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zoster sine herpete [keywords]
- Varicella-zoster. [JOURNAL ARTICLE]
- Handb Clin Neurol 2014.:265-283.
Primary infection with varicella-zoster virus (VZV), an exclusively human neurotropic α-herpesvirus, causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause zoster (shingles), dermatomal distribution pain, and rash on an erythematous base in one to three dermatomes. Zoster develops anywhere on the body. Skin lesions resolve within 1-2 weeks while complete cessation of pain usually takes 4-6 weeks. Unfortunately, zoster can be followed by chronic pain (postherpetic neuralgia), meningoencephalitis, cerebellitis, cranial nerve palsies, vasculopathy, myelopathy, and inflammatory eye disease. VZV reactivation also produces chronic radicular pain without rash (zoster sine herpete). In fact, all neurologic and ocular disorders listed above may also develop without rash. This review covers clinical, laboratory, and pathologic features of neurologic complications of VZV reactivation, including diagnostic testing to verify active VZV infection in the nervous system and the potential value of examining saliva for VZV DNA in patients with neurologic disease without rash. Additional perspectives are provided by discussions of the VZV genome, latency, pathogenesis, and immunity, and of the value of immunization of elderly individuals to boost cell-mediated immunity to VZV and prevent VZV reactivation.
- A case of herpes zoster uveitis with severe hyphema. [JOURNAL ARTICLE]
- BMC Ophthalmol 2014 May 29; 14(1):74.
Uveitis sometimes causes hyphema, but severe hyphema as a complication following herpes zoster uveitis has rarely been reported. We report a rare case of zoster sine herpete with unusually severe hyphema.A 41-year-old Japanese female developed hyphema filling almost one-half of the depth of the anterior chamber after a two-week history of unilateral anterior uveitis. Hyphema persisted for four weeks while sectorial iris atrophy became gradually apparent. Systemic prednisolone and valaciclovir resulted in prompt resolution of uveitis and hyphema. Serum anti-varicella zoster virus (VZV) IgG measured by enzyme immunoassay was 116 at presentation and decreased to 20.3 four month later. In addition, the antibody level in aqueous humor was almost 10-fold higher than that in serum examined 9 months after presentation. Because there was no skin lesion, this case was diagnosed as zoster sine herpete. The patient underwent cataract operation due to secondary cataract. The final visual acuity in decimal notation was 1.0, but complications such as severe iris atrophy, wide anterior synechiae, corneal opacity, and decrease in corneal endothelial cell count remained.Zoster sine herpete is an important differential diagnosis in a case of acute anterior uveitis with severe hyphema, although such cases are quite rare. Measurement of anti-VZV IgG levels by enzyme immunoassay in aqueous humor and serum would be useful in the diagnosis of VZV reactivation. Prompt diagnosis and administration of corticosteroids and anti-herpes virus medication may improve the outcome.
- A Case of Associated Laryngeal Paralysis Caused by Varicella Zoster Virus without Eruption. [Journal Article]
- Case Rep Med 2014.:916265.
We report a patient with significant weakness of the left soft palate, paralysis of the left vocal cord, and left facial nerve palsy. Although the patient showed no herpetic eruption in the pharyngolaryngeal mucosa and auricle skin, reactivation of varicella zoster virus (VZV) was confirmed by serological examination. She was diagnosed with zoster sine herpete. After treatment with antiviral drugs and corticosteroids, her neurological disorder improved completely. When we encounter a patient with associated laryngeal paralysis, we should consider the possibility of reactivation of VZV even when no typical herpetic eruption is observed.
- Isolated acute dysphagia due to varicella-zoster virus. [Journal Article]
- J Clin Virol 2014 Apr; 59(4):268-9.
We present a case of zoster sine herpete causing isolated acute dysphagia in an immunocompetent patient. The interest of this paper is the atypical presentation of varicella-zoster virus reactivation. A 77-year-old woman presented with a 3-day history of fever and worsening dysphagia for both liquid and solid foods. Cerebrospinal fluid examination revealed lymphocytic pleocytosis and PCR amplified varicella-zoster virus DNA with high antibody titers in both serum and cerebrospinal fluid. The panel was suggestive of a cranial neuritis due to varicella-zoster virus, involved cranial nerves, even in the absence of a cutaneous and mucosal rash. Varicella-zoster virus reactivation should be included in the differential diagnosis of isolated or multiple cranial nerve palsies, with or without zosteriform skin lesions. A prompt etiologic diagnosis can lead to early administration of antiviral therapy.
- Utility of real-time PCR analysis for appropriate diagnosis for keratitis. [Case Reports, Journal Article]
- Cornea 2013 Nov.:S71-6.
Real-time polymerase chain reaction (PCR) is a quantitative method to measure the amount of amplified PCR product in real time with high sensitivity. We have applied this method to detect pathogens in cases of keratitis with an unknown cause. The scraped corneal epithelium for epithelial keratitis or aqueous humor for stromal or endothelial keratitis was obtained and DNA was extracted. The DNA from specific pathogens was amplified using specific primers and TaqMan probe, and assessed quantitatively. Here, we review previously reported noteworthy examples of keratitis diagnosed by our real-time PCR system as follows: cases with Acanthamoeba keratitis whose causative pathogen was only detected by real-time PCR despite not being detected by histological examination and culture; zoster sine herpete with atypical pseudodendrite; acyclovir-resistant herpetic keratitis estimated by changes in viral DNA copy numbers before and after treatment; and corneal endotheliitis positive for cytomegalovirus, human herpes virus-7, or human herpes virus-8. Real-time PCR helps ophthalmologists to make an early diagnosis and provide appropriate treatment for keratitis with complex clinical appearances.
