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Ovid: Oxford Handbook of Accident and Emergency Medicine

Editors: Wyatt, Jonathan P.; Illingworth, Robin N.; Clancy, Michael J.; Munro, Philip T.; Robertson, Colin E. Title: Oxford Handbook of Accident and Emergency Medicine, 2nd Edition Copyright ©2005 Oxford University Press > Table of Contents > Chapter 5 – Infectious diseases Chapter 5 Infectious diseases P.210
Incubation periods Incubation period usually <1wk

Staphylococcal enteritis 1-6h
Salmonella enteritis 6-48h (usually 12-24h)
Bacillary dysentery (Shigella) 1-7days (usually 1-3days)
Botulism 12-96h (usually 18-36h)
Cholera 12h-6days (usually 1-3days)
Gas gangrene 6h-4days
Diphtheria 2-5days
Gonorrhoea 1-12days (usually 3-5days)
Legionnaires’ disease 2-10days (usually 7days)
Meningococcaemia 1-7days (usually 3days)
Scarlet fever 1-4days
Yellow fever 3-6days

Incubation period usually 1-3wks

Brucellosis 7-21days
Chickenpox 7-23days (usually ≈14days)
Lassa fever 3-16days
Leptospirosis 2-21days (usually 7-12days)
Malaria (falciparum) 7-14days (occasionally longer)
Malaria (vivax, malariae, ovale) 12-40days (occasionally >1yr)
Measles 10-18days (rash usually 14-18days)
Mumps 14-18days
Pertussis (whooping cough) 5-14days (usually 7-10days)
Poliomyelitis 3-21days (usually 7-10days)
Rubella 14-21days
Tetanus 1day-3 months (usually 4-14days)
Typhoid 8-21days
Typhus 4-21days

Incubation period usually >3wks

Amoebiasis 2wks-many months
Hepatitis A 3-5wks (usually 4wks)
Hepatitis B, Hepatitis C 6wks-6 months
HIV 3wks-3 months (anti-HIV appears)
Infectious mononucleosis 4-6wks
Rabies 4days-2yrs (usually 3-12wks)
Syphilis 10days-10wks (usually 3wks)

Duration of infectivity of infectious diseases

Chickenpox 5days before rash until last vesicle crusts
Hepatitis A 2wks before until 1wk after jaundice starts
Measles From initial symptoms to 5days after rash appears
Mumps 3days before to 1wk after salivary swelling
Pertussis 3days before until 3wks after start of symptoms
(3days if on erythromycin)
Rubella 1wk before to 5days after onset of rash
Scarlet fever 10-21days from onset of rash (1day if on penicillin)

P.211
Notifiable infectious diseases In Britain certain infectious diseases are ‘notifiable’. A doctor who knows or suspects a patient to be suffering from one is obliged to notify the local Public Health department. Use the special notification form if available. A small fee is payable to the notifying doctor. Telephone the consultant in Communicable Disease Control if investigation or control of an outbreak may be needed. Notifiable infectious diseases in Britain (ND)

  • Anthrax
  • Chickenpox**
  • Cholera
  • Diphtheria
  • Dysentery (amoebic or bacillary)
  • Encephalitis (acute)*
  • Erysipelas**
  • Food poisoning
  • Legionellosis**
  • Leptospirosis
  • Malaria
  • Measles
  • Membranous croup**
  • Meningitis*
  • Meningococcal infection
  • Mumps
  • Ophthalmia neonatorum*
  • Paratyphoid fever
  • Plague
  • Poliomyelitis (acute)
  • Puerperal fever**
  • Rabies
  • Relapsing fever
  • Rubella
  • Scarlet fever
  • Smallpox
  • Tetanus
  • Tuberculosis
  • Typhoid fever
  • Typhus
  • Viral haemorrhagic fever (eg Lassa fever)
  • Viral hepatitis
  • Whooping cough
  • Yellow fever

HIV infection and AIDS are not ‘notifiable’ diseases, but may be reported in strict confidence in the same way. Footnote *Notifiable only in England and Wales **Notifiable only in Scotland P.212
Childhood infectious diseases Children at risk 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. MeaslesND A virus infection spread by airborne droplets. Incubation period = 10-18days. Infectious from just before the onset of symptoms until 5days after the rash appears. Initial features (lasting ≈3days) are fever, malaise, coryza, conjunctivitis and cough. Koplik’s spots (small white spots like grains of salt) appear inside the cheeks. 1-2days later a red maculopapular rash starts behind the ears and spreads to the face and down the body. Treatment 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 malnourishedchildren die from measles, but in the UK the mortality is very low. MumpsND 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. Incubation period = 14-18days. Typical features 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 (p500). Rubella (German measles)ND 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 (http://www.hpa.org.uk/infections). The virus is spread mainly by the airborne route, with an incubation period of 2-3wks and infectivity from 1wk before symptoms until 5days 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. Treatment 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 GP or obstetrician. Whooping cough —see p645 P.213
P.214
Meningitis Causative organisms Meningitis may be bacterial, viral or occasionally fungal. Bacterial causes of meningitis include meningococci, pneumococci, Haemophilus influenzae, Listeria and TB. Other bacteria may also cause meningitis in neonates, the elderly and immunosuppressed patients. Clinical features of bacterial meningitis 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, neck stiffness, neurological signs or ↓ conscious level. Meningococcal meningitisND is caused by Neisseria meningitidis. It can result in septicaemia, coma and death within a few hrs 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 syndrome). Management Resuscitate if necessary and obtain venous access. Start antibiotics immediately (without waiting for investigations) if:

