Infectious disease

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2 Infectious disease

Chapter Contents

Approach to the patient with a suspected infection 29
Systemic multi-system infections 31
Skin and soft-tissue infections 42
Respiratory infections 48
Cardiological infections 52
Rheumatological infections 54
Neurological infections 54
Gastrointestinal infections 58
Hepatobiliary and pancreatic infections 63
Genitourinary infections 64
Systemic fungal infections 66
Helminthic infections 68
Sexually transmitted infections 71
Antimicrobial drugs 74

Approach to the patient with a suspected infection

Infectious diseases are the most common cause of illness in humans worldwide and can affect any organ. Fever is the cardinal symptom but not all infectious diseases will present with a fever. Fever can be defined as a temperature of ≥37.8°C, although this may vary between 37.5°C and 38.0°C.

• History should include overseas travel; animal contact; exposure to sick individuals; tick, insect or animal bites; sexual activity with risk factors; IV drug users; leisure activity, e.g. freshwater-borne infections.
• Examination should include ears, eyes, mouth and throat, and all systems, including rectal, vaginal and penile examination for STIs. Rashes and lymphadenopathy are common in infectious diseases.
• Investigations may not be required, particularly in the primary healthcare setting if the patient is relatively well. In general, the following investigations should be conducted in anyone who is unwell and requires hospital attention:

• FBC and ESR
• blood cultures
• serum save to microbiology
• U&E, liver biochemistry, glucose and CRP
• CXR
• urinalysis and culture
• if indicated by travel history — malaria — perform three blood smears if initial sample negative.

• Management

• Take samples for cultures and tests above.
• Give ‘blind’ antibiotics if the patient is unwell or if meningitis or septicaemia is likely. This ‘blind’ therapy should cover likely pathogens with broad-spectrum antibiotics, e.g. IV cefotaxime 8-hourly is often used.
• The regimen should be changed when the organism (and sensitivities) are identified.

Returning travellers (Table 2.1)

There are number of common illnesses that occur only in certain areas. The history should cover all recent travel. Most tropical illnesses are uncommon in the countries in which they occur; upper respiratory tract infections, urinary tract infections and viral infections are still common worldwide. However, some illnesses, such as malaria or dengue, are common. WHO advises that fever occurring in a traveller 1 week or more after entering a malaria risk area and up to 3 months after departure is a medical emergency because of the mortality associated with Plasmodium falciparum, though there have been well-reported cases of falciparum infection occurring after 3 months. Viral haemorrhagic fevers are also seen in patients returning from endemic areas, though these are very rare infections. Websites are a useful source of up-to-date information on geographic medicine and epidemics (e.g. www.cdc.gov/travel/destinat.htm).

Table 2.1 Causes of febrile illness in travellers returning from the Tropics and world-wide

Developing countries Specific geographical areas (see text)
Malaria Histoplasmosis
Schistosomiasis Brucellosis
Dengue World-wide
Tick typhus Influenza
Typhoid Pneumonia
Tuberculosis Upper respiratory tract infection
Dysentery Urinary tract infection
Hepatitis A Traveller’s diarrhea
Amoebiasis Viral infection

Fever of unknown origin (FUO)

One definition of a fever of unknown origin is ‘a fever persisting for more than 2 weeks, with no clear diagnosis despite intelligent and intensive investigation’. The definition of FUO has also been refined to include classical FUO, nosocomial FUO, neutropenic FUO and HIV-related FUO.

The causes of FUO, when determined, are infections (20–40%), e.g. endocarditis, TB, Lyme disease; connective tissue disease, e.g. polymyalgia (15–20%); malignancy, e.g. lymphoma (10–30%); and miscellaneous (e.g. drugs).

Fever and rash

The presentation of fever and rash in an adult has many potential causes. These range from severe life-threatening infections, such as meningococcal sepsis or toxic shock syndrome, to the usually mild infections of parvovirus or enterovirus. Travel-related illnesses include dengue, typhus or typhoid. Illnesses such as syphilis or HIV seroconversion illness can also present with a fever and rash.

Investigations

Initial investigations should include the following:

• FBC, LFTs, CRP
• blood cultures (repeated)
• skin biopsy for microscopy (Gram stain), culture or PCR if appropriate
• appropriate imaging.

A low platelet count would tend to indicate either a viral infection or possibly malaria. A lymphopenia may also indicate a viral infection, whereas a neutrophilia occurs in a bacterial infection. Treatment may be delayed until a diagnosis is made or appears highly likely. However, if serious infection, such as meningococcal sepsis, is suspected, then antimicrobial therapy must be started immediately.

Systemic multi-system infections

Sepsis

Sepsis is a leading cause of death worldwide and is usually the result of an overwhelming bacterial infection. Most infections, whether bacterial, fungal or viral, initiate a systemic inflammatory response with the release of vasodilatory and pro-inflammatory substances, including cytokines, histamine and prostaglandins. This results in endothelial damage, capillary leak and vasodilatation, causing tissue hypoperfusion. Additionally, the coagulation pathway is activated by a number of cytokines, resulting in microthrombi and further tissue ischaemia. The mortality rate for severe sepsis remains about 30%.

Clinical features

Patients are pyrexial (occasionally hypothermic) and often hypotensive, and have rigors, warm peripheries and a bounding pulse. Hypotension may not be present, particularly in children and young adults. They can be hyperglycaemic or, in severe cases, hypoglycaemic.

A consensus definition (1991) of sepsis immune response syndrome (SIRS) for adults considers two or more of the following features to be present:

• heart rate > 90 beats per min
• body temperature < 36°C or > 38°C
• respiratory rate > 20 breaths per min or PaCO2 < 4.3 kPa
• white blood cell count < 4 × 109/L or > 12 × 109/L, or > 10% immature (band) forms on film.

Septicaemia is defined as SIRS plus the detection of a positive blood culture. Bacteraemia is the presence of bacteria in the bloodstream without SIRS or in an asymptomatic patient.

Severe sepsis is sepsis complicated by organ dysfunction or hypotension.

Septic shock is sepsis with hypotension in adults with a systolic BP < 90 mmHg, a mean arterial pressure < 60 mmHg, or a reduction of > 40 mmHg in the systolic BP from baseline.

Management

Sepsis and septic shock should be treated urgently, as should the bacterial cause of the infection.

