Search

COVID-19 is one of the most disastrous respiratory diseases (after the 1918 influenza outbreak) spreading in the community. So far, it has killed 7,37,417 individuals. High variability in the viral genome and its greater ability to spread in the human community are badly affecting the comorbid individuals. Although infected individuals mainly possess respiratory issues, neurological manifestations in these individuals cannot be overlooked. The literature search is based on the recent development in the concerned field. We searched databases like PubMed, Google Scholar, and ScienceDirect using the keywords "COVID-19", "neurological manifestations", "CNS", and "PNS". The major neurological complications observed in these patients are encephalitis, necrotising haemorrhagic encephalopathy, Guillain-Barré Syndrome, smell/taste impairment, epileptic seizures, and abnormal states of consciousness. COVID-19 infection is just more than a cough, fever, and respiratory illness; it can cause indirect neurological complications in infected patients. It is therefore advised to treat and have a careful observation of the COVID-19 patients for neurological manifestations., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Introduction: Meningitis are the most common form of the nervous system infectious diseases. There are meningitis and/or encephalitis with bacterial and viral etiology. In epidemiological surveillance are highlighted meningitis and/or encephalitis caused by N. meningitidis, S. pneumoniae, H. influenzae and tick-borne encephalitis virus. Because vaccinations against these agents are common., Aim of the Study: The aim of the study is to assess the epidemiological situation of meningitis and encephalitis in Poland in 2017., Material and Methods: The epidemiological situation of meningitis and encephalitis in Poland was assessed on data from the annual bulletin “Infectious diseases and poisoning in Poland in 2017” and “Vaccinations in Poland in 2017”. (MP Czarkowski et al., Warsaw 2018, NIZP-PZH, GIS)., Results: In 2017 were registered 2 095 cases of meningitis and/or encephalitis in Poland. It means a 10.8% decrease in meningitis and/or encephalitis in Poland compared to 2016. With a general decrease in the number of infections of bacterial etiology, the number of cases of meningitis and/or encephalitis of S. pneumoniae, H. influenzae type B cases reported remains at the same level similar to last year. In contrast, the number of cases of etiology of N. meningitidis shows an increase of 25.4% compared to the previous year. Among all cases 57.9% were viral infections. In comparison to 2016 means a decrease in the percentage share of viral infections by 1.2 percentage points for bacterial infections. Among laboratory confirmed cases of neuroinfection with established etiology, the incidence caused by Neisseria miningitidis (122 cases), Streptococcus pneumoniae (171 cases) and tick-borne encephalitis (283 cases) are the most prevalent., Summary and Conclusion: There is a general downward trend in the number of meningitis and/or encephalitis cases, which may be due to introducing mandatory vaccination against S. pneumoniae. It can also mean an improvement in diagnostics given the decrease in unspecified meningitis and/or encephalitis. However meningitis and/or encephalitis remain a challenge for healthcare and epidemiological surveillance institutions., (© National Institute of Public Health – National Institute of Hygiene)

Members of the genera Alphavirus (family Togaviridae ) and Flavivirus (family Flaviridae ) are important zoonotic human and equine etiologic agents of neurologic diseases in the New World. In 2010, an outbreak of Madariaga virus (MADV; formerly eastern equine encephalitis virus) and Venezuelan equine encephalitis virus (VEEV) infections was reported in eastern Panamá. We further characterized the epidemiology of the outbreak by studying household contacts of confirmed human cases and of equine cases with neurological disease signs. Serum samples were screened using a hemagglutination inhibition test, and human results were confirmed using plaque reduction neutralization tests. A generalized linear model was used to evaluate the human MADV and VEEV seroprevalence ratios by age (in tercile) and gender. Overall, antibody prevalence for human MADV infection was 19.4%, VEEV 33.3%, and Mayaro virus 1.4%. In comparison with individuals aged 2-20 years, people from older age groups (21-41 and > 41 years) were five times more likely to have antibodies against VEEV, whereas the MADV prevalence ratio was independent of age. The overall seroprevalence of MADV in equids was 26.3%, VEEV 29.4%, West Nile virus (WNV) 2.6%, and St. Louis encephalitis virus (SLEV) was 63.0%. Taken together, our results suggest that multiple arboviruses are circulating in human and equine populations in Panamá. Our findings of a lack of increase in the seroprevalence ratio with age support the hypothesis of recent MADV exposure to people living in the affected region.

