Delayed-onset unilateral facial paralysis after mastoidectomy: A case report

Objective@#To discuss the case of a 36-year-old man who presented with left unilateral facial paralysis 11 days after mastoidectomy.@*Methods@#Design: Case Report Setting: Tertiary Government Training Hospital Patient: One@*Results@#A 36-year-old man with recurrent left ear discharge of 30 years duration underwent left canal wall-down mastoidectomy and was discharged well after 3 days. On follow up after 8 more days, he was noted to have House Brackmann IV left facial paralysis. Following 5 days methylprednisolone, neurologic evaluation and physical therapy rehabilitation, facial paralysis improved in the ensuing weeks until House-Brackmann I was achieved at week 12.@*Conclusion@#Delayed-onset Facial Palsy (DFP) following tympanomastoid surgery may be approached conservatively, including steroids, acyclovir, and, if with a history of herpes or varicella infection, immunization can be given. Prognosis for DFP is good especially when the facial nerve is identified intraoperatively during otologic surgeries

Understanding the hepatitis B core positive liver donor

The increasing number of patients on the Singapore national liver transplant waiting list and the lack of donor livers have necessitated a review of the limited use of marginal donor liver grafts. Some grafts are of good quality but are considered marginal due to positive donor antibody to hepatitis B virus core protein serology, and negative hepatitis B surface antigen (HBsAg) and hepatitis B DNA. The fear is of viral reactivation during periods of intense immunosuppression. This is made possible by the ability of the hepatitis B virion to reside in a dormant state within the hepatocyte nucleus despite HBsAg clearance, i.e. the occult hepatitis B infection (OBI). In truth, appropriate selection of recipients and effective post-transplantation immunoprophylaxis significantly reduce the risk of hepatitis B viral reactivation. This article explains the confusion surrounding OBI and reviews current recommendations on how to manage such donor liver grafts.

Seroepidemiology of Epstein Barr virus in men who have sex with men in Chongqing area / 中国感染与化疗杂志

Objective To investigate the seroepidemiology of Epstein-Barr virus (EBV) and human immunodeficiency virus (HIV) in adult men who have sex with men (MSM) in Chongqing area. Methods Nonprobability sampling method was used to test EB-CA-IgG, EB-NA-IgG and EB-VCA-IgM in the sera of 1082 MSMs from the clinical trials of HIV/AIDS treatments in Chongqing area from 2012 to 2015, and 1059 healthy individuals by means of enzyme-linked immunosorbent assay. The results were analyzed by Chi-square test. The difference was considered statistically significant when P<0.05. Results The 1082 MSM included 130 HIV positive and 952 HIV negative subjects. The prevalence of prior EBV infection was 92.6% in total MSM population, 88.5% in HIV-positive MSM, and 93.2% in HIV-negative MSM. The prevalence in total MSM and HIV negative MSM was significantly higher than that in control group (89.9%). Prior EBV infection was not?found?in?0.5%?of?the?total?MSM,?0.8%?of?HIV?positive?MSM?and?0.4%?of?HIV?negative?MSM,?all?significantly?lower?than?that?of control group (5.0%) (P<0.05).?Finally,?the?rate?of?EBV?reactivation?in?HIV?positive?MSM?(10.0%)?was?significantly?higher?than?that in control group (3.8%) and in HIV negative MSM group(4.1%) (P<0.005). Conclusions EBV infection is highly prevalent in MSM, higher than that in the general population. The rate of EBV reactivation in HIV negative MSM is similar to that in general population. The rate of seroepidemiology-based EBV reactivation is significantly higher in HIV positive MSM, which may be associated with the immunocompromised status post HIV infection.

Hepatic Failure Caused by Reactivation of YMDD Mutants Occurring during Preemptive Lamivudine Therapy

Reactivation of hepatitis B virus (HBV) replication is a frequent phenomenon in patients receiving immunosuppressants or chemotherapy. It was recently reported that regional therapy, such as transarterial chemotherapy (TAC) or radiotherapy, can also induce HBV reactivation in patients with hepatocellular carcinoma (HCC), and this can be prevented by preemptive lamivudine treatment. We report an unusual case of fatal hepatitis caused by reactivation of the tyrosine-methionine-aspartate-aspartate (YMDD) lamivudine-resistant strain in a 51-year-old male patient with HCC who was receiving preemptive lamivudine therapy. This patient received combined helical tomotherapy and TAC for the treatment of HCC with pulmonary metastasis. HBV reactivation and hepatitis exacerbation occurred after 2 months of therapy, but preemptive antiviral therapy was continued. Laboratory tests showed that the serum HBV DNA level had increased by more than 10,000-fold and a severe elevation of the aminotransferase level to 1,060 U/L. Although adefovir was added to lamivudine immediately after detecting the YMDD mutants, the patient eventually died of hepatic failure. Our experience suggests that for preemptive therapy, the use of potent antiviral drugs with a low risk of drug resistance as well as close viral monitoring are important for chronic HBV carriers undergoing intensive anticancer therapy.