• Patients should have close monitoring (intensive care) and be adequately supported with IV fluid volume replacement, inotropes and adequate oxygenation.
• Therapy to optimize the mixed venous oxygen saturation has been shown to improve survival from sepsis significantly.
• Adjunctive therapy of severe sepsis with activated protein C (drotrecogin alfa activated) may be of benefit. Evidence for other adjunctive therapies, such as the use of steroids, is disappointing. Tight glycaemic control is now not recommended (p. 539).
• Blood tests should include FBC, U&E, LFTs and CRP.
• Blood cultures × 2 (at least) should be taken from different sites prior to antibiotic therapy.
• Early IV antibiotic therapy should be given. The exact choice of antibiotic depends on the probable source of sepsis. If the source of sepsis is completely unknown, then choose antibacterial agents that treat a broad range of Gram-positive and Gram-negative bacteria (such as co-amoxiclav 1.2 g IV 3 times daily, cefotaxime 1 g twice daily IV to maximum of 8 g daily, plus gentamicin 5–7 mg/kg IV daily).
• Neutropenic sepsis may often be caused by Pseudomonas aeruginosa and these patients should be treated with an antipseudomonal β-lactam antibiotic (such as piperacillin/tazobactam 4.5 g 6-hourly IV infusion or meropenem 1 g 8-hourly) plus an aminoglycoside. If there is a permanent IV line in situ, then glycopeptides may need to be added. Failure of fever to resolve should indicate the need to investigate the possibility of a fungal or viral infection and/or to use a glycopeptide to treat resistant gram negative infections.
• Asplenic patients can develop sepsis from encapsulated organisms, e.g. Streptococcus pneumoniae, Neisseria meningitidis or Haemophilus influenzae. Give a third-generation cephalosporin (ceftriaxone IV infusion 2–4 g daily ± vancomycin 1–1.5 g IV infusion 12-hourly).

Meningococcal septicaemia

Neisseria meningitidis is found worldwide. There are five major serogroups. The organism is carried asymptomatically in the nasopharynx of 5–20% of the general population. Invasion into the bloodstream (septicaemia-causing disease) depends on both host and bacterial factors.

Presentation is with the classic triad of headache, fever and neck stiffness, though this is not always the case (p. 54). Septicaemia causes septic shock with fever, myalgia and hypotension, and may be accompanied by a petechial or haemorrhagic rash. The case fatality rate is approximately 10%.

N.B. If not treated immediately, patients can deteriorate rapidly, with shock, disseminated intravascular coagulation, multi-organ failure and death.

Diagnosis

Diagnosis is frequently clinical with:

• presence of a rash (Fig. 2.1)
• Gram stain showing diplococci in CSF (not always necessary) or aspirate of petechiae
• culture of blood, CSF or aspirate
• PCR of above samples if necessary.
image

Fig. 2.1 Meningococcal septicaemia showing a purpuric rash.

Management (Box 2.1)

Start antibiotics immediately.

• cefotaxime 2 g 6-hourly IV for 7 days or
• benzyl penicillin 2.4 g 4-hourly by IV infusion.

Box 2.1 Meningococcal meningitis and meningococcaemia emergency treatment

Suspicion of meningococcal infection is a medical emergency requiring treatment immediately

Clinical features

• Petechial or non-specific blotchy red rash
• Fever, headache, neck stiffness

All these features may not be present — and meningococcal infection may sometimes begin like any apparently non-serious infection

Immediate treatment for suspected meningococcal meningitis at first contact before transfer to hospital or investigation

• Benzylpenicillin 1200 mg (adult dose) slow IV injection or intramuscularly
• Alternative if penicillin allergy — cefotaxime 2 g IV ×4 daily

In meningitis, minutes count; delay is unacceptable

On arrival in hospital

• Routine tests including blood cultures immediately
• Watch out for septicaemic shock

Patient contacts in the household and ‘kissing’ contacts should be given prophylaxis with oral rifampicin 600 mg 6-hourly for 2 days or ciprofloxacin 500 mg single dose to eradicate bacteria from the nasopharynx. Group C disease contacts should be offered immunization.

Malaria

Malaria in humans is caused by Plasmodium falciparum (most severe form), Plasmodium vivax, Plasmodium ovale, Plasmodium malariae or rarely Plasmodium knowlesi, which are transmitted by the Anopheles mosquito. P. vivax and P. malariae may recur after many years, but P. falciparum and P. malariae do not recur, although individuals may be reinfected. P. falciparum causes a potentially fatal malaria that results in about 1–2 million deaths annually, most in children in sub-Saharan Africa. The other causes of malaria are very rarely fatal and may be regarded as the benign malarias.

Clinical features

Patients present with fever and other generalized features, such as malaise, headache, vomiting, diarrhoea and sweats, 10–21 days (occasionally months) after a mosquito bite. Symptoms can be mild or severe with complications (e.g. cerebral malaria) (see below). Repeated infections cause ill health, anaemia and hypersplenism with splenomegaly.

Diagnosis

• Peripheral blood film can detect asexual forms of the appropriate Plasmodium. This is usually done by microscopy. A single negative blood film examination does not exclude malaria and should be performed three times on three consecutive days. Speciation of malaria parasites should be performed by a skilled examiner if necessary. If there is any doubt as to the species or whether or not an infection is present, then the infection should be assumed to be P. falciparum until it can be proven otherwise.
• Antigen detection kits are available for P. falciparum and other malarias that rely on the detection of parasite histidine-rich protein 2 or lactate dehydrogenase.
• Real-time PCR for P. falciparum and some benign malarias is marginally more sensitive and specific than microscopy but is expensive, difficult to perform and not yet in routine clinical practice.

P. falciparum infection causes about 200 million infections worldwide annually. WHO advises that fever occuring in a traveller one week or more after entering a malaria risk area and up to three months after departure is a medical emergency because of the mortality associated with P. falciparum. Cases have been reported up to 5 years after leaving a malarial area. Three blood films should be performed. Falciparum malaria is divided into severe and uncomplicated forms.

Severe malaria can present differently in adults and children, but may be defined as the presence of the following features:

• Glasgow coma score ≤ 9/15
• hypoglycaemia (blood glucose ≤ 2.2 mmol/L)
• severe anaemia (Hb ≤ 5 g/dL)
• renal failure
• acidosis (pH < 7.25), hyperlactataemia (≥ 5 mmol/L)
• hyperparasitaemia (> 5%)
• Respiratory distress.

The case fatality rate of severe malaria remains between 15 and 30%, despite adequate antiparasitic treatment and good supportive management.

Management of uncomplicated falciparum malaria

The treatment of malaria varies, depending on the resistance patterns to antimalarial chemotherapy and will vary over time. Up-to-date advice should be sought if there are doubts as to the appropriate therapy. There is very little chloroquine-sensitive falciparum malaria. Treatments for uncomplicated falciparum malaria are shown in Table 2.2.