Citrobacter freundii is considered a ubiquitous organism and an opportunistic pathogen. Reports of C. freundii-associated disease in mammals have been very limited. We report an outbreak of C. freundii septicemia and encephalitis in sheep, with a high mortality rate; 13 adult sheep were found dead over a 6-d period on a farm in central China that housed ~1,370 sheep. Three animals were autopsied and showed septicemia, congestion of meningeal vessels, and pleural effusion. C. freundii was isolated in abundance in pure culture from 19 of 21 organs. All 3 C. freundii isolates had similar antimicrobial resistance phenotypes for 10 of the 11 agents tested, and were sensitive to 8 of the 11 agents. We reproduced C. freundii infection in sheep experimentally by oral or subcutaneous inoculation routes, and recovered the challenge organism from all of the experimentally infected sheep. Intramuscular injection of enrofloxacin protected sheep against an otherwise fatal challenge. Our results suggest that C. freundii played a major role in this disease outbreak.

We describe the first reported outbreak of West Nile virus (WNV) infection in humans in Serbia in August to October 2012 and examine the association of various variables with encephalitis and fatal outcome. Enzyme-linked immunosorbent assay (ELISA) was used for detection of WNV-specific IgM and IgG antibodies in sera and cerebrospinal fluid. A total of 58 patients (mean age: 61 years; standard deviation: 15) were analysed: 44 were from Belgrade and its suburbs; 52 had neuroinvasive disease, of whom 8 had meningitis, while 44 had encephalitis. Acute flaccid paralysis developed in 13 of the patients with encephalitis. Age over 60 years and immunosuppression (including diabetes) were independently associated with the development of encephalitis in a multivariate analysis: odds ratio (OR): 44.8 (95% confidence interval (CI): 4.93–408.59); p=0.001 (age over 60 years); OR: 10.76 (95% CI: 1.06–109.65); p=0.045 (immunosuppression including diabetes). Respiratory failure requiring mechanical ventilation developed in 13 patients with encephalitis. A total of 35 patients had completely recovered by the time they were discharged; nine patients died. The presence of acute flaccid paralysis, consciousness impairment, respiratory failure and immunosuppression (without diabetes) were found to be associated with death in hospital in a univariate analysis (p<0.001, p=0.007, p<0.001 and p=0.010, respectively).

Background: An 8-year era of interrupted indigenous measles transmission in Bulgaria came to an end in April 2009 when a large epidemic occurred that would eventually claim 24,253 cases and 24 deaths; infants, children and young adults of the Roma community were disproportionally affected. Compared with Western Europe, case-fatality rate and proportion of medical complications were uncharacteristically high., Methods: To disentangle underlying drivers of the outbreak and reasons for these medical complications, we assembled a number of national ecologic variables as well as regional individual-level data for 206 measles cases, randomly selected from national medical records. We conducted a logit regression analysis of data from individuals with medical complications., Results: Ecologic socio-economic predictors were not associated with measles cases by region, although the proportion of medical complications differed considerably. Individual-level data from a region with high medical complications revealed that mother's education [odds ratio (OR) 0.79; 95% confidence interval (CI) 0.68-0.92], immunization status of the child (OR 0.28; 95% CI 0.08-0.94) and households declaring an income (OR 0.31; 95% CI 0.10-0.93) decreased the risk for developing severe medical complications such as pneumonia or encephalitis from a measles infection., Discussion: The extent of this outbreak with a high case-fatality rate and high proportion of medical complications calls for resolute public health action. We found vaccination and maternal education to be crucial conduits of curbing medical complications from measles infections. Ultimately, the goal is measles elimination in Europe by 2015, and these data hint at intervention entry points.