  • the patient is shocked/deteriorating or if
  • there is any suspicion of meningococcal infection (especially a petechial or purpuric rash)

Give IV cefotaxime (2g in an adult; 80mg/kg in a child) or IV ceftriaxone (2g in an adult; 80mg/kg in a child). Chloramphenicol is an alternative if there is a history of anaphylaxis to cephalosporins (see BNF). Initial investigations are FBC, U&E, glucose, blood cultures, serum for polymerase chain reaction and serology, clotting screen and CXR. Throat swab (positive in 40% of meningococcal patients even after antibiotic therapy has started). Urine culture. Aspiration or scraping of petechial rash may show meningococci by microscopy, polymerase chain reaction or culture. LP is required if meningitis is suspected, but ensure CT scan is performed first if there are focal neurological signs or suspicion of ↑ICP (confusion/coma, hypertension, bradycardia or papilloedema). Do not perform LP if there is a coagulopathy. Provide supportive treatment including:

  • O2
  • IV fluids
  • Pressure area care
  • Monitor conscious level, T°, BP, ECG, SaO2 and fluid balance.
  • Consult an expert early and discuss starting dexamethasone (0.15mg/kg) in an attempt to ↓ the risk of post-meningitis deafness, which is especially relevant in children.

See also http://www.britishinfectionsociety.org or http://www.meningitis.org P.215
Prophylaxis of meningococcal 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 (p211) immediately about any suspected meningococcal infection and obtain advice about antibiotic prophylaxis. Prophylactic antibiotics (rifampicin or ciprofloxacin) are needed for the patient’s family and close contacts. Hospital and ambulance staff usually need prophylaxis only if they have given mouth to mouth ventilation. Rifampicin is given 12hrly for 2days (5mg/kg for child aged <1yr; 10mg/kg at 1-12yrs; 600mg at age >12yrs. It makes the urine orange or brown, discolours soft contact lenses and ↓effectiveness of OCP for ≈4wks (see BNF)—give appropriate warnings and record this in the notes. Ciprofloxacin is given as a single dose of 500mg (adults only): it is not licensed for chemoprophylaxis of meningitis. Tell contacts of meningococcal patients to report to a doctor at once if they develop symptoms. TB meningitis 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 (p222), which may be apparent on CXR. 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 meningitis 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 Fungal meningitis is usually part of disseminated infection in immunosuppressed patients, (eg those with AIDS (p232), 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. P.216
Gastroenteritis/food poisoningND 1 Diarrhoea 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. A baby’s parents 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 >6months, normal stool frequency ranges from 1 stool on alternate days to 3 stools daily. Diarrhoea and vomiting 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 (E. coli VTEC 0157). Stool microscopy and culture 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. Food poisoning is a notifiable disease (p211). Immediate notification by telephone is mandatory once an outbreak is suspected. The food eaten, symptoms and incubation period may suggest the organism or toxin involved (see below). CO poisoning (p202) may cause malaise and vomiting in several members of a family and be misdiagnosed as food poisoning. History Record the duration of symptoms, 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). Examination 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%): Clinical evidence of mild dehydration

  • thirst
  • ↓ urinary output (in a baby <4 wet nappies in 24h)
  • dry mouth

Clinical evidence of moderate dehydration

  • sunken fontanelle in infants
  • sunken eyes
  • tachypnoea due to metabolic acidosis
  • tachycardia

Clinical evidence of severe dehydration

  • ↓ skin turgor on pinching the skin
  • drowsiness/irritability

P.217
Food poisoning characteristics

Cause Incubation Food Symptoms*
Staph. aureus 1-6h Meat, milk D, V, P, shock
Bacillus cereus 1-16h Rice D, V, P
Salmonella 6-48h Meat, eggs D, V, P
Escherichia coli 1-2days Any food D, V, P
E. coli VTEC 0157 1-2days Meat, milk D, V, P
Campylobacter 1-3days Meat, milk fever, P, D
Shigella 1-3days Any food bloody D, V, fever
Vibrio parahaem 2-3days Seafood watery D
Cholera 12h-6days Water, seafood D (watery), shock
Rotavirus 1-7days D, V, fever, cough
Botulism 12-96h Preserved food V, paralysis
Scombrotoxin < 1h Fish D, flushing, sweating
Chemicals < 2h Food, water various
Mushrooms < 24h Mushrooms D, V, P, hallucinations
* D = diarrhoea, V = vomiting, P = abdominal pain

P.218
Gastroenteritis/food poisoningND 2 Treatment Most cases are self-limiting, but careful attention to ensure adequate fluid replacement is essential. Hospital treatment 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 <3months 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 5mins, repeated as necessary). Oral rehydration therapy (ORT) is effective in most patients with gastroenteritis (< 5% dehydration). Standard ORT formulations (eg Dioralyte®, Rehidrat®) contain glucose, sodium, potassium and chloride and either citrate or bicarbonate (details are in the BNF). Glucose is important to enhance the absorption of sodium and water.