Table 2.2 Drug treatment of uncomplicated malaria in adults

Type of malaria Drug treatment
Plasmodium vivax, P. ovale, P. malariae Chloroquine 600 mg
300 mg 6 hours later
300 mg 24 hours later
300 mg 24 hours later
P. falciparum (almost all are resistant to chloroquine) Quinine 600 mg 3 times daily for 7 days
Plus
Doxycycline 200 mg once daily for 7 days
Or
Clindamycin 450 mg 3 times daily for 7 days
(Fansidar (SP) (pyrimethamine and sulfadoxine) 3 tablets as single dose with or following quinine)
Or
Malarone 4 tablets daily for 3 days
Or
Riamet (artemether with lumefantrine) 4 tablets 12-hourly for 3 days
  Alternative therapy
  Artesunate-mefloquine 12/25 mg/kg daily for 3 days
Or
Dihydroartemisinin/piperaquine 6.3 mg/kg daily for 3 days

Management of severe falciparum malaria (Box 2.2)

• In non-endemic countries, all cases of falciparum malaria should be admitted to hospital for at least 1–2 days to ensure there is no immediate deterioration. It can be a medical emergency and require intensive care therapy.
• Artesunate 2.4 mg/kg single bolus by IV injection can be given if available, then at 12 and 24 hours, thereafter daily until oral medication can be tolerated. It does not cause hypoglycaemia. A recent trial found a lower death rate in patients with severe malaria treated with artesunate compared to quinine-treated patients. Artemisinin resistance has been reported in Cambodia. Artesunate is also available as rectal suppositories. However, if artesunate is difficult to obtain then quinine therapy should not be delayed.
• Quinine salts is an alternative. 20 mg/kg IV loading dose (max. 1.2 g) given over 4 hours, followed by 10 mg/kg IV over 4 hours 3 times daily should be used to treat severe malaria. IV administration may induce hypoglycaemia, and any patient receiving IV quinine should have a glucose infusion and regular (4-hourly) blood glucose monitoring. Quinine may be given orally as soon as the patient is able to tolerate oral medication (600 mg 3 times daily) to complete a week of therapy.
• Exchange transfusion is of unproven benefit in the treatment of severe malaria; it has a number of complications and should only be used in adults with a parasitaemia of > 10% after specialist advice has been sought.

Box 2.2 Drug treatment of severe chloroquine-resistant P. falciparum malaria in adults

Full hospital facilities

• Artesunate 2.4 mg/kg by IV injection, then 1.2 mg/kg over 4 hours every 8 hours

or

• Quinine salt 20 mg/kg IV infused over 4 hours, followed by 10 mg/kg

No infusion available

• Quinine dihydrochloride (diluted 1 : 1 in water) given by divided IM injection (regimen as for IV) — half into each thigh

No injection available

• Artemisinin rectal suppositories (limited availability)
• Rectal quinimax or quinine

Management of non-falciparum malaria

Non-falciparum malarias can be treated with oral chloroquine 600 mg, then 300 mg after 8 hours, then 300 mg daily for 2 days. There is some reported chloroquine-resistant malaria in Papua New Guinea and treatment can be with riamet or malarone (dosages in Table 2.2). P. vivax and P. ovale have hypnozoites that may persist and cause a recurrence of infection many years later. Patients with vivax or ovale infection should receive primaquine 15 mg daily for 2–3 weeks following successful treatment, to eradicate hepatic hypnozoites and prevent relapse. Anyone who is about to receive primaquine should have their glucose-6-phosphate dehydrogenase (G6PD) status checked, as primaquine use is associated with haemolysis in patients with G6PD deficiency (p. 216). WHO guidelines www.who.int/topics/malaria/en.

Prevention of malaria

• Avoidance of mosquito bites with mosquito repellants and permethrin-impregnated bed-nets can reduce transmission of malaria by similar amounts to chemoprophylaxis. The advice given to travellers to the tropics about the risks of malaria at their destinations and the need for malaria chemoprophylaxis should be up to date, as it changes over time.
• Currently available alternatives for chemoprophylaxis in adults are atovaquone/proguanil (malarone 1 tablet daily), mefloquine 250 mg weekly and doxycycline 100 mg daily.
• Chloroquine-resistant P. falciparum is so common that there are very few places where chloroquine 300 mg weekly/proguanil 200 mg daily prophylaxis can currently be recommended.
• Prophylaxis should usually be started a week (malarone — only 1 day) before travel and continued for 4 weeks after return. It should also be stressed in advice to patients that malaria chemoprophylaxis is not 100% effective; should they become febrile after return from a malarial area, they should still suspect malaria.

Dengue

Dengue is caused by a flavivirus that is carried by the daytime-biting Aedes mosquito. It is found throughout most of the tropics and is particularly common in South-East Asia and the Caribbean. The incubation period is about 5–7 days.

Clinical features

An acute febrile illness with very severe musculoskeletal pain, severe headache with retro-orbital pain, severe malaise, lymphadenopathy and sometimes a maculo-papular rash occur. The fever subsides after 3–4 days and then returns.

Dengue haemorrhagic fever (DHF) may occur as a result of a second or subsequent infection with a different dengue serotype and may be caused by an abnormal immune response to dengue infection. It presents with severe bleeding (haematemesis and melaena), a severe capillary leak and hypotension.

Investigations

Investigations show a low platelet count, normal white cell count and sometimes mildly abnormal liver biochemistry. See Figure 2.2 for the course and timing of diagnosis.

image

Fig. 2.2 Dengue infection: course and timing of diagnosis.

(From Halstead SB 2007, with permission.)

Treatment

There are no specific antiviral therapies currently available for the treatment of dengue fever but adequate fluid replacement in DHF is essential; blood transfusion is given if necessary. Corticosteroids are of no proven benefit. Convalescence is slow.

Leptospirosis

Leptospirosis is a zoonosis caused by a number of species of the genus Leptospira. Leptospirosis is found worldwide, but is particularly common in South-East Asia. A chronic renal infection in the animal reservoir (usually rodents) is the usual source of infection in humans, disease in humans being acquired through contact with water contaminated with rodent urine. Around 90% of infections are thought to result in a self-limiting febrile illness, but some result in a severe and potentially fatal illness. The incubation period is 5–14 days.

Clinical features

The main features of severe leptospirosis are fever, anorexia, jaundice, myalgia, conjunctival suffusion, and hepatic and renal failure. The case fatality rate of severe leptospirosis is about 5–40%.

Diagnosis

Diagnosis of leptospirosis is by culture or serological tests. There should be early liaison with the laboratory, as specialized culture techniques improve diagnosis.