Since 2006, an unprecedented epidemic of highly pathogenic Porcine reproductive and respiratory syndrome virus (HP-PRRSV) infection has emerged and prevailed in mainland China, causing so called high fever disease with a nervous symptom that is different from typical porcine reproductive and respiratory syndrome. To investigate this syndrome, the brains of pigs inoculated with HP-PRRSV were analyzed. The nucleic acid of HP-PRRSV was detected in brains by reverse transcription polymerase chain reaction. Histological examination demonstrated nonsuppurative encephalitis with lymphohistiocytic perivascular cuffing and infiltration of these leukocytes into the neuropil. Furthermore, transmission electron microscopy revealed that the HP-PRRSV that infected the endothelial cells crossed the blood-brain barrier into the central nervous system then induced cellular damage to neurons and neuroglial cells. These results provide a general insight into the pathway of HP-PRRSV invasion into brain tissue and the pathogenesis of nonsuppurative encephalitis.

Objective: To identify the etiology of an aseptic encephalitis outbreak (ten cases) in a hospital of Xiamen city from 11 to 17 May, 2011., Methods: A total of ten patients' throat swabs, anal swabs and cerebrospinal fluid were collected and detected by RT-PCR for pan-enterovirus. The samples containing detectable pan-enterovirus were tested by PCR with genotype-specific general primers located in VP1 region of enterovirus genotype A, B and C (HEV-A, B and C). The PCR products of VP1 segment were purified and sequenced, and phylogenetic analysis was performed. Meanwhile, the pathogens in those samples were isolated in Vero cell culture. Homologous analysis of VP1 sequences were carried out for the cultured virus samples and the original clinical samples to identify the outbreak etiology., Results: Among the ten cases, seven cases were positive for pan-enterovirus nucleic acid. When tested by genotype-specific PCR, the throat and anal swab samples from those 7 patients were positive with HEV-B VP1 primers. Meanwhile, the HEV-B VP1 segments were sequenced and phylogenetic analyzed, which indicated the seven cases were all infected by enterovirus Echo 30. The sequences from those samples had homology of 95.3% - 97.1% with the epidemic strains in Zhejiang, 2004. Out of the seven cases, the sequences of XM2, XM3, XM4, XM8 throat swab samples and XM3, XM6 throat samples showed 99.4% - 100.0% homology which were different from the sequence of XM1, and the homology was 92.8% - 93.4%. Furthermore, the viruses were isolated using Vero cells from XM1, XM2, XM3, XM4 and XM8 throat swab samples, and the VP1 sequence showed more than 99.9% homology with the original specimens., Conclusion: The local outbreak of aseptic encephalitis was caused by Echo 30 of enterovirus genotype B, and the epidemic strains may have different genetic background.

Background: Bovine herpesvirus 5 (BoHV-5) is a member of the subfamily Alphaherpesvirinae responsible for meningo-encephalitis in young cattle. The first case of bovine meningo-encephalitis associated with a herpesvirus infection was reported in Australia. The current geographical distribution of BoHV-5 infection is mainly restricted to South America, especially Brazil and Argentina. Outbreaks of BoHV-5 are regularly observed in Argentina suggesting the circulation of the virus in the bovine population., Results: Seventeen field strains of BoHV-5 isolated from 1984 to now were confirmed by differential PCR and subjected to restriction endonuclease analysis (REA). Viral DNA was cleaved with BstEII which allows the differentiation among subtypes a, b and non a, non b. According to the REA with BstEII, only one field strain showed a pattern similar to the Argentinean A663 strain (prototype of BoHV-5b). All other isolates showed a clear pattern similar to the Australian N569 strain (prototype of BoHV-5a) consistent with the subtypes observed in Brazil, the other South-American country where BoHV-5 is known to be prevalent. The genomic region of subtype b responsible for the distinct pattern was determined and amplified by PCR; specifically a point mutation was identified in glycoprotein B gene, on the BstEII restriction site, which generates the profile specific of BoHV-5b., Conclusions: This is the first report of circulation of BoHV-5a in Argentina as the prevailing subtype. Therefore the circulation of BoHV-5b was restricted to a few years in Argentina, speculating that this subtype was not able to be maintained in the bovine population. The mutation in the gB gene is associated with the difference in the restriction patterns between subtypes "a" and "b".

