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Shingles (herpes zoster)
This is produced by reactivation of latent VZV from the dorsal root ganglion of sensory nerves, and most commonly involves the thoracic dermatomes (Fig. 5.5) and the ophthalmic division of the trigeminal nerve.
Burning discomfort develops in the affected dermatome, followed 3 to 4 days later by a vesicular rash. There may be viraemia and distant ‘satel- lite’ lesions. Severe, extensive or prolonged disease suggests underlying immunosuppression, for example, HIV. Chickenpox may be caught from shingles, but not vice versa.
Complications
• Ophthalmic trigeminal involvement: may lead to corneal ulceration, and requires ophthalmology review. • Ramsay Hunt syndrome: facial palsy, ipsi- lateral loss of taste and buccal ulceration and a rash in the external auditory canal. • Postherpetic neuralgia: can be difficult to treat, but may respond to amitriptyline or gabapentin. • Myelitis/encephalitis: rare.
Early therapy with aciclovir helps to limit early- and late- onset pain and to prevent the development of postherpetic neuralgia. VZV vaccination is now offered to patients aged 70 and 78 years in the UK to prevent shingles.
Systemic viral infections without exanthem
Complications
• Epididymo- orchitis: occurs in 25% of postpubertal males, with testicular atro- phy, although sterility is unlikely. Oophoritis is less common. • Mumps menin- gitis: complicates 10% of cases, with lymphocytes in the CSF. • Encephalitis.
• Transient hearing loss and labyrinthitis: uncommon. • Spontaneous abortion.
Management and prevention
Analgesia for symptoms is sufficient. There is no evidence that glucocorti- coids are of value in orchitis. Mumps vaccine is one of the components of the combined MMR vaccine.
Influenza
This is an acute systemic viral illness predominantly affecting the respira- tory system, caused by influenza A or B viruses. Seasonal changes in hae- magglutinin (H) and neuraminidase (N) glycoproteins allow the organism to evade natural immunity and cause outbreaks or epidemics of varying severity.
Clinical features
Influenza is highly infectious by respiratory droplet spray from the earliest stages of infection. Incubation is 1 to 3 days, and onset is with fever, mal- aise, myalgia and cough. Viral or superadded bacterial pneumonia is an important complication. Myositis, myocarditis, pericarditis and encephalitis are rare complications.
Acute infection is diagnosed by viral antigen or RNA detection in a naso- pharyngeal sample.
Management involves early diagnosis, scrupulous hand hygiene and infection control to limit spread by coughing and sneezing. Neuraminidase inhibitors such as oseltamivir (75 mg twice daily for 5 days) can reduce the severity of symptoms if started within 48 hours of symptom onset.
Prevention involves seasonal vaccination of vulnerable groups, for example, people over 65 years, children aged 2 to 7 years, the immuno- suppressed and those with chronic illnesses.
Avian influenza is the transmission of avian influenza A from sick poultry to humans, causing severe disease. Human–human spread is rare. Swine influenza, caused by a H1N1 strain infecting humans, spread around the world from Mexico in 2009.
Infectious mononucleosis and Epstein- Barr virus
Infectious mononucleosis is a syndrome of pharyngitis, cervical lymphade- nopathy, fever and lymphocytosis (also known as glandular fever), most often caused by EBV, a gamma herpesvirus. In developing countries, subclinical infection in childhood is virtually universal. In developed coun- tries, primary infection may be delayed until adolescence or later. Saliva from asymptomatic excreters is the main means of spread, either by droplet infection or environmental contamination in childhood, or by kissing among adolescents and young adults. Infectious mononucleosis is not highly con- tagious, so case isolation is unnecessary.
In addition to EBV, an infectious mononucleosis syndrome may result from infection with CMV, herpesvirus 6 or 7, HIV- 1 or toxoplasmosis.
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Clinical features
• Prolonged prodrome of fever, malaise and headache. • Lymphade- nopathy, especially posterior cervical. • Pharyngeal inflammation or exudates. • Persisting fever and fatigue. • Splenomegaly. • Palatal petechiae. • Periorbital oedema. • Clinical or biochemical hepatitis.
• A nonspecific rash.
Complications
Common: Include an antibiotic- induced rash (classically amoxicillin), severe laryngeal oedema and postviral fatigue.
Less common: Cranial nerve palsies, meningoencephalitis, haemolytic anaemia, splenic rupture, glomerulonephritis, pericarditis, pneumonitis and thrombocytopenia.