Treatment

Treatment of severe disease is with benzyl penicillin 1.2 g IV 4 times daily or ceftriaxone 1 g IV daily. Doxycycline 100 mg twice daily may be used in mild disease. Jarisch–Herxheimer reactions have been reported after treatment.

Plague

Sporadic cases (as well as occasional epidemics) of plague occur worldwide, the majority in sub-Saharan Africa, although disease is occasionally seen in the southern states of the USA. Plague is caused by a Gram-negative bacillus, Yersinia pestis. The main reservoirs are rodents. The usual vector is the rat flea.

Clinical features

Clinical manifestations of plague are bubonic, septicaemic, pneumonic, pharyngeal and meningitis.

Diagnosis

Diagnosis is by clinical suspicion and culture of Y. pestis from blood, sputum or aspirate of a bubo. A rapid immunodermatographic dipstick test is also available, and has high sensitivity and specificity.

Treatment

The treatment of choice is streptomycin 15 mg/kg IM twice daily for at least 7 days or gentamicin 5 mg/kg IV daily for 10 days. Oral tetracycline, quinolones and chloramphenicol are also effective. Post-exposure prophylaxis is with doxycycline or ciprofloxacin.

Brucellosis

Brucellosis is a zoonosis and nearly all human infections result from direct or indirect exposure to animals. Farmers, veterinarians and abattoir workers are particularly at risk. Spread is following direct contact with infected animals or by the consumption of unpasteurized dairy products from cows, goats or sheep. The pathogens are members of the genus Brucella: in humans usually B. abortus, B. melitensis and B. canis. Brucellosis has a worldwide distribution, although it has been eliminated from the UK. It is especially common in the Mediterranean, India and the Arabian Peninsula.

Clinical features

The onset is insidious, with an incubation period about 2–4 weeks. Symptoms are initially non-specific, although specific ones include an ‘undulant’ fever, malodorous sweat and a peculiar taste in the mouth. Brucellosis can affect nearly any organ of the body and includes lymphadenopathy, hepatosplenomegaly, sacro-iliitis, arthritis, osteomyelitis and meningoencephalitis. Chronic brucellosis can last over a year. Symptoms may also recur over long periods.

Investigations

• White cell count is normal/low. CRP and ESR are variable.
• Blood and bone marrow cultures (which have a higher yield) should be performed. Brucella may also be cultured from CSF, lymph nodes or liver biopsies. There should be liaison with the laboratory, as a prolonged incubation is required and laboratory transmission of Brucella should be prevented.
• Serological tests with rising antibody titres on ELISA may aid diagnosis if culture results remain negative.

Treatment

• WHO recommends treatment for 6 weeks with doxycycline 200 mg daily and rifampicin 600–900 mg daily, but relapses occur.
• Doxycycline 200 mg daily for 6 weeks and streptomycin 1 g IM daily for 2–3 weeks or gentamicin are also used.

Listeriosis

Listeria monocytogenes causes an infection of many animal species. It is also widespread in the environment in soil and decayed matter. The organism can grow at low temperatures and may be transmitted in foods such as unpasteurized cheeses and pâtés.

Clinical features

• In healthy adults, Listeria causes a self-limiting febrile gastroenteritis, the incidence of which is unknown. A brainstem encephalitis can occur in healthy adults; CSF examination may be normal, although these patients are often bacteraemic and MRI may be useful.
• In pregnant women, neonates, and elderly or immunosuppressed patients, Listeria can cause serious problems.

• In pregnancy bacteraemia usually occurs in the last trimester and presents as a flu-like illness, but infection of the fetus can lead to septic abortion, premature labour and stillbirth. Early treatment may prevent fetal loss but the rate remains about 50%.
• In neonates Listeria may manifest as an early-onset sepsis in the premature infant, acquired in utero. A second, late-onset form occurs about 2 weeks after birth and usually presents as a meningitis.
• In the elderly and the immunocompromised Listeria usually causes meningitis or bacteraemia; a variety of other focal infections have been described.

Investigations

Listeriosis is established by culture of blood, CSF or other body fluids.

Treatment

The treatment of choice for adult listeriosis is ampicillin plus gentamicin. Co-trimoxazole is also effective.

Q fever

Infection with the obligate intracellular pathogen Coxiella burnetii, which is widespread in many animals, is the cause of Q fever. Transmission to humans is usually via dust, aerosol and unpasteurized milk; spore formation means that the infection can remain in the environment for long periods.

The incubation period is 2–4 weeks. Onset is insidious, with fever, myalgia and headache, but pneumonia and hepatitis may occur. Occasionally, endocarditis or other focal infections may cause chronic illness.

• Diagnosis is made serologically or by nested PCR (low sensitivity).
• Treatment is with doxycycline 200 mg daily for 14 days. The addition of chloroquinine is used in chronic infection.

Lyme disease

Lyme disease is found in North America, Europe and Asia, and is caused by infection with the spirochaete Borrelia burgdorferi, of which there are several genomic species. It is a zoonosis transmitted to man by ixodid ticks, the main animal reservoir being deer or occasionally other mammals. Infections usually occur after visiting woodland.

There are three stages of Lyme infection:

• Stage 1 disease is a localized infection, presenting about a week after the tick bite with erythema migrans (a macular rash), lymphadenopathy, and associated fever and headache.
• Stage 2 disease occurs several days to weeks after the appearance of erythema migrans. Some patients may develop a more widespread rash, and after several weeks or months around 15% of untreated cases develop neurological complications such as meningitis, encephalitis, cranial or peripheral neuritis, or radiculopathies. About 5% of patients develop cardiac involvement. Myalgia and arthritis may also occur at this stage.
• Stage 3 disease commonly causes a chronic arthritis (usually of the knees), but may also cause chronic encephalomyelitis and other neurological disorders or acrodermatitis chronica atrophicans. The evidence for persistent infection at this stage is lacking.

Diagnosis

This may occasionally be established by finding spirochaetes in CSF or skin samples. Serodiagnosis is usually performed to confirm the diagnosis, with an IgM response detectable in the first month. Some care should be taken in interpreting results, as false positives may occur.

Treatment

• Amoxicillin 500 mg 3 times daily for 14–21 days or doxycycline 100 mg twice daily for 14–21 days can be used to treat early infection or isolated facial palsies. The duration of amoxicillin or doxycycline treatment should be increased to 30–60 days for stage 2 disease.
• Ceftriaxone 2 g IV daily for 14–28 days should be used if there is neurological involvement or cardiac involvement, e.g. second- or third-degree atrioventricular block.
• Prevention is necessary in tick-infested areas with repellants and protective clothing. Ticks must be removed promptly.