Background: The threat of emerging infections and recognition of novel immune-mediated forms of encephalitis has raised the profile of this condition in recent years. Incidence is poorly defined and most cases have an unknown cause. There is currently much interest in identification of new microbial agents of encephalitis, but no work has investigated systematically reasons for lack of pathogen identification in studies., Methods: We systematically reviewed published literature on incidence and etiology of encephalitis in non-outbreak settings and explored possible explanations for the large number of cases of unknown etiology., Results: Annual incidence ranged from 0.07 to 12.6 cases per 100,000 population with an evident decrease over time (p = 0.01). The proportion of cases with unknown etiology was high across studies (>50% in 26 of 41 studies), with strong evidence of heterogeneity in study findings (p < 0.001). Our meta-regression identified study period, setting, and subsyndrome to be the main contributors to between-study variation, rather than methodologic factors such as study design, case definitions, sample types, and testing strategies., Conclusions: Our findings support the hypothesis that new and emerging infectious agents, or new forms of immune-mediated encephalitis, may be responsible for cases currently of unknown cause and encourage the ongoing global effort to identify these. Our review highlights research areas that might lead to a better understanding of the causes of encephalitis and ultimately reduce the morbidity and mortality associated with this devastating condition.

A recent Hendra virus outbreak at a veterinary clinic in Brisbane, Queensland, Australia, involved 5 equine and 2 human infections. In contrast to previous outbreaks, infected horses had predominantly encephalitic, rather than respiratory, signs. After an incubation period of 9-16 days, influenza-like illnesses developed in the 2 persons before progressing to encephalitis; 1 died. Both patients were given ribavirin. Basal serum and cerebrospinal fluid levels were 10-13 mg/L after intravenous administration and 6 mg/L after oral administration (isolate 90% inhibitory concentration 64 mg/L). Both patients were exposed to infected horses, 1 during the late incubation period in a horse. The attack rate for veterinary clinic staff exposed to infected horses was 10%. An isolate from this outbreak showed genetic heterogeneity with isolates from a concurrent, but geographically remote, outbreak and from previous outbreaks. Emergence of Hendra virus is a serious medical, veterinary, and public health challenge.

Background: In addition to classical manifestations of Chikungunya infection, severe infections requiring hospitalization were reported during outbreaks in India in 2006., Objectives: To describe the systemic syndromes and risk groups of severe Chikungunya infections., Study Design: We prospectively investigated suspected Chikungunya cases hospitalized in Ahmedabad, Gujarat during September-October 2006, and retrospectively investigated laboratory-confirmed Chikungunya cases hospitalized with neurologic syndromes in Pune, Maharashtra. Hospital records were reviewed for demographic, comorbidity, clinical and laboratory information. Sera and/or cerebrospinal fluid were screened by one or more methods, including virus-specific IgM antibodies, viral RNA and virus isolation., Results: Among 90 laboratory-confirmed Chikungunya cases hospitalized in Ahmedabad, classical Chikungunya was noted in 25 cases and severe Chikungunya was noted in 65 cases, including non-neurologic (25) and neurologic (40) manifestations. Non-neurologic systemic syndromes in the 65 severe Chikungunya cases included renal (45), hepatic (23), respiratory (21), cardiac (10), and hematologic manifestations (8). Males (50) and those aged >or=60 years (50) were commonly affected with severe Chikungunya, and age >or=60 years represented a significant risk. Comorbidities were seen in 21 cases with multiple comorbidities in 7 cases. Among 18 deaths, 14 were males, 15 were aged >or=60 years and 5 had comorbidities. In Pune, 59 laboratory-confirmed Chikungunya cases with neurologic syndromes were investigated. Neurologic syndromes in 99 cases from Ahmedabad and Pune included encephalitis (57), encephalopathy (42), and myelopathy (14) or myeloneuropathy (12)., Conclusions: Chikungunya infection can cause systemic complications and probably deaths, especially in elderly adults.

This is the first of two papers which critically examine the relationship between the 1918/19 influenza pandemic and encephalitis lethargica (EL). The role of influenza in the etiology of EL was vigorously debated until 1924. It is notable, however, that the unitarian camp were largely reactive in their argumentation; while the influenza skeptics provided detail descriptions of EL and the features they argued to be unique or at least unusual, influenza supporters focused on sequentially refuting the evidence of their opponents. The impression which emerges from this debate is that the individual features identified by the skeptics were not absolutely pathognomic for EL, but, on the other hand, their combination in one disorder had not previously been described for any other disease.

