3.8 Modelos lineales: problemas de valor inicial
3.8.2 Sistemas resorte-masa: movimiento libre amortiguado
Varicella zoster virus (VZV) belongs to the herpes virus family and cause varicella that is the chickenpox and the herpes zoster that is the shingles (Fig. 9.19). Varicella zoster virus causes a benign exanthematous illness manifested by prodromal symptoms and vesicular rash.
Figure 9.17: Herpetic dendrite in a graft stained with florescein dye (Courtesy: Medical Photographic Imaging Centre, Royal Victorian Eye and Ear Hospital, Melbourne)
Figure 9.18: Geographic ulcer in a graft stained with Rose Bengal dye (Courtesy: Medical Photographic Imaging Centre, Royal Victorian Eye and Ear Hospital, Melbourne)
After acute infection the VZV travels down the peripheral axons to cells in the dorsal root ganglion where it remains in the latent phase.
The herpes zoster occurs due to reactivation of the VZV within the dorsal root ganglion and virions travel to skin or mucous membrane or skin along the axonal transport.
EPIDEMIOLOGY
The annual incidence of herpes zoster is 1.5/1000 to 3.0/
1000 cases. The incidence is more in patients more than 75 years of age. There is no predilection for gender, race, or seasonal variation.
Herpes zoster has a greater preponderance in cases with altered cell mediated immunity, those taking immunosuppressive agents, organ transplant recipients, syphilis, tuberculosis, and those having HIV. It is also precipitated by physical or emotional stress.
The varicella zoster keratitis occurs in two forms:
• Primary (varicella)
• Recurrent (herpes zoster).
The ocular manifestations are uncommon in varicella but common in ophthalmic zoster. The various ocular manifestations in ophthalmic VZV include:
• Eye lesions which are manifested as pocks on lids and lid margins.
• Keratitis occurs rarely in cases of VZV.
• Epithelial keratitis with or without pseudodendrites occurs more rarely.
• Disciform keratitis with uveitis of varying duration can occur.
Ophthalmic varicella zoster infection is accompanied by keratouveitis that varies in severity according to immune status of the patient. The manifestations of ophthalmic varicella zoster infection are benign in children as compared to adults who have severe and sometimes blinding disease. Corneal complications in ophthalmic zoster are associated with skin eruption in areas supplied by branches of the nasociliary nerve.
Differences between dendrites of HSV and HZV infections (Table 9.6).
TREATMENT OF OPHTHALMIC VARICELLA ZOSTER
• Intravenous and oral acyclovir has been used successfully for treatment of herpes zoster ophthal-micus. This treatment regime is particularly important in immunocompromised patients. The appropriate timing of the therapy is vital. Therapy needs to be started within 72 hours after appearance of the rash. The use of oral acyclovir in a dosage of 800 mg five times daily for 10-14 days has been recommended. Although varicella zoster virus keratopathy is an uncommon indication for penetrating keratoplasty, effective visual rehabili-tation can be achieved in these patients. Careful postoperative management, frequent lubrication, and lateral tarsorrhaphies to protect the corneal surface are major factors in the successful outcome of these cases.25
ADENOVIRAL INFECTIONS
It is causative agent for epidemic keratoconjunctivitis which is predominantly caused by the serotypes 8, 19, and 37. The infection is highly contagious, with approximately 10 percent transmission in household contacts via hands and fomites. Transmission has also been associated with instrumentation, industrial trauma [shipyard workers (i.e. shipyard eye)], contaminated ophthalmic solutions, and the hands of health care workers. Corneal trauma facilitates infection. After an 8 days incubation period, an insidious onset of unilateral red eye occurs, which spreads to involve both eyes.
Patients have photophobia, tearing, and pain (indicating corneal involvement). Children may have fever and lymphadenopathy. Malaise and headache are reported.
Inflammation may persist for weeks, and residual scarring and visual impairment may occur. The associated findings in epidemic keratoconjunctivitis are:
• Severe follicular keratoconjunctivitis.
TABLE 9.6
Differentiation between dendrites of herpes simplex and zoster
Feature HSV VZV
Overall Fine, lacy Thick ropy
Epithelium Linear defect with Elevated, painted-on bared stroma, appearance surrounded by
edematous epithelial cells
Staining Base stains with Minimal fluororescein fluorescein staining
Diseased border epithelial cells stain with rose bengal
Terminal bulbs Frequent None
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• Palpebral edema.
• Preauricular lymphadenopathy is not common but is a pathognomonic finding with adenovirus infection.
• Hemorrhagic conjunctivitis may develop.
In stage I corneal epithelial vesicle like elevations are present which are 25 to 30 microns and barely perceptible on slit lamp. Two to five days later ,the lesions coalesce with each other , become clearly visible on slit lamp and involve deeper epithelium. These are the classical deep epithelial punctuate keratitis lesions which may resolve or progress further (Fig. 9.20). In stage III faint subepithelial infiltrates are present beside the deep punctate keratitis. Stage IV is characterized by nummular opacities which may be present months to weeks after the initial episode (Fig. 9.21).
Visual haziness or impairment resulting from keratitis develops due to the occurrence of nummular opacities (Fig. 9.21) and may persist for months to years.
A molecular assay for detection of human adenovirus based on automated nucleic acid extraction and real time polymerase chain reaction is being evaluated for the diagnosis of ocular adenoviral infections. The new molecular assay is suitable for rapid diagnosis of adenoviral keratoconjunctivitis in the routine diagnostic laboratory. It allows for a rapid diagnosis of adenoviral keratoconjunctivitis.26
Management
Medical management can range from cold compresses and artificial tears to topical vasoconstrictors (e.g.
Figure 9.21: Healed adenoviral keratoconjunctivitis (nummular opacities)
Figure 9.20: Subepithelial infiltration in adenoviral keratoconjuncti-vitis
naphazoline) and steroids (vexol, flarex, pred forte) two to four times daily. Recently, cidofovir an antiviral drug used intravenously to treat cytomegalovirus retinitis appears to be effective in adenoviral keratoconjunctivitis.
The topical form creates a faulty viral DNA structure.
Twice daily instillation is recommended.27
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