Usual dose of ORT:
infant 1-11½ 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. Recommence normal feeds and diet after 24h (or earlier if the 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 for ORT are liable to be dangerously inaccurate. If nothing else is available, one may use salt 2.5mL (half a standard 5mL spoonful) and sugar 20mL (four × 5mL spoonfuls) in 1 pint (500mL) of cooled boiled water. Drugs other than ORT are rarely required in gastroenteritis. An antiemetic (eg prochlorperazine 12.5mg IM or prochlorperazine 3mg buccal) is occasionally helpful in adults, but do not use it in children, in whom the side effects can be troublesome. Prolonged vomiting requires investigation and usually hospital admission. Anti-diarrhoeal drugs (eg kaolin, codeine phosphate, loperamide) are contraindicated in children and rarely needed in adults: they may aggravate nausea and vomiting and occasionally cause ileus. Antibiotics 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 5days) or ciprofloxacin (500mg bd PO for 2days: see the BNF or data sheet about side effects and warnings). P.219
P.220
Infestations Worms 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). Other helminthic infections include roundworms, hookworms and tapeworms. Obtain advice from departments of tropical medicine (see p238). Lice Humans may be infected by the body louse (Pediculosis humanis corporis), head louse (Pediculosis humanis capitis) or the ‘crab’/pubic louse (Phthirus pubis). Head lice 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 permethrin, malathion or carbaryl, repeated after 7days (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. Infection by body lice 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. Crab lice are usually transmitted sexually. They cause itching in pubic hair areas. Occasionally children become infested on eyelashes or eyebrows. Treat with permethrin, malathion or carbaryl (see BNF). Sexual partners or other family members may also need treatment. Consider other coexisting venereal diseases. Fleas 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 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 4-6wks, 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 malathion or permethrin (see BNF). Treat all members of the household at once. Calamine lotion and an oral antihistamine may help to relieve itching. P.221
Ticks 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 disease is caused by a tick-borne spirochaete, Borrelia burgdorferi, and it occurs in the UK, most of Europe, the US and in 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 2-40days 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 or encephalitis may develop. Arthritis associated with Lyme disease is more common in North America than in the UK. Myocarditis and heart block occur occasionally. Refer to an Infectious Diseases specialist for confirmation and treatment if Lyme disease is suspected. P.222
TuberculosisND The Mycobacterium genus is characterized by its acid-fast staining (ie it is resistant to being decolourized with acid after it has been stained using 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. Presentation TB can involve almost any organ of the body. Primary infection is usually pulmonary and often asymptomatic. Post-primary infection may present with malaise, weight loss and night sweats and with localised symptoms depending on the organs involved. Pulmonary TB may result in cough, haemoptysis, pneumonia and pleural effusion (p101). Miliary TB, with blood-borne infection of many organs, develops over 1-2wks 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. TB meningitis causes headaches and vomiting, sometimes with neck stiffness, cranial nerve palsies and papilloedema. Tuberculous osteomyelitis usually affects the spine, with collapse of adjacent vertebrae and a paravertebral abscess. Patients may present with swollen lymph nodes from tuberculouslymphadenitis or with sinuses or cold abscesses from bone or soft tissue infection: microscopy of the discharge will show acid-fast bacilli. Treatment Refer patients with suspected TB to an appropriate specialist for assessment and treatment. Isolation is required for patients with untreatedpulmonary TB. Notify the local Public Health department (p211). P.223
AnthraxND 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 pulmonary 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 may cause cutaneous or pulmonary anthrax, which may be fatal. Cutaneous anthrax starts with a red papule which develops into an ulcer (‘malignant pustule’) with a black centre. The lesion is not painful, but may itch. Malaise and fever may occur and in a few cases, life-threatening septicaemia develops. Penicillin ↓ risk of complications from cutaneous anthrax. The clinical diagnosis is confirmed by microscopy and culture of the pustule. Pulmonary anthrax starts within 48hrs of exposure with a flu-like illness, followed by breathlessness and shock. Septicaemia and meningitis may be 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 (p211). Post-exposure prophylaxis with antibiotics can prevent anthrax if started early enough. Press enquiries must be anticipated after any case of anthrax, especially if anthrax spores have been released deliberately. Further information is available from: http://www.hpa.org.uk/infections P.224
Streptococcal infections Streptococcus pyogenes and other streptococci may reside without symptoms, but can cause sore throats (pharyngitis and tonsillitis—see p530), soft tissue infections (cellulitis, erysipelas and lymphangitis—see p503), scarlet fever and occasionally endocarditis and septicaemia. Later, non-suppurative sequelae of streptococcal infections include erythema nodosum, rheumatic fever (p475) and glomerulonephritis. Streptococci and/or staphylococci may cause necrotizing fasciitis, impetigo and toxic shock. Scarlet feverND Some streptococcal infections are associated with scarlet fever. There is a diffuse erythematous rash with spots of ↑ erythema around slightly raised hair follicles, making the skin feel rough. During the first 1-2days 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 ‘red strawberry tongue’. At 10-14days after onset of the rash, skin may peel from palms and soles. Treat with penicillin or erythromycin for 14days. Complete recovery is usual. Infective endocarditis Endocarditis may develop on previously normal heart valves, as well as on diseased or prosthetic valves. IV drug abusers are liable to staphylococcal infection of the tricuspid valve, with fever and pneumonia from septic PE. The commonest organism is S. viridans, but many others have been implicated. Many acute cases involve Staphylococcus aureus and present with acute heart failure. Clinical features 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. Treatment On suspicion of endocarditis, admit immediately for investigation (blood cultures, echocardiography) and treatment. Cellulitis and erysipelas Treat these bacterial skin infections with antibiotics as described on p503. Necrotizing fasciitis This is a rare and severe bacterial infection of soft tissues. It can occur with or without obvious trauma and may follow illicit heroin injection (‘muscle popping’). Strep. pyogenes is often involved, sometimes with Staphylococcus aureusor 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. Initial symptoms and signs may be vague, with severe pain but little on examination, except for tenderness of the affected area, sometimes with slight erythema and swelling. The patient is usually pyrexial. Infection can spread rapidly and cause marked soft tissue swelling with discolouration, 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. Treatment involves resuscitation with IV fluids and antibiotics, and prompt surgery to debride the affected area and excise necrotic tissues. Similar infections, often with anaerobic organisms, may involve the abdomen, perineum and scrotum (Fournier’s gangrene). P.225
Staphylococcal infections Staphylococcus aureus is involved in many infections of wounds, soft tissues (p399), joints and bones (p472). Staphylococci may also cause impetigo, scalded skin syndrome, food poisoning, pneumonia, endocarditis, toxic shock syndrome, septicaemia and meningitis. Impetigo A highly infectious superficial skin infection caused by staphylococci or streptococci. It may involve normal skin or complicate a pre-existingcondition such as eczema or scabies. Lesions often start around the mouth/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 7days, max 10days) and give PO flucloxacillin or erythromycin if lesions are widespread or there is cellulitis or pyrexia. Scalded skin syndrome 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 (toxicepidermal necrolysis, Lyell’s syndrome) occur in children. Admit for nursing and medical care. Toxic shock syndrome 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 give anti-staphylococcal antibiotics. Remove tampons and send for culture. Refer to ITU. Involve a surgeon if there is any associated abscess which requires drainage. Staphylococcal septicaemia Occurs particularly in debilitated or immunocompromised patients and in IV drug abusers. 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 (p214) and the rash may be similar. P.226