Visceral leishmaniasis

Visceral leishmaniasis (kala-azar) is caused by Leishmania donovani, L. infantum or L. chagasi, and is present in India, Asia, Africa, the Mediterranean and South America. In central India, humans are the main host and the disease occurs in epidemics. In most other areas, it is a zoonosis; the main animal reservoirs are dogs and foxes, although in Africa it is carried by rodents. Visceral leishmaniasis is a common opportunistic infection of advanced HIV disease in Mediterranean coastal regions.

Clinical features

The incubation period is usually 1–2 months but may be much longer. Fever and splenomegaly are common features, pancytopenia and hepatomegaly are often present, and lymphadenopathy is common in Africa. If the infection is untreated, death usually occurs within a year with worsening pancytopenia and weight loss.

Diagnosis

This is confirmed by finding the parasite in aspirates of bone marrow, liver, lymph node or spleen, though in inexperienced hands these can occasionally be mistaken for histoplasmosis.

• Nucleic acid amplification and specialized culture techniques are available from specialist centres.
• Serology can be useful.

Treatment

• The drug of choice is IV amphotericin B (preferably given in the liposomal form), but this is expensive and is not widely available in many areas where the disease is prevalent.
• Miltefosine may be an oral alternative to amphotericin B.
• In areas where resources are limited, pentavalent antimony salts are used, but these are toxic drugs and should be given after specialist advice.

Rickettsial diseases

Rickettsia and the closely related species, Orientia, are small intracellular bacteria that are spread by arthropods (ticks, lice, mites). The reservoir of infection is usually mammalian (often rodent) but may be human. The incubation period is 4–21 days and rickettsial illnesses are characterized by fever, rash and headache. A black spot or eschar may be present at the site of the tick bite, which is painless. Renal failure and haematological, neurological or cardiovascular abnormalities may complicate the illness, but these are rare.

Diagnosis

This can be confirmed serologically.

Treatment

• Doxycycline 100 mg twice daily for 5–7 days and rifampicin 600 mg daily are also effective if tetracyclines cannot be used.
• Prophylaxis for scrub typhus is with weekly oral doxycycline 200 mg, but only in highly endemic areas.

Epstein–Barr virus (EBV)

This herpes virus commonly causes infections, mainly in adolescents and young adults worldwide. It is probably transmitted in saliva and by aerosol.

Clinical features

• Infectious mononucleosis (sometimes referred to as glandular fever) produces a fever, headache, malaise, lymphadenopathy and sore throat. A transient macular rash is common if amoxicillin is given. Mild hepatitis and splenomegaly are common. Severe complications, such as meningoencephalitis, myocarditis and splenic rupture, are rare.
• A post-viral syndrome may occasionally occur after the acute infection, with patients feeling lethargic for a number of months. Like other herpes viruses, EBV remains latent for life but reactivation in the immunocompetent is controversial.

EBV is implicated in the aetiology of a number of malignancies, including Burkitt’s lymphoma, nasopharyngeal carcinoma and post-transplant lymphoma, and in HIV disease with primary cerebral lymphoma, Hodgkin’s lymphoma and oral leucoplakia.

Investigations

• Specific IgG and IgM EBV antibodies detect the infection.
• PCR is available for the detection of EBV DNA in CSF and other body fluids; this may be particularly useful in the diagnosis of meningoencephalitis or primary cerebral lymphoma in HIV infection.

Treatment

Most cases of EBV infection require no specific treatment. The efficacy of antiviral treatment of EBV-associated tumours or EBV in immunosuppressed patients remains unproven; steroids may be of use in some complications, such as thrombocytopenia or haemolysis.

Skin and soft-tissue infections

Skin infections result in a number of different conditions. The most common organisms causing skin infections are group A streptococci and Staphylococcus aureus.

• Impetigo — weeping exudative area, often on the face, with a honey-coloured crust on the surface due to Staph. aureus or group A streptococci.
• Cellulitis — confluent erythema of the skin, often tender. Cellulitis affects the lower leg or sometimes the face, and is associated with a high temperature. It is commonly caused by a streptococcus, or less frequently a staphylococcus.
• Folliculitis — inflammation of hair follicles, presenting as tender papules and pustules. Folliculitis is very commonly caused by Staph. aureus.
• Boils — deep-seated inflammation of the skin, causing painful red swellings, sometimes with pus. Boils are usually caused by staphylococci.

Treatment

Treatment should be started empirically and should cover both Staph. aureus and streptococcal infections. If oral therapy is appropriate, then flucloxacillin 500 mg 4 times daily and amoxicillin 500 mg 3 times daily are reasonable choices; the duration of therapy depends on response, but is usually around a week. Clindamycin 300–450 mg 4 times daily, clarithromycin 500 mg orally 2 times daily for 7 days or another macrolide is used in penicillin-allergic patients.

In severe or extensive infections, high-dose IV benzyl penicillin 1.2–1.8 g IV 4-hourly and flucloxacillin 1–2 g IV 6-hourly will be required. High-dose IV clindamycin or a macrolide is used in penicillin-allergic patients. Collections of pus may need to be drained, and in cellulitis elevation of the affected limb speeds recovery.

Meticillin-resistant Staph. aureus (MRSA)

The mec-A gene in Staph. aureus makes it resistant to meticillin, oxacillin, flucloxacillin and nearly all other β-lactam antibiotics. The incidence of MRSA has increased over the last 25 years and in some hospitals more than 50% of Staph. aureus are MRSA; the prevalence of community-acquired MRSA is increasing.

Like meticillin-sensitive Staph. aureus (MSSA), MRSA is usually a harmless skin colonizer, particularly in hospital inpatients. However, both can cause a variety of invasive infections, e.g. soft-tissues infections, bacteraemias, pneumonias and line infections. The case fatality rate of invasive MRSA infections is greater than that of MSSA. Eradication of MRSA carriage is possible, though sometimes difficult. Isolation of patients, strict hand washing, good IV catheter care and other infection control procedures should be observed. Control of the use of antibiotics in hospitals and good infection control policies are vital to prevent spread.

Community-acquired MRSA (CA-MRSA) may have different resistance profiles to hospital strains (often retaining sensitivities) as regards tetracycline, clindamycin and co-trimoxazole. It often produces the exotoxin Panton–Valentine leucocidin and is an increasingly common cause of soft-tissue infections, particularly in the USA (USA300 strain).

Treatment

Treatment of MRSA infection depends on the source of the infection and the sensitivity of the MRSA.

Antibiotics active against MRSA include the glycopeptides (vancomycin and teicoplanin), rifampicin, the tetracyclines and fusidic acid.