Encephalitis lethargica (EL) was first reported in 1917 in central Europe. It became epidemic in the winter of 1918/1919 concurrently with the pandemic of influenza, and by then had reached Russia and North America. It spread throughout the world in epidemic form, mainly in the succeeding winters, up to 1927. By then about 65 000 cases had been reported, although the true number worldwide can only be guessed at. EL mortality was about 30% in the acute stage, and similar during recurrences. Half of the survivors had persistent or recurrent neuro-psychiatric illness, with Parkinsonism a frequent end stage. Most contemporary observers attributed EL to a virus and some believed it was specifically a post-influenzal complication. The epidemiology of EL mostly points to an infective cause, e.g. a seasonal respiratory or gastrointestinal virus with infrequent encephalitic expression but the ability to persist, flare and progressively damage the brain. However, any link with the influenza virus strain of 1918/1919 remains hypothetical. The aetiological theories that have been applied to EL are reviewed and the question is raised whether broader laboratory investigation might now reveal a continuing low endemicity of EL and identify its cause.

In the first half of the 20th century, during the Spanish flu pandemic, more than half a million people died from a mysterious disease sleeping sickness which was named 'encephalitis lethargica'. Despite extensive research, the cause of the disease has not yet been established. In the Netherlands many doctors published cases in the Nederlands Tijdschrift voor Geneeskunde (Dutch Journal of Medicine), also when chronic forms of the disease arose. An attempt to treat patients suffering from the chronic disease with levodopa initially had spectacular results but eventually lead to a new disappointment as a result of severe side effects. The experiment was stopped prematurely. Encephalitis lethargica is still being sporadically diagnosed in the 21st century. Recent research suggests that an autoimmune response targeted at the basal ganglia, possibly caused by a streptococcal infection, plays a role in the aetiology of the disease.

Background: We investigated an outbreak of severe neurologic disease and pneumonia that occurred among students at 4 schools in Rhode Island., Methods: We identified cases of encephalitis, encephalomyelitis, and pneumonia that occurred among schoolchildren from 1 September 2006 through 9 February 2007, and we performed serologic tests, polymerase chain reaction (PCR) analysis, and culture for the detection of multiple pathogens in oropharyngeal and nasopharyngeal specimens. Students with positive results of M. pneumoniae IgM serologic testing and no alternative diagnosis were considered to be infected with M. pneumoniae. At school A, we used questionnaires to identify students and their household contacts who made visits to physicians for pneumonia and cough. We compared observed and expected rates of pneumonia., Results: Rates of pneumonia among elementary students (122 cases/1000 student-years) were > 5-fold higher than expected. Three students had encephalitis or encephalomyelitis, and 76 had pneumonia. Of these 2 groups of students, 2 (66%) and 57 students (75%), respectively, had M. pneumoniae infection. M. pneumoniae was detected by PCR in 10 students with pneumonia; 5 of these specimens were cultured, and M. pneumoniae was isolated in 4. Of 202 households of students attending school A, 20 (10%) accounted for 61% of visits to physicians for pneumonia or cough. Of 19 household contacts of students with pneumonia, 8 (42%) developed pneumonia and 6 (32%) reported visits for cough., Conclusions: M. pneumoniae caused a community-wide outbreak of cough illness and pneumonia and was associated with the development of life-threatening neurologic disease. Although M. pneumoniae was detected in schools, its transmission in households amplified the outbreak. Interrupting household transmission should be a priority during future outbreaks.

An atypical outbreak of West Nile virus (WNV) occurred in Ngorban County, South Kordophan, Sudan, from May to August 2002. We investigated the epidemic and conducted a case-control study in the village of Limon. Blood samples were obtained for cases and controls. Patients with obvious sequelae underwent cerebrospinal fluid (CSF) sampling as well. We used enzyme-linked immunosorbent assay (ELISA) and neutralization tests for laboratory diagnosis and identified 31 cases with encephalitis, four of whom died. Median age was 36 months. Bivariate analysis did not reveal any significant association with the risk factors investigated. Laboratory analysis confirmed presence of IgM antibodies caused by WNV in eight of 13 cases, indicative of recent viral infection. The unique aspects of the WNW outbreak in Sudan, i.e. disease occurrence solely among children and the clinical domination of encephalitis, involving severe neurological sequelae, demonstrate the continuing evolution of WNV virulence. The spread of such a virus to other countries or continents cannot be excluded.