TetanusND An acute and often fatal disease, common in much of Asia, Africa and South America, especially in neonates. Now rare in developed countries: 30-40cases/yr 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. Incubation period is usually 4-14days, but may be 1day to 3months. In 20% of cases there is no known wound. Tetanus occasionally occurs after surgery or IM injections. Clinical features 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. Differential diagnoses Dystonic reaction to metoclopramide or phenothiazines, strychnine poisoning, quinsy or dental abscess, meningitis, rabies. Procyclidine or benztropine relieve muscle spasms from drug-induced dystonia, but are unlikely to affect tetanus; diazepam may relieve dystonia or tetanic spasms. Management Obtain senior medical and anaesthetic help. Monitor breathing, ECG and BP. Refer to ITU. Control spasms with diazepam. Paralyse and ventilate if breathing becomes inadequate. Clean and debride wounds. Give penicillin and metronidazole and human tetanus immune globulin. Prognosis Depends on severity of disease and quality of care. Short incubation (<4days) and rapid progression suggest severe disease and high mortality. With expert intensive care, the mortality in adults is <10%, but neonatal tetanus is often fatal. Immunization Tetanus is eminently preventable by immunization and by proper care of wounds (p396). P.227
Gas gangrene This is a rapidly spreading infection of muscle by clostridial bacteria (anaerobic toxin-producing Gram +ve bacilli), usually Clostridium perfringens (formerly called C. welchii). It is fatal if untreated. It often involves wounds of the hip and buttocks, amputations for vascular disease or severe muscle injuries (eg gunshot wounds). Occasionally, gas gangrene of the perineum occurs without trauma. Incubation period is usually <4days (sometimes a few hrs). Sudden severe pain occurs at the wound site. Generalized toxicity develops rapidly, 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 onset of symptoms. Diagnosis depends on clinical features. Severe pain necessitates wound inspection (remove/window any POP). Obtain immediate senior surgical advice if gas gangrene is suspected. Wound discharge may contain Gram +ve bacilli. X-rays may show soft tissue gas, but its absence does not exclude gas gangrene. Treatment Refer for immediate surgical removal of all infected tissue, antibiotics (metronidazole with penicillin or clindamycin) and possibly hyperbaric O2 and gas gangrene antitoxin. BotulismND The exotoxin of Clostridium botulinum paralyses autonomic and motor nerves by blocking acetylcholine release at nerve synapses and myoneural junctions. Infection follows 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. IV drug users may develop botulism after IM or SC injections of contaminated drugs. Incubation period is 12-72h. 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. Clinical signs result from involvement of autonomic and motor nerves: dry mouth, cranial nerve palsies (ptosis, squint, fixed pupils, weakness of tongue), limb weakness with muscle flaccidity. Consciousness and sensation are preserved. Hypotension and ileus may occur. Fever is unusual. Differential diagnoses are Guillain-Barré syndrome, myasthenia gravis, brainstem stroke, diphtheria, poisoning (atropine, anticholinergics or organophosphates), paralytic rabies. Botulism may be misdiagnosed as staphylococcal food poisoning, paralytic shellfish poisoning, CO or mushroom poisoning. Management Obtain senior help. Assess and monitor breathing, ventilate if necessary and admit to ITU. Botulinum antitoxin (see BNF) and possibly penicillin are needed. 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. P.228
Sexually transmitted diseases The commonest sexually transmitted disease (STD) is non-specific genital infection. Other common diseases include 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 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. Genital ulcers and sores 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). Other causes of painless ulcers include carcinoma and trauma (possibly self-inflicted). Urethritis 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, FBs or from attempts at self-treatment with intraurethral chemicals. Gonorrhoea usually has a shorter incubation period (3-5days) than non-gonococcal urethritis (eg chlamydia 7-14days), 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 4h before the appointment, in order to allow serial urine samples to be taken. Reiter’s disease 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 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. Complications include prostatitis, epididymitis, salpingitis, Bartholin’s abscess; rarely septicaemia with arthritis, fever, rash (maculopapular initially then pustular) and endocarditis. P.229
HepatitisND Hepatitis A (infectious hepatitis) ND 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 3-5wks. There may be fever, malaise, anorexia and nausea for 2-7days before jaundice develops. Jaundice is more common in adults than in children and is associated with dark urine, pale stools and tender hepatomegaly. Treatment is symptomatic, but alcohol should be avoided. Infectivity is greatest shortly before jaundice develops, so isolation is of little value. Arrange follow-up by a specialist or GP. There is usually complete recovery over several wks. Hepatitis BND Hepatitis B is transmitted by infected blood (eg shared needles in drug abusers, tattooing, needlestick injury) and by sexual intercourse. The incubation period is 6wks to 6months. 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 ‘universal precautions’ (p236) are essential when handling all blood samples and ‘sharps’. The management of needlestick injury is described on p404. Hepatitis C, D and END Hepatitis C and D are spread in the same way as hepatitis B and may cause hepatic failure or chronic liver disease. No immunization is available. Hepatitis E is similar to hepatitis A, but has a high mortality in pregnancy. Refer to a specialist for follow-up. Leptospirosis (Weil’s disease)ND Weil’s disease, caused by the spirochaete Leptospira interrogans, is spread by contact with infected rat’s urine, often in canals, rivers or sewers. The leptospires enter the body through small breaks in the skin or via mucous membranes of the eyes or nose. After ≈10 days there is fever, headache, vomiting, diarrhoea, a haemorrhagic rash, conjunctival reddening, jaundice and renal failure. The mortality is ≈1%. Refer to an Infectious Diseases unit. Treatment is with penicillin or doxycycline with supportive care and haemodialysis if necessary. Prophylactic penicillin or doxycycline is reasonable for people who fall into waterways contaminated with leptospires. P.230
Herpes virus infections Varicella zoster Chickenpox 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 3-4days. Fever, malaise and muscle aches may occur in adults. Transmission of infection may occur before the onset of disease 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 (acyclovir) and/or varicella-zoster immune globulin. Consider aciclovir also for adults and older adolescents (see BNF). Shingles 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 1-4days. 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. Antiviral treatment (aciclovir, famciclovir or valaciclovir) ↓ risk of post-herpetic pain if given early (within 72h of start of rash). Dose: aciclovir 800mg five times daily for 7days. Antiviral treatment is also indicated in patients with immune deficiency or ophthalmic zoster, who need immediate specialist referral. Provide analgesia. Antibiotics may be required for secondary infection. Herpes simplex Primary herpes simplex infections often cause painful vesicles and ulceration involving the mouth or genitalia (p538). The virus may be inoculated locally into skin by trauma (‘herpes gladiatorum’, ‘scrumpox’) or by contamination of fingers causing herpetic paronychia (whitlow). Infection of the cornea may cause dendritic ulcers (p520). Herpes simplex meningitis and encephalitisND are uncommon but may be fatal, especially in immunodeficient patients. Do not incise a suspected whitlow. Cover it with a dressing and advise care to avoid spread of infection to lips or eyes. The herpes simplex virus persists in sensory ganglia and may be reactivated by stimuli such as sun, cold, trauma or viral respiratory infections. Recurrence of cold sores of the lips is often preceded by a tingling sensation: aciclovir cream or tablets may prevent the development of vesicles. Secondary bacterial infection of skin lesions may require antibiotics. P.231
Infectious mononucleosis (glandular fever) 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 ß-haemolytic streptococcus. In severe cases there is marked oedema of the throat with tonsillar swelling and a membranous exudate (‘anginose’ infectious mononucleosis). Swallowing and breathing may be difficult. A rash is uncommon unless ampicillin or amoxicillin are given (this rash does not signify allergy to penicillins in general). Complications of infectious mononucleosis include respiratory obstruction, ruptured spleen (spontaneously or after minor trauma), thrombocytopenia, jaundice, meningitis, encephalitis, facial palsy and acute polyneuritis (some- times causing respiratory failure). Investigations Take FBC and blood film (for atypical lymphocytes), request Monospot test or Paul-Bunnell test (which may be -ve initially). Differential diagnosis includes cytomegalovirus and toxoplasmosis. Treatment 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 PO on day 1, 15mg PO tds on days 2-3, 10mg PO tds on days 4-5, 5mg PO tds on days 6-7). Steroids are also helpful in patients with neurological complications. Concurrent ß-haemolytic streptococcal infection requires erythromycin (500mg PO tds), which would also treat the rare unrecognised case of diphtheria. P.232
Human immunodeficiency virus 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. Structure and pathogenesis 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 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↓, so the patient develops profound cellular immunodeficency. Although other complex mechanisms are also involved, CD4 cell counts provide a useful index of disease stage and progress. Transmission 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 coexistent STD)
  • risk of vertical 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 to health care workers from an HIV positive source carry a risk of ≈0.3%.