• Serious invasive MRSA infections should, in general, be treated with a glycopeptide (e.g. vancomycin 1 g IV twice daily), and often a second agent is added, such as rifampicin for MRSA pneumonia, fusidic acid for MRSA osteomyelitis, or gentamicin or rifampicin for MRSA endocarditis.
• MRSA bacteraemia should be treated for at least 2 weeks but, for example, MRSA endocarditis or osteomyelitis must be treated for longer.
• Less serious infections, such as mild cellulitis, can be treated with two oral agents, such as a tetracycline, co-trimoxazole or a combination of fusidic acid and rifampicin.
• Newer agents include linezolid, quinupristin/dalfopristin, daptomycin and tigecycline. Linezolid may have advantages over vancomycin; linezolid has better penetration into lung tissue and skin, but the clinical benefit is yet to be confirmed. These new drugs should not yet be used as first-line treatment for MRSA infections.

Glycopeptide-intermediate Staph. aureus (GISA) and vancomycin-resistance in Staph. aureus (VRSA)

• GISA develops because of changes in cell wall synthesis.
• VRSA, which has acquired the van A gene from vancomycin-resistant enterococci, has also been reported but is rare.

Staphylococcal toxic shock syndrome (TSS)

TSS is an acute febrile illness characterized by a generalized erythematous rash that nearly always starts within the first 24 hours of illness, desquamating after about 1 week. The most common symptoms include fever (>40° C), hypotension, and diffuse rash with desquamation. TSS ranges in severity from a mild disease to a severe life-threatening illness. It is due to toxin production by Staph. aureus. TSS toxin-1 (TSST-1) acts as a superantigen that stimulates non-specific T-cell proliferation. For streptococcal toxic shock syndrome, see below.

In the early 1980s, most cases of TSS were in menstruating females and associated with retained tampons. Recently, TSS has been less often associated with menstruation.

• Treatment is by removal of the source of the staphylococcal infection and treatment with flucloxacillin 1–2 g IV 4 times daily.

Post-streptococcal syndromes

Strep. pyogenes infections usually cause localized throat or skin infections. However, there are a number of immune-associated, generalized complications of Strep. pyogenes.

Rheumatic fever

This is a multi-system inflammatory disorder, occurring in children and young adults as a result of a pharyngeal infection with a group A streptococcus. It is due to molecular mimicry between cell wall M proteins of some group A streptococcus strains, and cardiac laminin and myosin and synovial membrane. Rheumatic fever is much less common in Western Europe and the USA than in other parts of the world; this may be due in part to the treatment of streptococcal infections, e.g. sore throats. The diagnosis of rheumatic fever is made according to the revised Duckett–Jones criteria. The major criteria are carditis, polyarthritis, chorea, erythema marginatum and subcutaneous nodules, while the minor criteria include fever and arthralgia.

• Diagnosis. This is made on the basis of two or more major criteria, or one major criterion plus two or more minor criteria, with evidence of recent streptococcal infection, e.g. positive throat cultures or raised antistreptolysin O titre.

• Treatment

• Aspirin/NSAIDs produce a dramatic response.
• Bed rest is advised. Steroids are used if carditis is present but their efficacy remains unproven.
• Streptococcal infections should be eradicated with oral phenoxymethylpenicillin 500 mg 4 times daily for 10 days.
• Prophylaxis. Oral phenoxymethylpenicillin 250 mg twice daily, until the age of 20 years or for 5 years after the latest attack, is used for prophylaxis against further episodes of rheumatic fever. This is most common after an episode of carditis. Erythromycin is used if the patient is allergic to penicillin.
• Complications. Chronic rheumatic valvular disease develops in just over half of those who have acute rheumatic fever complicated by carditis (after 10–20 years). The mitral and aortic valves are mainly affected.

Other post-streptococcal syndromes

• Scarlet fever is a diffuse, erythematous, 1–2 mm, ‘sandpaper’-like rash that results from the production of pyrogenic exotoxin (erythrogenic toxin, types A, B and C) produced by group A streptococcus, usually after a pharyngeal infection. The rash usually starts on the head and then proceeds downwards, but sparing the palms and soles. The rash often exhibits a linear character in the axillary folds (Pastia’s lines). Scarlet fever is diagnosed clinically and with a culture-positive throat swab.
• Streptococcal toxic shock syndrome (STSS) is a febrile illness associated with a streptococcal infection. It is similar to staphylococcal TSS and results from the production of superantigens produced by streptococcal infections.
• Glomerulonephritis — see p. 343.

Cat scratch fever

This is caused by Bartonella henselae. Regional lymphadenopathy occurs 1–2 weeks after infection. This resolves after weeks or months and is not accompanied by systemic symptoms. Doxycycline can be used.

Herpes simplex (HSV)

HSV1 is spread by direct contact and droplet infection. The primary illness produces a fever with painful blisters on the face or a painful gingivostomatitis. Recrudescence of HSV blisters appears as cold sores.

• Treatment is with topical aciclovir; if infection is severe, use oral aciclovir 200 mg 5 times daily for 5 days.

Myositis

Pyomyositis is an acute bacterial infection of skeletal muscle that is usually caused by Staph. aureus and occasionally by streptococci or other organisms.

• Treatment is with prompt surgical debridement with benzyl penicillin 1.2 g IV 4 times daily and flucloxacillin 500 mg 4 times daily.

Gas gangrene

Gas gangrene is caused by infection with Clostridium perfringens or occasionally with other species of Clostridia. It is characterized by the absence of pus and the presence of gas in the tissues. It may be difficult to distinguish from necrotising fasciitis, except during surgery, though the presence of gas on X-ray and crepitation in the tissues is useful.

• Treatment is with prompt surgical debridement and high-dose benzyl penicillin 2.4 g IV 6 times daily and clindamycin 1.2 g IV 4 times daily. Hyperbaric oxygen therapy is also advised, although there is no RCT to support the use of this therapy.

Necrotising skin and soft-tissue infections

These are defined as soft-tissue infections spreading along the fascial planes with or without an overlying cellulitis. They are serious infections with mortality as high as 40%. Clinically, these patients are very unwell and pain is a prominent symptom, out of proportion to the skin findings. The causative organism is usually group A streptococcus, though other organisms can cause this syndrome; if the infection follows abdominal surgery or a testicular infection (Fournier’s gangrene), then mixed infections with anaerobic and aerobic organisms (synergistic gangrene) occur. Vibrio vulnificans infection may be contracted from sea water.

• Diagnosis is made clinically and these patients should be rapidly assessed by a specialist surgeon. High white cell count and high CRP are usually present. US/CT may be helpful but should not delay early surgery.
• Treatment is with wide and aggressive surgical debridement, which may need to be repeated on a number of occasions.