Long- term: Some forms of Hodgkin’s lymphoma, Burkitt’s lymphoma, lymphoproliferative disease in the immunosuppressed and nasopharyngeal carcinoma (in China and Alaska).
Investigations
• Atypical lymphocytes on blood film. • Monospot test (heterophile anti- body absorption test): may initially be negative, so should be repeated if clinical suspicion is high. • EBV IgM antibodies.
Management
Treatment is symptomatic, for example, aspirin gargles to relieve a sore throat. Oral glucocorticoids may be required to relieve laryngeal oedema.
Chronic fatigue may respond to graded exercise programmes. Contact sports should be avoided until splenomegaly has resolved, to avoid splenic rupture.
Cytomegalovirus
CMV circulates readily among children. There is a second period of virus acquisition in teenagers and adults up to 35 years of age, with significant sexual and oral spread. The infection is transferred by contact with an excreter, who sheds virus in saliva, urine and genital secretions.
Most postchildhood CMV infections are asymptomatic, but some adults develop an illness resembling infectious mononucleosis. Lymphadenopa- thy, pharyngitis and tonsillitis are found less often than in infectious mono- nucleosis, whereas hepatomegaly is more common. Complications include meningo- encephalitis, Guillain–Barré syndrome, autoimmune haemolytic anaemia, myocarditis and rashes. Immunocompromised patients can develop hepatitis, oesophagitis, colitis, pneumonitis, retinitis, encephalitis and polyradiculitis. CMV infection during pregnancy carries a 40% risk of fetal infection, causing rashes, hepatosplenomegaly and a 10% risk of neu- rological damage to the fetus.
Atypical lymphocytes are seen less commonly than in infectious mono- nucleosis, and the monospot test is negative. Detection of CMV- specific IgM antibodies confirms the diagnosis, and treatment is symptomatic in the immunocompetent. In immunosuppressed patients, diagnosis is by PCR virus detection and treatment is with IV ganciclovir or oral valganciclovir.
Dengue
The dengue flavivirus is spread by the vector mosquito Aedes aegypti and is endemic in South- East Asia, the Pacific, Africa and the Americas.
The incubation period following a mosquito bite is 2 to 7 days, with a pro- drome of malaise and headache, followed by a morbilliform rash, arthralgia, pain on eye movement, headache, nausea, vomiting, lymphadenopathy and fever. The rash spreads centrifugally, spares the palms and the soles, and may desquamate on resolution. The disease is self- limiting, but con- valescence is slow.
Dengue haemorrhagic fever and dengue shock syndrome: These more severe manifestations occasionally complicate infection: circulatory failure, features of a capillary leak syndrome and DIC with haemorrhagic complications such as petechiae, ecchymoses, epistaxis, GI bleeding and multiorgan failure. Other complications include encephalitis, hepa- titis and myocarditis. Case fatality with this aggressive disease may approach 10%.
Investigations
• Detection of a fourfold rise in antidengue IgG antibody titres. • Amplifica- tion of dengue RNA by PCR.
Management and prevention
Management is supportive, including fluid replacement and management of shock and organ dysfunction. Insecticides that control mosquito levels help to limit transmission. Aspirin should be avoided, and steroids are ineffective. A recently licensed vaccine is available.
Yellow fever
Yellow fever is a flavivirus infection that is a zoonosis of monkeys in the tropical rainforests of West and Central Africa and South and Central America. It is transferred to humans by infected Aedes or Haemagogus mosquitoes, and is a major public health problem, causing 200 000 infections per year, mainly in sub- Saharan Africa, with a mortality of around 15%.
The incubation period is 3 to 6 days, and the acute phase is usually char- acterised by a mild febrile illness lasting less than a week. Fever remits, then recurs in some cases after a few hours to days. In severe cases, the dis- ease returns with rigors and high fever, severe backache, abdominal pain, nausea, vomiting, bradycardia and jaundice. This may progress to shock, DIC, hepatic and renal failure with jaundice, petechiae, mucosal haemor- rhages, GI bleeding, seizures and coma.
Diagnosis in blood is by detecting virus (RT- PCR) or IgM or rising IgG antibodies.
Management
Treatment is supportive, with careful fluid and electrolyte balance, urine output and BP measurement. Blood transfusions, plasma expanders and peritoneal dialysis may be necessary. Isolation is needed to prevent cross- infection. Vaccination prevents disease for at least 10 years.