Influenza is a zoonotic respiratory virus that affects birds, mammals, and humans. Influenza viruses are unique in their genetic instability, which frequently results in antigenic drift or shift. Antigenic shifts are responsible for influenza epidemics. Influenza A pandemics have been responsible for millions of deaths during the past several hundred years. In terms of virulence and lethality, the 1918 to 1919 influenza pandemic was the worst in history. It was unique in its predilection and lethality among young healthy adults. There has never been a satisfactory explanation for the unusual virulence of the 1918 to 1919 pandemic.

In the present work, evidence of Listeria monocytogenes antigens based on the avidin-biotin complex (ABC) immunoperoxidase technique was performed on formalin-fixed central nervous system tissues (CNS) from a total of 23 natural cases of encephalitis (four ovine and 19 bovine). Listeria monocytogenes serotype 4 was isolated from 10 of 17 cultured specimens. Meningoencephalitis characterized by focal necrosis, microabscesses, perivascular cuffing, and gliosis with presence of macrophages and/or neutrophils was observed at histological examination. Positive L. monocytogenes antigens were successfully identified by immunohistochemistry (IHC) in the CNS of all 23 cases. Paraffin-embedded tissues assayed were stored up for 17 years. Morbidity of the outbreaks was between 0.3-3% and 0.1-1% for ovine and bovine cases, respectively. In all the ovine cases, flocks involved were under extensive grazing conditions. In nine of the 19 bovine cases (47.3%), supplementation with corn silage was used. The ABC test can help as a practical tool for the diagnosis of natural cases of L. monocytogenes encephalitis on formalin-fixed specimens from ovine and bovine.

Emerging infectious diseases involving zoonosis have become important global health problems. The 1998 outbreak of severe febrile encephalitis among pig farmers in Malaysia caused by a newly emergent paramyxovirus, Nipah virus, is a good example. This disease has the potential to spread to other countries through infected animals and can cause considerable economic loss. The clinical presentation includes segmental myoclonus, areflexia, hypertension, and tachycardia, and histologic evidence includes endothelial damage and vasculitis of the brain and other major organs. Magnetic resonance imaging has demonstrated the presence of discrete high-signal-intensity lesions disseminated throughout the brain. Nipah virus causes syncytial formation in Vero cells and is antigenically related to Hendra virus. The Island flying fox (Pteropus hypomelanus; the fruit bat) is a likely reservoir of this virus. The outbreak in Malaysia was controlled through the culling of >1 million pigs.

We review the clinical courses and outcomes of an outbreak of enteroviral infection that occurred in 5 children with acute lymphoblastic leukemia during a 2-month period in a hematology-oncology unit. Three patients presented with encephalitis and 2 with parotitis. Three of the 5 patients recovered uneventfully and 2 died, 1 of chronic encephalitis and 1 of acute brain stem encephalitis.

Encephalitis lethargica (EL) was a complex and mysterious disease that appeared around the same time as the great influenza pandemic of 1918. The contemporaneous relationship of the 2 diseases led to speculation that they were causally related. Contemporary and subsequent observers conjectured that the influenza virus, directly responsible for the deaths of more than 20 million people, might also have been the cause of EL. A review of the extensive literature by observers of the EL epidemic suggests that most contemporary clinicians, epidemiologists, and pathologists rejected the theory that the 1918 influenza virus was directly responsible for EL. Disappearance of the acute form of EL during the 1920s has precluded direct study of this entity. However, modern molecular biology techniques have made it possible to examine archival tissue samples from victims of the 1918 pandemic in order to detect and study the genetic structure of the killer virus. Similarly, tissue samples from EL victims can now be examined for evidence of infection by the 1918 influenza virus.