Diagnosis and HIV testing IgG antibodies to HIV provide evidence of infection and form the basis of current blood tests. Interpret results remembering that these antibodies may not appear until 3months after exposure. HIV testing is not appropriate in A&E, 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 the Terrence Higgins Trust (Tel. 0845 1221 200), or the National AIDS Helpline (24h freephone 0800 567 123). Natural history of HIV infection HIV infection progresses through a number of phases which form the basis of the 2 commonly used classification systems (WHO and CDC systems). Acute infection is usually sub-clinical, but may produce a non-specific febrile illness (lethargy, arthralgia, myalgia) 6wks after exposure. A long asymptomatic period (≈10yrs) follows. Some patients develop Persistent Generalized Lymphadenopathy (PGL). PGL is unexplained lymphadenopathy (>1cm) at two non-inguinal sites for 3months. Patients become symptomatic as their immunity↓, developing unusual infections and tumours. Many are ‘indicator diseases’ used to diagnose AIDS (see below). The label ‘AIDS’ has significant psychological connotations. Most patients with AIDS survive > 2yrs. Anti-retroviral drugs (AZT, DDI or DDC) delay onset of AIDS in symptomatic patients and ↑ length of survival. P.233
Initial presentation of HIV to A&E Many HIV +ve patients attending A&E 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. Centers for Disease Control classification of HIV infection

