viral infection

Shingles (herpes zoster)
After initial infection, VZV persists in latent form in the dorsal root ganglion of sensory nerves and can reactivate
in later life.
Clinical features
Burning discomfort occurs in the affected dermatome, where discrete vesicles appear 3–4 days later., paraesthesia occurs without rash (‘zoster sine herpete’). Severe disease, a prolonged duration of rash, multiple dermatomal involvement or recurrence suggests underlying Immune deficiency, including HIV. Chickenpox may be contracted from a case of shingles but not vice versa. Although thoracic dermatomes are most commonly involved ,the ophthalmic division of the trigeminal nerve is also frequently affected; vesicles may appear on the cornea and lead to ulceration. This condition can lead to blindness .
Bowel and bladder dysfunction occur with sacral nerve root involvement. The virus occasionally causes cranial nerve palsy, myelitis or encephalitis. Post-herpetic neuralgia causes troublesome persistence
of pain for 1–6 months or longer, following healing of the rash. It is more common with advanced age.
Management
Early therapy with aciclovir or related agents has been shown to reduce both early- and late-onset pain, especially in patients over 65 years. Postherpetic neuralgia requires aggressive analgesia, along
with agents such as amitriptyline 25–100 mg daily or gabapentin.
Capsaicin cream (0.075%) may be helpful.

Infectious mononucleosis (IM) and Epstein-Barr virus (EBV)
It is most often caused by EBV infection, but a variety of other viral infections (CMV, HHV-6, HIV-1) and toxoplasmosis can produce a similar clinical syndrome.
.The virus is usually acquired from asymptomatic excreters via saliva, either by droplet infection or environmental contamination in childhood, or by kissing among adolescents and adults.
Clinical features
fever, headache and malaise. This is followed by severe pharyngitis, which may include tonsillar exudates, and non-tender anterior and posterior cervical lymphadenopathy. Palatal petechiae, periorbital oedema, splenomegaly, inguinal or axillary lymphadenopathy, and macular, petechial or erythema multiforme rashes may occur. In most cases fever resolves over 2 weeks, and fatigue and other abnormalities settle over a further few weeks. Death is rare but can occur due to respiratory obstruction, haemorrhage from splenic rupture or thrombocytopenia, or encephalitis.
diagnosis of IM outside the usual age in adolescence and young adulthood is difficult. in adults over 30 years of age it can be severe and prolonged. In both groups pharyngeal symptoms are often absent. IM may present with jaundice, as a PUO or with a complication.
Complications of infectious mononucleosis
Common
• Severe pharyngeal oedema
• Antibiotic-induced rash (80-90% with ampicillin)
• Prolonged post-viral fatigue
• Hepatitis , Jaundice


Uncommon Neurological
• Cranial nerve palsies
Polyneuritis ,Transverse myelitis
• Meningoencephalitis
Haematological
• Haemolytic anaemia
• Thrombocytopenia


Renal
• Abnormalities on urinalysis
• Interstitial nephritis


Cardiac
• Myocarditis
• ECG abnormalities
• Pericarditis


Rare
• Ruptured spleen
• Respiratory obstruction
• Agranulocytosis
• X-linked lymphoproliferative syndrome


EBV-associated malignancy
• Nasopharyngeal carcinoma
• Burkitt s lymphoma
• Primary CNS lymphoma
• Hodgkin s disease (certain subtypes only)
• Lymphoproliferative disease in immunocompromised
Investigations
Atypical lymphocytes
.A heterophile antibody is present during the acute illness and convalescence, which is detected by the Paul-Bunnell or Monospot test.
Specific EBV serology (immunofluorescence) can be used to confirm the diagnosis if necessary.
Management
symptomatic. If a throat culture yields a ?-haemolytic streptococcus, a course of penicillin should be prescribed. Administration of ampicillin or amoxicillin in this condition commonly causes an itchy macular rash, and should be avoided. When pharyngeal oedema is severe, a short course of corticosteroids, e.g. prednisolone 30 mg daily for 5 days, may help. Antivirals are not sufficiently active against EBV.
contact sports should be avoided until splenomegaly has completely resolved because of the danger of splenic rupture. Unfortunately, about 10% of patients with IM suffer a chronic relapsing syndrome.
Cytomegalovirus (CMV)
CMV, like EBV, circulates readily among children. A second period of virus acquisition occurs among teenagers and young adults, peaking between the ages of 25 and 35 years, rather later than with EBV infection. Most post-childhood infections are therefore acquired from asymptomatic excreters who shed virus in saliva, urine, semen and genital secretions. Sexual transmission and oral spread are common
Clinical features
Most post-childhood CMV infections are subclinical, although some young adults develop an IM-like syndrome and some have a prolonged influenza-like illness lasting 2 weeks or more. Physical signs resemble those of IM, but in CMV mononucleosis hepatomegaly is relatively more common, while lymphadenopathy, splenomegaly, pharyngitis and tonsillitis are found less often. Jaundice is uncommon and usually mild. Unusual complications include meningoencephalitis, Guillain-Barré syndrome, autoimmune haemolytic anaemia, thrombocytopenia, myocarditis and skin eruptions such as ampicillin-induced rash. Immunocompromised patients can develop hepatitis, oesophagitis, colitis, pneumonitis, retinitis, encephalitis and polyradiculitis.
Women who develop a primary CMV infection during pregnancy have about a 40% chance of passing CMV to the fetus, causing congenital infection and disease at any stage of gestation. Features include petechial rashes, hepatosplenomegaly and jaundice; 10% of infected infants will have long-term CNS sequelae such as microcephaly, cerebral calcifications, chorioretinitis and deafness.
Investigations
Atypical lymphocytosis is not as prominent as in IM and heterophile antibody tests are negative. LFTs are often abnormal, with an alkaline phosphatase level raised out of proportion to transaminases. Serological diagnosis depends on the detection of CMV-specific IgM antibody plus a four-fold rise or seroconversion of IgG. In the immunocompromised, antibody detection is unreliable and detection of CMV in an involved organ by PCR, culture or histopathology establishes the diagnosis. A positive culture of CMV in the blood may be useful in transplant populations but not in HIV-positive individuals, since in HIV infection CMV reactivates at regular intervals but these episodes do not correlate well with episodes of clinical disease.
Management
Only symptomatic treatment is required in the immunocompetent patient. Immunocompromised individuals are treated with ganciclovir 5 mg/kg i.v. 12-hourly or with oral valganciclovir 900 mg 12-hourly for at least 14 days. Foscarnet or cidofovir is also used in CMV treatment of immunocompromised patients who are resistant or intolerant of ganciclovir-based therapy.