pains, especially in the back, followed by severe diarrhoea, abdominal pain, dry throat, a maculopapular rash, conjunctivitis, and gastrointestinal bleeding. Isolate and treat as for suspected Lassa fever.

Diseases with similar features (plus in some cases jaundice) include dengue (see graphic  p.248), Crimean-Congo fever (central Africa, parts of Eastern Europe, and Asia) and yellow fever (Africa and South America). The initial management is the same as for Lassa fever.

Severe acute respiratory syndrome (SARS) is a viral respiratory illness caused by a coronavirus. SARS was first recognized in March 2003, but probably originated in November 2002 in the Guangdong province of China, where the virus has been found in wild animals. SARS spread to several countries, causing deaths in south-east Asia and Canada in March to May 2003. Few cases have occurred since then. No cases are known at the time of writing, but there is concern that SARS may re-emerge from China.

SARS is spread by respiratory droplets produced when an infected person coughs, sneezes, or uses a nebulizer. The virus can also spread when someone touches an object contaminated by infectious droplets and then touches his/her mouth, nose, or eyes.

The incubation period of SARS is usually 2–7 days, but may be up to 10 days. The illness starts with fever (>38°C), usually associated with rigors, headache, muscle pains and malaise. Diarrhoea may occur. Some patients have mild respiratory symptoms initially. A dry cough develops after 2–7 days, with increasing breathlessness from hypoxia caused by pneumonia. Consider the possibility of SARS in a patient with these symptoms who, within 10 days of the onset of illness, has visited an area where SARS may occur (especially China) or worked in a laboratory holding SARS virus samples.

CXR may be normal or may show patchy infiltrates, and later areas of consolidation. WCC is usually normal or ↓ initially (lymphopenia).

If SARS is suspected, get expert help (ED consultant, Infectious Diseases specialist, and infection control staff) and isolate the patient (if possible in a negative pressure room). Ensure that the minimum number of staff have contact with the patient. Staff who do have contact must wear masks or respirators (of FFP3 standard), goggles, gowns and gloves, with strict handwashing and careful disposal of all items. Provide the patient with an N95 mask or a surgical mask. Record SpO2 and give O2 if necessary, but avoid flow rates of >6L/min, to minimize virus aerolization. If bronchodilators are needed, use a spacer inhaler rather than a nebulizer. Maintain a list of all contacts. Expect press enquiries.

An expert will help to assess to decide about admission. Those admitted should ideally be placed in a negative pressure isolation room with full infection control measures. Treat as for community-acquired pneumonia (graphic  p.110).

Further information about SARS is available from:

is common in the UK and many other countries, particularly during winter. Most people are ill for only a few days with fever, muscle aches, coughing and nausea, but there are some deaths, especially in elderly people.

occurs when a new subtype of influenza A emerges, which can spread easily from person to person and which is different from previous strains (so there is no pre-existing immunity). Influenza pandemics occurred in 1918–1919 (with 40–50 million deaths worldwide, including many children and young adults), and also in 1957 and 1968. Another pandemic could develop at any time. There was concern about influenza A subtype H5N1, which infected poultry in Hong Kong in 1997 and 2003 and spread to birds across south-east Asia, with carriage by migrating birds across Asia and to Europe and Africa. This avian flu infected many millions of birds and some people in south-east Asia and Turkey who had been in close contact with infected chickens. The mortality in these cases was high. In 2009 influenza A subtype H1N1 caused a pandemic of swine flu which started in Mexico and spread to many other countries. Most patients with swine flu had only mild illness but a minority developed severe infection, and some died.

Human-to-human spread of H1N1 or H5N1 flu is rare, at the time of writing, but another pandemic could develop if the virus mutates again.

Like SARS (see graphic  p.251) flu is spread by droplets coughed or sneezed into the air, or by direct contact with hands contaminated with the virus.

Consider the possibility of avian flu or swine flu in a patient with fever ≥38°C and cough or breathlessness, who in the last 7 days has been in an area affected by H1N1 or H5N1 influenza. Laboratory staff and health care workers in contact with cases of severe unexplained respiratory illness could also be at risk.

Isolate the patient and treat with precautions against transmission of the virus, as for SARS (graphic  p.251). Antiviral treatment with oseltamivir or zanimivir may be considered, depending on current guidelines.

Clinical guidelines about the assessment of suspected cases and the management of influenza patients will be updated as the situation changes and if another pandemic develops. Information is available from the UK Health Protection Agency: www.hpa.org.uk/infections/topics_az/influenza/pandemic

Notes
*

Notifiable only in England and Wales.

**

Notifiable only in Scotland.

1 Lalloo DG et al. (2007) UK malaria treatment guidelines. Journal of Infection  54: 111–121.

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