Reactivation of latent bovine herpesvirus type 5 in cattle with polioencephalomalacia induced by ammonium sulphate

In the state Mato Grosso do Sul, Brazil, outbreaks of meningoencephalitis by BoHV-5 and polioencephalomalacia (PEM) display similar epidemiological features, suggesting that meningoencephalitis may be associated with reactivation of a latent BoHV-5 infection, during the development of PEM. To test this hypothesis, four 7-8 months old steers negative for BoHV-5 antibodies were inoculated intranasally with BoHV-5 and received amprolium from day 35 to day 105 after inoculation. Because PEM was not produced during this period, ammonium sulphate was given from day 114 to day 180 after inoculation. Two uninfected control steers received amprolium and ammonium sulphate for the same periods. All inoculated cattle developed antibodies against BoHV-5 after inoculation and the virus was isolated from nasal swabs, indicating that they were infected. Two inoculated steers had clinical signs of PEM after 118 and 146 days after virus inoculation. One was euthanized after a clinical manifestation period of seven days and had severe lesions of PEM and meningoencephalitis. BoHV-5 was isolated from the central nervous system of this animal. The other animal recovered but continued to manifest chronic signs of PEM and was euthanatized. On histological examination, the cerebral cortex, caudate nucleus and thalamus had multifocal areas of malacia and mild meningoencephalitis of the cortex. BoHV-5 was not isolated from the brain. One uninfected control steer had signs of neurological disease on day 158 and had lesions of PEM without meningoencephalitis at necropsy. The simultaneous production of PEM and diffuse meningoencephalitis, with isolation of BoHV-5, in one steer treated with ammonium sulphate, 118 days after BoHV-5 inoculation, suggests that latent BoHV-5 was reactivated in this animal submitted to experimental induction of PEM.

No Mato Grosso do Sul surtos de meningoencefalite por herpesvírus bovino-5 (BoHV-5) e polioencefalomalacia (PEM) apresentam características epidemiológicas semelhantes, o que sugere que a meningoencefalite pode estar associada com a reativação de uma infecção latente por BoHV-5 em animais com PEM. Para testar esta hipótese, 4 garrotes de 7-8 meses de idade, sem anticorpos séricos para BoHV-5 foram inoculados intranasal com BoHV-5 e receberam amprólio desde o dia 35 até o dia 105 após inoculação. Como não foi reproduzida PEM durante este período, os animais receberam sulfato de amônia desde o dia 114 até o dia 180 após inoculação. Dois bovinos controles, não inoculados, receberam amprólio e sulfato de amônia durante os mesmos períodos. Todos os bovinos inoculados apresentaram anti-corpos contra BoHV-5 após a inoculação e o vírus foi isolado de suabes nasais, indicando que foram infectados. Dois bovinos inoculados tiveram sinais clínicos de PEM após 118 e 146 dias da inoculação de vírus. Um que foi eutanasiado após um curso clínico de 7 dias apresentou lesões severas de PEM e meningoencefalite. BoHV-5 foi isolado do sistema nervoso central. O outro se recuperou, mas continuou a apresentar sinais crônicos de PEM. No exame histológico o córtex cerebral, núcleo caudato e tálamo apresentavam áreas multifocais de malacia e no córtex havia moderada meningoencefalite. BoHV-5 não foi isolado do encéfalo. Um garrote controle, não inoculado, apresentou sinais nervosos aos 158 dias após inoculação e na necropsia apresentava lesões de PEM, mas sem meningoencefalite. A reprodução simultânea de PEM e encefalite difusa em um animal tratado com sulfato de amônia, 118 dias após a inoculação de BoHV-5 e o re-isolamento do vírus do animal infectado sugere que a infecção latente por BoHV-5 foi reativada no animal submetido a indução experimental de PEM.