An unusual complication of tooth exfoliation and osteonecrosis following herpes zoster infection of trigeminal nerve: a case report and literature review.

Osteonecrosis following herpes zoster infection is a rare but severe complication, and clinicians' awareness is important for early detection and management of this condition. A case of herpes zoster of the left maxillary division of the trigeminal nerve is reported in a young female having no concurrent predisposing factors, with accompanying rare complications of alveolar bone necrosis and rapid tooth exfoliation. Acyclovir was used to manage the case effectively. The previously reported similar cases in the literature have been reviewed and the pathophysiology of tooth exfoliation and osteonecrosis by varicella zoster viruses is discussed.

Herpes zoster associated with tooth resorption and periapical lesions.

A 72-year-old woman presented with multiple periapical lesions and resorption of teeth in a single quadrant 17 years after an attack of herpes zoster (shingles) of the maxillary division of the trigeminal nerve. It is possible that cases of tooth resorption that were previously classified as idiopathic may have a viral aetiology and we suggest that these patients should be asked about a previous attack of shingles.

Maxillary herpes zoster with corneal involvement in a HIV positive pregnant woman.

Corneal involvement in maxillary herpes zoster is very rare. This report presents the case of a 32 years old 7 months pregnant para2+1 female, who presented with vesiculopapular rashes with hyperpigmented crusts over the maxillary area of the face on the left side with periocular oedema, conjunctivitis and mild punctate keratitis in the left eye. She was HIV positive and was on treatment with the highly active antiretroviral therapy. She was treated with topical and systemic acyclovir with rapid resolution of the ocular features.

[Varicella zoster virus infection involving the maxillary branch of the trigeminal nerve].

Herpes zoster is an infection caused by reactivation of the latent varicella virus in the sensory ganglia. The mechanisms responsible for Varicella zoster virus (VZV) reactivation are poorly understood. Yet, it is believed that decreased cellular immunity can be a trigger for it's reactivation. The occurrence of herpes zoster in young people may point to an underlying immunodeficiency. Therefore, the possibility of concomitant HIV infection must be eliminated. Herpes zoster manifests as a vesicular rash along a sensory dermatome, usually preceded by pain or paresthesia of the involved cutaneous area. The most commonly affected dermatomes are those of the thorax and abdomen, followed by the cranial nerves, especially the trigeminal nerve. The maxillary nerve is the least frequently affected branch of the trigeminal nerve and only rarely causes ocular injury. This is a case history of a young patient infected with VZV involving the maxillary branch of the trigeminal nerve, complicated by secondary bacterial infection of the ipsilateral hemiface. The literature regarding the epidemiology, pathogenesis, complications and the proper treatment of herpes zoster is reviewed with an emphasis on the involvement of cranial nerves.

Maxillary zoster with corneal involvement.

A case, of maxillary zoster with corneal involvement in a young patient is described. Corneal involvement in maxillary zoster (Medline search) is rare.

Herpes zoster with progression to acute varicella zoster virus-meningoencephalitis.

BACKGROUND: Acute meningoencephalitis (ME) from varicella zoster virus (VZV) reactivation is a rare and serious complication of herpes zoster (HZ). OBJECTIVES AND METHODS: As early diagnostic detection is mandatory to prevent long-term sequelae, any clinical indication is helpful to identify patients that are at higher risk of the development of VZV-ME. In order to find such risk factors, the clinical data of 38 patients consecutively hospitalized for the treatment of HZ over a 1-year period were analyzed. RESULTS: Four of the 38 patients with HZ developed ME. Of these, three had involvement of the trigeminal nerve branch, one including an ophthalmic affection, and one presented with disseminated HZ. All were women with an average age of 83.5 years, in comparison with patients with HZ but without ME who had an average age of 69.3 years and a female preponderance of 60%. The first clinical signs of ME were rapidly progressing somnolence and meningism. Patients with HZ-ME were treated with intravenous acyclovir, oral glucocorticosteroids, and antiseizure therapy, and recovered almost completely without major residual symptoms. CONCLUSION: Progression of HZ to ME seems to occur more often than normally believed. Female patients above 80 years of age with either ophthalmic involvement or disseminated HZ are at a potentially high risk of the development of ME. The general recommendation of starting oral glucocorticosteroids from day 1 of antiviral treatment in older patients must be questioned, as it may stimulate VZV replication and dissemination.

Dissemination of wild-type and gC-, gE-and gI-deleted mutants of Aujeszky's disease virus in the maxillary nerve and trigeminal ganglion of pigs after intranasal inoculation.

Aujeszky's disease virus (ADV) is a well known neurotropic virus in pigs. In the present study the mechanism of spread of ADV along the maxillary nerve and the role of the viral envelope glycoproteins gC, gE and gI in this process was examined in pigs. The Ka parental strain of ADV and its gC-, gE- and gI-deleted mutants were inoculated intranasally in pigs, after which virus dissemination in the maxillary nerve and the trigeminal ganglion was monitored at time intervals by means of virus isolation. The parental strain was isolated from both the nasal mucosa and the trigeminal ganglion at 21 h post-inoculation (p.i.), whereas the middle part of the connecting maxillary nerve was positive only after 48 h p.i. It appears, therefore, that ADV travels from the nasal mucosa via the nerve towards the ganglion in a non-infectious form, and then replicates in the neuronal somas, after which infectious virus is transported towards the nasal mucosa. Although all mutants were present at 48 h p.i. in the nasal mucosa and the trigeminal ganglion, the appearance of infectious virus in the maxillary nerve was clearly delayed with gE- and gI- mutants. It is suggested that glycoproteins gE and gI are involved in the axonal transport of infectious ADV away from neuronal cell bodies, also called anterograde transport.

Tracking the spread of a lacZ-tagged herpes simplex virus type 1 between the eye and the nervous system of the mouse: comparison of primary and recurrent infection.

The spread of herpes simplex virus type 1 (HSV-1) during primary ocular infection and after reactivation of latent infection in the trigeminal ganglion (TG) was examined in the mouse using a genetically modified virus containing the lacZ reporter gene under the control of the immediate-early 110 promoter. Whole tissue mounts of the eye and lids, their sensory nerves, and TG with the attached dorsal root entry zone (DRE) into the central nervous system (CNS) were stained for beta-galactosidase. Sixteen hours after inoculation of the cornea by scarification, staining was found in the scarified epithelium of the cornea and in the unscarified conjunctiva. By 24 h, staining was also seen in a few TG neurons and by 96 h their number had greatly increased and their distribution was more widespread. Stained cells (identified as Schwann cells by their staining for glial fibrillary acidic protein [GFAP] or S-100) in the TG were first seen close to stained neurons at 40 h, and by 48 h lines of such cells extended partway toward the periphery and toward the DRE. By 72 h, these lines had reached the periphery and the DRE where the adjacent CNS was also stained. In the cornea, stained cells with the morphology and arrangement of Schwann cells were seen from 40 to 120 h. After reactivation of latent infection, 10 of 22 samples had positively stained neurons. In eight samples, corneal and lid epithelial cells were stained. No stained Schwann cells were seen in the TG; however, branched networks of such cells were present in the cornea and the lids. This detailed sequential analysis has provided new information on the involvement of Schwann cells in the pathogenesis of primary and recurrent HSV-1 disease in the TG and the cornea.