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

Some indicator diseases for AIDS in HIV +ve patients

  • Pneumocystis carinii pneumonia
  • 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 and AIDS 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. P.234
Presentation of HIV +ve patients Many patients with symptomatic HIV infection bypass A&E and liaise directly with the specialist unit caring for them. Assessment of HIV +ve patients is difficult in A&E, 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: Respiratory problems As CD4 counts ↓, Pneumocystis carinii pneumonia (PCP) becomes more likely and is the commonest indicator diagnosis of AIDS. A non-productive cough combines with dyspnoea and fever. CXR may reveal bilateral diffuse interstitial shadowing of both mid-zones. Obtain blood and sputumcultures, rehydrate with IV fluids as necessary and refer urgently for IV co-trimoxazole or pentamidine 9 steroids. Occasionally, PCP may present with fulminant respiratory failure needing emergency tracheal intubation and IPPV. Other common infections include pulmonary TB, Aspergillus and Cryptococcus. IV drug abusers are at special risk of bacterial infection: usually H. influenzae or Strep. pneumoniae. Neurological problems Strongly suspect Cryptococcus neoformans meningitis in HIV +ve patients presenting with headache, fever and sometimes ↓ conscious level. Neck stiffness and photophobia are rare, despite advanced infection. Obtain a CT scan to exclude space-occupying lesions (cerebral toxoplasmosis may present similarly, with focal signs or fits) before urgent LP and CSF examination. 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 9 dementia. Eye problems The most significant ophthalmological problem is CMV retinitis, occurring in 15% of patients. This presents with orbital pain, redness, photophobia and ↓ VA. Fundoscopic appearances are characteristic: perivascular haemorrhages and exudate that have been called ‘pizza pie’. Refer for urgent ophthalmological assessment and treatment with ganciclovir or foscarnet. Gastrointestinal problems Nausea, vomiting, diarrhoea and weight loss are common complaints and can be due to drug therapy. Dysphagia may reflect oesophageal candidiasis, herpes simplex, CMV or Kaposi’s sarcoma, all requiring specialist investigation and treatment. CMV colitis can cause a serious illness, characterized by abdominal pain, diarrhoea and fever. Obtain plain x-rays if the recognised 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. Hepatitis viruses are particularly likely to complicate the picture in IV drug abusers, many of whom are infected with hepatitis B and C viruses. P.235
Muco-cutaneous problems 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. Drug reactions and side effects 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. P.236
HIV and A&E staff A&E 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 A&E staff is largely in the form of needlestick injury (p404). This is reflected in the recommended universal precautions which should be followed for contact with all emergency patients. Precautions for A&E staff:

  • ensure up-to-date immunization against tetanus and hepatitis B
  • cover any open wounds or weeping dermatitis
  • wear gloves during any contact with patient’s blood or other body fluids
  • wash hands before and after every patient contact
  • consider wearing double gloves during invasive procedures
  • use goggles and mask to protect if aerosolization is anticipated
  • wear a mask if the patient may have pulmonary TB
  • avoid handling needles directly or using hand-held needles
  • never re-sheathe needles
  • place used needles immediately into a ‘Sharps bin’
  • wash contaminated surfaces with 1:10 bleach
  • pregnant staff should not treat patients with AIDS (concern about CMV and herpes simplex virus)

Handling HIV +ve patients 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 might have received outside hospital, does not extend into the A&E department. 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. HIV +ve staff The risk to patients from A&E 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. Needlestick injury: see p404. P.237
P.238
Imported infectious diseases Patients may present in A&E with infectious diseases acquired abroad. It is essential to ask where a patient has been, especially in the 6wks before the onset of symptoms. The most common imported diseases are bowel infections causing diarrhoea (p216). Less common, but very important diseases include malaria (p240), typhoid (p241), Legionnaires’ disease and hepatitis (p229). Rabies (p242) and viral haemorrhagic fevers such as Lassa fever (p243) 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) http://www.heartsol.wmids.nhs.uk Telephone 0121 424 2000
Liverpool (School of Tropical Medicine) http://www.liv.ac.uk/lstm Telephone 0151 708 9393 Fax 0151 705 3370
London (Hospital for Tropical Diseases) http://www.thehtd.org Telephone 0207 387 9300 Fax 0207 388 7645
Oxford(Churchill Hospital) Telephone 01865 220 289 Fax 01865 222 901
http://www.jr2.ox.ac.uk/ndm/Tropical_Medicine/pages/home.htm
Glasgow (Gartnavel General Hospital) Telephone 0141 201 3000 Fax 0141 201 3466

A useful public access website provided by the NHS which gives information for people travelling abroad from the UK is http://www.fitfortravel.scot.nhs.uk Pyrexia of unknown origin in travellers Think of and check for malaria (p240) in any febrile patient who has been in a malarious area. Consider Lassa fever (p243) in someone who has been in West Africa in the previous 3wks. Typhoid (p241) often presents as a septicaemic illness with constipation rather than diarrhoea. TB (p222) and brucellosis may cause fever and sweating at night. Investigations (warn lab of possible risks) 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. Management Barrier nurse in a cubicle. Wear gown, gloves, goggles, and mask. Record vaccination and prophylaxis history, together 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. P.239
Severe Acute Respiratory Syndrome Background SARS is a viral respiratory illness caused by a coronavirus. SARS was first recognised 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. A 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. Spread 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. Features The incubation period of SARS is usually 2-7days but may be up to 10days. The illness starts with fever (>38°C), sometimes associated with rigors, headache, muscle pains and malaise. Diarrhoea may occur. Some patients have mild respiratory symptoms initially. A dry cough develops after 2-7days, with increasing breathlessness from hypoxia caused by pneumonia. Consider the possibility of SARS in a patient with these symptoms who, within 10days 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. Management If SARS is suspected, get expert help (A&E consultant, Infectious Diseases specialist and infection control staff) and isolate the patient in a side room. Ensure that the minimum number of staff have contact with the patient. Staff who do have contact must wear masks or respirators (of N95 standard), goggles, gowns and gloves, with strict handwashing and carefuldisposal of all items. Provide the patient with an N95 mask or a surgical mask. Record SaO2 and give O2 if necessary, but avoid flow rates of >6litres/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 (p109). Further information about SARS is available on several websites:

P.240
MalariaND Malaria is common in many tropical and subtropical countries. It is a parasitic infection transmitted by mosquitoes. There are four varieties, caused by Plasmodium falciparum, P. vivax, P. ovale and P. malariae. 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. Malaria in the UK Many cases occur in travellers from malarious areas, especially P. vivax infections from the Indian subcontinent and P. falciparuminfections from Africa, South-East Asia and Central and South America. Malaria often develops despite antimalarial tablets, because of drug resistance or incorrect dosage. Exclude malaria as the cause of any febrile illness within 2months of return from a malarious area. Common misdiagnoses are influenza and viral hepatitis. Clinical features The incubation period is usually 7-14days for P. falciparum and 12-40days for other types of malaria, but occasionally it is much longer (>1yr), especially in P. malariae and P. vivax infections. There is malaise, fatigue, fever and headache followed by paroxysms lasting 8-12h of rigors, vomiting and then severe sweating. The fever may become periodic (48h in P. ovale orP. vivax infections and 72h in P. malariae). Haemolytic anaemia, splenomegaly and jaundice may occur, but lymphadenopathy is not a feature. P. falciparum may cause cerebral malaria with coma, fits, oculogyric crisis and focal neurological signs. Diarrhoea, cardiac failure, pulmonary oedema and shock may occur. Deterioration can be rapid. Investigations Consider Lassa fever (p243) in recent visitors to West Africa. Send blood for thin and thick film examination for malaria in any ill patient who has been in a malarious area. Repeated blood films may be needed. If falciparum malaria is possible, start treatment without waiting for the blood results. Other investigations are FBC (malaria may cause anaemia, neutropenia and thrombocytopenia), U&E (renal failure is possible), blood glucose (hypoglycaemia may be severe) and urine testing (haemolysis may occur – ‘black water fever’). Treatment of falciparum malaria Careful monitoring is needed ± ITU. Obtain expert advice from a tropical disease specialist (p211), especially if the patient is severely ill or has come from Thailand or adjacent countries where there is widespread drug resistance. Give quinine, orally or IV depending on the severity of illness (oral dose: quinine sulphate 600mg (adult) or 10mg/kg (child) every 8hrs for 7days; IV dosage: quinine dihydrochloride 10mg of base/kg in 500mL dextrose/saline over 4h). Alternative drugs are mefloquine or malarone (proguanil with atovaquone). In drug resistant infections, doxycycline or Fansidar® (pyrimethamine and sulfadoxine) may be required in addition to quinine. See BNF. Treatment of benign malarias (P. vivax, ovale, malariae) Refer to Infectious Diseases unit for treatment and follow-up. Usual treatment is chloroquine. A course of primaquine is also needed to prevent relapse in vivax and ovale infections, but glucose-6-phosphate dehydrogenase levels need to be checked before primaquine is used, since it may cause haemolysis in G-6-PD deficient patients. P.241
TyphoidND and paratyphoidND (enteric fever) 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 8-14days but may be up to 21days. Initial symptoms 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. Physical examination This may be normal. There may be a relative bradycardia (i.e. 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. Investigations FBC (slight leucopenia is common), blood films for malaria, U&E, blood cultures. CXR (for signs of TB or pneumonia). Treatment Isolate and barrier nurse. Admit suspected cases to an Infectious Diseases unit and notify the local consultant in Communicable Disease Control immediately. The usual drug treatment is with ciprofloxacin or chloramphenicol. P.242
PoliomyelitisND 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. Resuscitate and ventilate if necessary and refer to ITU. The differential diagnosis includes Guillain-Barré syndrome (p138) and organophosphate poisoning (p200). RabiesND Rabies is a viral infection of mammals which 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, 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 p400. Expert advice about post-exposure treatment is available in the UK from the Viral Zoonosis Unit of the Health Protection Agency (telephone 020 8200 4400). The Department of Health’s Memorandum on Rabies: Prevention and Control (2000) is available from: http://www.doh.gov.uk/rabies/memorandumrabies/rabies.pdf See also: http://www.hpa.org.uk/infections/tropics_az/rabies/menu.htm Clinical features The incubation period of rabies is usually 3-12wks, but can vary from a few days to >2yrs. 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 ↑paralysis, but no episodes of spasm or hyperactivity. Rabies is almost always fatal, even with ITU treatment. Management If suspected, barrier nurse the patient in a quiet room with the minimum of staff, who must wear gowns, gloves, masks and eye protection. 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. P.243
Viral haemorrhagic feversND Lassa fever 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 3wks. There is a high mortality, Early symptoms 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 3wks. However, malaria and typhoid are much more common and need urgent diagnosis and treatment. Management If Lassa fever is possible, barrier nurse the patient in a cubicle by staff wearing gloves, gowns, googles and masks. Take special care to avoid needlestick injuries. 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 (p240). Warn the lab 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. Ebola fever and Marburg fever 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 4-10days. 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. Other viral haemorrhagic fevers Diseases with similar features (plus in some cases jaundice) include dengue (southern Asia, South America and the Carribean), 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.

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