• Antibiotic therapy for group A streptococcus is with high-dose benzyl penicillin 2.4 g IV 6 times daily and clindamycin 1.2 g IV 4 times daily.
• If a synergistic infection is suspected, then treatment should cover anaerobes and Gram-negative organisms; suitable drugs could include ampicillin, gentamicin and metronidazole; ampicillin, gentamicin and clindamycin; or co-amoxiclav, gentamicin and metronidazole.

Bite wounds

The major problem resulting from bite wounds is infection, but this will depend on the site, extent and cause.

• Dog bites. These are the commonest type of bite (80%) but only a few become infected. The oral flora of dogs contains streptococci, staphylococci, Pasteurella multocida and Capnocytophaga canimorsus.

• Treatment. If the bite is infected, give co-amoxiclav 500 mg 8-hourly for 7 days. This can also be used as prophylaxis for 3–5 days.

• Cat bites. Most of these become infected and prophylaxis with co-amoxiclav should always be given.

• Treatment. If the bite is infected, give co-amoxiclav or doxycycline 100 mg daily. Increase the duration to 2 weeks for cellulitis and longer for osteomyelitis.

• Wild animal bites. The danger here is rabies and vaccination must be given (p. 56). Co-amoxiclav is a reasonable choice for prophylaxis.

General measures for bite wounds

• Investigations include culture of swabs from wounds.
• Foreign bodies should be removed and the wound irrigated.
• Do not suture unless the bite is on the face.
• Elevate if possible.
• Give antibiotics as above.
• If there is a fracture, X-ray the relevant area. Vaccinate against rabies (p. 57).

Varicella zoster virus (VZV) infection

Primary infection with VZV is in childhood in Europe and the Americas. In some countries (e.g. in South Asia) transmission is different, with more infections in adults.

The primary infection with VZV causes chickenpox, which almost never occurs again in the same person. Chickenpox is infectious from 2 days before the start of the rash until all the vesicles have crusted. The incubation period of chickenpox is 14–21 days. There is a brief ‘flu-like prodromal illness, which may be absent in the young. A rash then develops, with macules rapidly progressing to vesicles, mainly on the head and trunk. The rash occurs in ‘crops’, with skin lesions in all stages typically present on the body. Eventually, the vesicles crust and heal without scarring. Chickenpox is highly infectious and is spread from infected lesions and by the respiratory route. After recovery, VZV remains latent for life in spinal nerve roots. The illness tends to be more severe in adults, particularly pregnant women, smokers and the immunosuppressed. Complications of chickenpox include pneumonia, bacterial superinfection of skin lesions and meningo-encephalitis. VZV can cross the placenta and infection in pregnancy leads to fetal damage in about 2% of cases, mostly in infections before 20 weeks’ gestation.

Shingles is a secondary reactivation of latent VZV infection in the distribution of one or sometimes two dermatomes. The vesicles of shingles are identical to those in chickenpox. Shingles mainly affects the elderly but can occur at any age. Post-herpetic neuralgia may occur after herpes infection and causes severe debilitating pain. Shingles involving the ophthalmic division of the trigeminal nerve has a high rate of complications. Disseminated shingles infection can occur in the immunosuppressed patients (particularly in late HIV infection), when the rash is seen over many dermatomes and appears similar to chickenpox. Shingles lesions may transmit infection to non-immune individuals.

Diagnosis

Diagnosis is clinical but, if necessary, can be confirmed with immunofluorescence, electron microscopy or viral culture of vesicle fluid.

Treatment

• Healthy children with chickenpox usually require no treatment and infection results in lifelong immunity.
• Adults with chickenpox should be given antiviral treatment, if they present within 72 hours of onset, with aciclovir (800 mg oral 5 times daily for 7 days) or oral valaciclovir or famciclovir.
• Severe VZV infection, particularly in the immunosuppressed or pregnant women, should be treated with IV aciclovir (10 mg/kg IV 3 times daily).
• Zoster immune immunoglobulin (ZIG) can be used as post-exposure prophylaxis in the immunocompromised or pregnant, with no past infection with chickenpox who has been exposed to VZV.
• An effective varicella vaccine is available but is not recommended as routine in all countries.
• Shingles is also treated with aciclovir (800 mg orally 5 times daily for 7 days), as early treatment reduces the duration of symptoms and the occurrence of neuralgia.
• Prophylactic therapy with aciclovir can be used to prevent HSV and VZV in immunocompromised patients. In the USA varicella zoster vaccine is recommended for all people over 65 years.

Leprosy (Hansen’s disease)

Leprosy is caused by Mycobacterium leprae, an acid-fast bacillus. The majority of cases are in India and Brazil. The prevalence of leprosy has decreased since a successful WHO treatment campaign.

The incubation period is very variable but is usually 2–6 years. The signs of leprosy are usually skin lesions, usually anaesthetic and thickened peripheral nerves. Leprosy is classified between two polar extremes of tuberculoid (high degree of cell-mediated immunity (CMI)) and lepromatous (impaired CMI), depending on the host’s immune reaction to the infection (Ridley–Jopling system).

Diagnosis and treatment

It is not possible to culture M. leprae but diagnosis is made clinically and on microscopic examination of tissue. The type of treatment and its duration depend on the type of leprosy. Rifampicin, clofazimine and dapsone are the main drugs used (p. 87).

Respiratory infections

Upper respiratory tract infections

Pharyngitis

Most throat infections are caused by viruses and do not need antimicrobial therapy, but it is difficult to differentiate between viral and bacterial causes in all patients. Patients with three of the following are more likely to have bacterial rather than viral infection: fever, purulent tonsils, cervical lymphadenopathy and absence of cough. Strep. pyogenes (Lancefield group A β-haemolytic streptococcus) is the major bacterial cause of pharyngitis and is commoner in the age group 5–15. A history of contact with a patient with proven Strep. pyogenes infection is helpful in diagnosis.

• Investigations. Rapid antigen detection tests may be helpful but, like throat cultures, will also be positive in those who have throat colonization with Strep. pyogenes.
• Treatment. If antibacterial treatment is given, the first choice should be oral phenoxymethylpenicillin 500 mg 4 times daily for 10 days. Amoxicillin and ampicillin should not be given unless infection with EBV can be ruled out. For penicillin-allergic patients, a macrolide (e.g. erythromycin 250 mg 4 times daily or 500 mg twice daily) or an oral cephalosporin can be given for 10 days. Rarer bacterial causes of pharyngitis include Arcanobacterium haemolyticum, which can be treated with erythromycin.

Diphtheria

See p. 49.