- Pathogenesis and current approaches to control of varicella-zoster virus infections. [Journal Article, Research Support, N.I.H., Extramural, Review]
- Clin Microbiol Rev 2013 Oct; 26(4):728-43.
Varicella-zoster virus (VZV) was once thought to be a fairly innocuous pathogen. That view is no longer tenable. The morbidity and mortality due to the primary and secondary diseases that VZV causes, varicella and herpes zoster (HZ), are significant. Fortunately, modern advances, including an available vaccine to prevent varicella, a therapeutic vaccine to diminish the incidence and ameliorate sequelae of HZ, effective antiviral drugs, a better understanding of VZV pathogenesis, and advances in diagnostic virology have made it possible to control VZV in the United States. Occult forms of VZV-induced disease have been recognized, including zoster sine herpete and enteric zoster, which have expanded the field. Future progress should include development of more effective vaccines to prevent HZ and a more complete understanding of the consequences of VZV latency in the enteric nervous system.
- Infectious neuropathies. [Journal Article, Review]
- Curr Opin Neurol 2013 Oct; 26(5):510-5.
Infectious neuropathies are heterogeneous neuropathies with multiple causes. They still represent an important world health burden and some of them have no current available therapy.Leprosy incidence has decreased by 50% during the last years, but leprosy-related neuropathies still cause severe disability. The pure neuritic leprosy is a diagnostic challenge that may require nerve biopsy or nerve aspiration cytology. The treatment itself may lead to a 'reversal reaction', which further causes injuries to the nerve. HCV-related neuropathies may be related or not to the presence of cryoglobulins. The absence of vasculitis, the most frequent form is a peripheral sensory neuropathy involving small nerve fibers, and more accurately diagnosed by pain-related evoked potentials. HIV-related neuropathy has become the major neurological complication of HIV infection. Both HIV-induced neuropathy and antiretroviral toxic neuropathy are clinically indistinguishable. The existence of an isolated chronic polyneuropathy due to Borrelia burgdorferi remains highly controversial. Lastly, an active infectious ganglioneuritis caused by varicella zoster virus, producing shingles, is the most frequent infectious neuropathy in the world and may cause various neurological complications. Zoster sine herpete remains frequently undiagnosed.Recent data have improved our knowledge and diagnostic tools of infectious neuropathies. Treatment of the injured nerves is not yet available, and prevention and rapid diagnosis remain the main priorities for the clinician.
- Unusual trigeminal autonomic pain heralding hemichorea due to zoster sine Herpete vasculopathy. [Case Reports, Journal Article]
- Pediatr Neurol 2013 Sep; 49(3):205-8.
Varicella zoster virus primary infection is responsible for chickenpox, whereas secondary infection or reactivation can lead to a variety of clinical scenarios. If latent infection is established in trigeminal ganglion, the reactivation can determine viral migration to cerebral arteries, which causes a cerebral vasculopathy and subsequently an ischemic stroke.Here we report on a child experiencing recurrent episodes of headache mimicking a trigeminal autonomic cephalalgia, in the absence of any skin rash, which were followed by the occurrence of an ipsilateral hemiparesis associated with a choreic movement disorder a month later.Magnetic resonance angiography showed evidence of a right-sided infarction of basal ganglia and anterior limb of the internal capsule, corresponding to the vascular territory of the recurrent artery of Heubner, as a consequence of a focal varicella zoster virus arteriopathy.We suggest that the recognition of this prodromal manifestation, which can be interpreted as a zoster sine herpete, could provide clinicians an extremely useful time window to start promptly with a prophylactic treatment.
- Varicella-zoster meningoencephaloradiculoneuropathy in an immunocompetent young woman. [Case Reports, Journal Article]
- J Clin Virol 2013 Aug; 57(4):361-2.
The clinical manifestations of varicella-zoster virus infections can be divided into primary infection with chickenpox and reactivated infection with dermatomal shingles, disseminated herpes zoster, zoster sine herpete and varicella-zoster virus encephalitis, meningitis and vasculopathy. We present a case of zoster sine herpete leading to meningitis with cranial and peripheral nerve palsies. A 17-year-old woman was admitted to hospital with intermittent fever, drowsiness, slowness and subsequent frontal headache and horizontal diplopia. Cerebrospinal fluid examination revealed lymphocytic pleocytosis and PCR amplified varicella-zoster virus DNA. Laboratory and clinical findings were suggestive of meningoencephaloradiculoneuropathy, stemming from varicella-zoster virus and affecting cranial and peripheral nerves. Only 5% of patients with zoster develop cranial and peripheral nerve palsies. Diagnosis is imperative in order to initiate prompt antiviral therapy so as to minimize morbidity and the risk of death.
- Spinal arteriovenous malformation masquerating zoster sine herpete. [Journal Article]
- Korean J Pain 2013 Jan; 26(1):72-5.
Zoster sine herpete (ZSH) is difficult to diagnosis during an acute period due to the absence of the characteristic zosteriform dermatomal rash; therefore, progression to postherpetic neuralgia is more common than typical zoster. In addition, misdiagnosis of other neuropathic pain as ZSH is common in clinical situations. Here, we report a case of spinal arteriovenous malformation that mimics ZSH. This is a rare condition; therefore, high clinical suspicion for a correct diagnosis and proper examination are not easy. However, early diagnosis and definitive treatment are essential to prevent neurologic deficit and mortality.