Acute laryngo-tracheobronchitis (croup)

This causes paroxysms of cough with breathlessness and stridor. It is caused initially by viral infections, e.g. parainfluenza, complicated by bacterial infection. The voice is hoarse with a barking cough (croup) and audible laryngeal stridor.

• Treatment. Oral corticosteroids and nebulized adrenaline (epinephrine) are helpful. Oxygen with adequate rehydration is necessary.

Epiglottitis

This presents with a sudden onset of fever, sore throat and stridor, which may rapidly progress to complete airway obstruction. In children, the bacterial causes of epiglottitis include group A streptococcus, Strep. pneumoniae and Staph. aureus. Capsulated strains of H. influenzae, e.g. type b, are now rare in countries that immunize against this pathogen (Hib vaccine). A swab from the epiglottis may reveal the causative organism, but this could potentially provoke airway obstruction and should only be carried out if facilities for intubation are present. Blood cultures should also be taken.

• Treatment. Cefotaxime 50 mg/kg IV 4 times daily or ceftriaxone 50 mg/kg IV daily is the first-choice agent. For patients who are allergic to cephalosporins, chloramphenicol 25 mg/kg IV 4 times daily is used. Epiglottitis is rare in adults but the spectrum of bacteria is similar to that seen in children and cefotaxime, ceftriaxone or chloramphenicol can be used at adult doses.

Coryza

Coryza (the common cold) is caused by viruses. There are currently no effective antimicrobial treatments.

Sinusitis

Most episodes of sinusitis are viral and will resolve without antimicrobial therapy. The symptoms of bacterial infection are maxillary/facial pain, and purulent discharge after 7–10 days. The likely organisms are Strep. pneumoniae, H. influenzae, Moraxella catarrhalis, group A streptococcus, Staph. aureus and anaerobes in chronic infection.

• Treatment. Appropriate antibacterials include amoxicillin 500 mg 3 times daily for 7 days, oral doxycycline 200 mg, followed by 100 mg daily for 7 days or erythromycin 250 mg 4 times daily or 500 mg twice daily for 7 days. If there is a failure to respond or the patient has recently received antibacterial treatment, co-amoxiclav 625 mg 3 times daily for 7 days or ciprofloxacin 500 mg twice daily for 7 days, combined with metronidazole 400 mg twice daily for 7 days, can be used. Chronic infection usually requires surgery.

Otitis media

This is predominantly an infection of children. Most episodes are viral and will resolve without antimicrobial treatment. Although bacterial infection may occur with Strep. pneumoniae, H. influenzae, group A streptococcus and Staph. aureus, use of antibacterials is of questionable value, as most cases get better without treatment.

• Treatment. If the child remains unwell for more than 3 days, antibacterials can be used, including amoxicillin (< 2 years, 125 mg 3 times daily; 2–10 years, 250 mg 3 times daily; > 10 years, 500 mg 3 times daily, all for 5 days). If the patient is allergic to penicillin, erythromycin (< 2 years, 125 mg 4 times daily; 2–8 years, 250 mg 4 times daily; > 8 years, 250–500 mg 4 times daily) can be given for 5 days or azithromycin (15–25 kg, 200 mg daily; 26–35 kg 300 mg; 36–45 kg 400 mg daily) for 3 days.

Diphtheria

Diphtheria is caused by pharyngeal or cutaneous infection with toxigenic strains of Corynebacterium diphtheriae and, rarely, toxigenic strains of C. ulcerans. Classical diphtheria presents with a membranous pharyngitis, cervical lymphadenopathy and oedema of the surrounding soft tissues. The membrane, which is not always present, is typically grey, thick and adherent. Laryngeal involvement also occurs, and causes hoarseness and stridor. Nasal diphtheria may present as a bloody nasal discharge. Cutaneous diphtheria is commoner in tropical countries and usually affects the legs. The lesions start as vesicles and progress to form ulcers.

• Diagnosis. Diagnosis relies on a combination of clinical and laboratory findings, with the demonstration of a toxigenic isolate of C. diphtheriae from throat, nose or skin swabs.
• Treatment. A combination of antitoxin to neutralize the toxin and antibacterials to eradicate the organism is needed, though the benefit of antitoxin in cutaneous infection is uncertain. Appropriate antibacterials include IV erythromycin 40 mg/kg a day, until the patient can swallow, when oral erythromycin 500 mg 4 times daily or oral phenoxymethylpenicillin 250 mg 4 times daily can be given. Antibacterials should be given for 14 days and a throat swab taken to check for elimination of the organism. If the culture is still positive, a further 10 days’ treatment is needed. Cases should also be immunized in the convalescent stage. Close contacts require antibacterial prophylaxis with erythromycin 500 mg 4 times daily for 7 days. If cultures are positive from close contacts, a further 10 days’ treatment is needed. Those contacts who have not been immunized in the preceding 12 months require vaccine. Non-toxigenic strains of C. diphtheriae may cause severe pharyngitis, which can be treated with oral erythromycin 500 mg 4 times daily for 7 days or phenoxymethylpenicillin 250 mg 4 times daily for 7 days.

Measles

This is a vaccine-preventable viral infection and no specific antiviral treatment is available. The incubation period ranges from 7 to 18 days. There is a prodromal illness with fever, conjunctivitis, cough and often diarrhoea. This is followed, usually 2 or 3 days later, with a rash that starts on the face and spreads to the trunk, lasting for 4–7 days. Measles is a self-limiting illness but complications are relatively frequent. Diagnosis is by demonstration of viral antigen on PCR in nasopharyngeal aspirates or urine, or by demonstration of IgM antibody in blood or saliva. Otitis media and pneumonia may follow and antibacterials can be used for these complications. Inosine pranobex has been used to treat the rare complication, subacute sclerosing panencephalitis, but there is little evidence of any benefit.

Mumps

This is a vaccine-preventable viral infection and no specific antiviral treatment is available. The incubation ranges from 18 to 21 days. Mumps is a febrile illness characterized by inflammation of the salivary glands, particularly the parotids, which are swollen and tender. It is a self-limiting illness and complications are rare. Aseptic meningitis, orchitis and oophoritis and pancreatitis may occur. Diagnosis is usually by demonstration of IgM antibody in blood or saliva.

Rubella (German measles)

Rubella is a worldwide viral disease spread by droplets. The incubation is 14–21 days; the rash begins 7 days after the onset of malaise, fever, conjunctivitis and lymphadenopathy. The rash is pinkish red, macular and discrete. Treatment is supportive and complications are rare. Congenital rubella syndrome affects fetuses in ~80% of women who contract the disease in the first trimester.

Prevention is with the MMR vaccine.

Lower respiratory tract infections

Influenza

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