At least 70 wild green sea turtles, Chelonia mydas, died in the Moreton Bay area of southeast Queensland, Australia over 6 wk in spring 1991. Based on the necropsy of 24 turtles, there was a severe enteritis or encephalitis associated with Caryospora cheloniae, a coccidial pathogen previously recorded only in farm-reared Ch. mydas hatchlings. Infection was characterized by the presence of coccidia in extra-intestinal lesions. Oocysts were observed to sporulate, after which sporozoites escaped into seawater to form a novel stellate configuration. We conclude that C. cheloniae is pathogenic for life stages other than hatchling Ch. mydas and that naturally-occurring coccidiosis is a significant disease of free-living Ch. mydas.

Verminous encephalitis attributed to Chandlerella quiscali was diagnosed in a flock of emus (Dromaius novaehollandiae). Clinically affected birds showed torticollis and progressive ataxia. Filarioid parasites with morphological characteristics resembling C. quiscali were identified in one case. Histologic lesions in the brain and spinal cord consisted of mild to moderate perivascular cuffing and scattered areas of variable mild necrosis. Parasites observed within the parenchyma of the brain and spinal cord often were not associated with either necrosis or an inflammatory reaction. Ivermectin administered subcutaneously at 4-week intervals at a dose rate of 200 micrograms/kg body weight appeared to prevent clinical signs in flocks in the presumed endemic area.

We report here nine cases of encephalitis secondary to exanthematous diseases diagnosed from March to June 1990 at the University Hospital in Monterrey, Mexico. Two of the cases were secondary to measles, three to rubella, and four to varicella. One patient with varicella died, and the histopathological study showed findings compatible with viral encephalitis. The sex distribution was four males and five females with ages ranging from two to fourteen years. The most common clinical manifestations were hemiparesia, intracranial hypertension, meningism and altered consciousness. The CSF examination showed lymphocytic pleocytosis (mean = 295 cells), increased protein levels (mean = 118 mg/dL) and a normal glucose value in eight cases. These findings and the presence of an exanthematous disease suggested viral invasion of the CNS. Magnetic resonance imaging showed high intensity signal areas mainly in the frontal and temporal lobes. In this paper we compare the relative incidence of encephalitis secondary to exanthematous diseases in our geographical area during the last four years.

From May 1985 to December 1989, while doing blood counts on hospitalized children in Bombay, over 300 blood smears showed an impressive number of activated monocytes (AMs) and hemophagocytes (HPs). Many AMs resembled macrophages. The AM-HPs were visible in blood for 1-10 days, accompanied by a neutrophilia and a marked thrombocytopenia. Clinical features associated with these smears were fever, unresponsiveness to antibiotics, symptoms referable to the CNS and respiratory and/or gastrointestinal tracts, and bleeding. Ninety percent of affected children were under 2 years of age. The illness resolved completely or was fatal in 30%, with bleeding or respiratory failure, within 2 weeks. Children older than 2 years had underlying illness and high fever, and 40% died. Surgical candidates had obstructive gastrointestinal pathologic findings, from the stomach to the ileum. Babies under 1 month of age died, with clinical signs of deterioration and bleeding. Bone marrows were unremarkable. Few or no AM-HPs were seen. The fibrin split product tests were positive. Liver function test results were normal. Autopsies on six cases revealed edema and bleeding or thrombosis in the lungs, brain, and gastrointestinal tract. Only one neonate had a mild histiocytic infiltration in the lungs and liver. Features in common with and differences from virus-associated hemophagocytic syndromes are discussed.

The authors examined 9 children aged from 13 months to 9 years who, while being in a general hospital, contracted enteroviral encephalitis induced by Coxsackie B3 virus with a possible involvement of Coxsackie B1 virus. This report on a group hospital outbreak of enteroviral encephalitis appears to be the first of the kind in the available literature. The authors discuss the possibility of enteroviral encephalitis and Economo's encephalitis being identical in nature.

During and after a Rift Valley fever epidemic in Southern Mauritania, we observed 348 patients infected by RVF virus. 17 of them had encephalitis. These belonged to 2 groups, acute febrile forms with short duration and possibility of death, and sub-acute forms, with a longer duration and with sequelae. They were pure encephalitis, without clinical or biological meningeal signs. We also noticed 5 brutal ocular attacks, running very slowly, with sequelae.

Acute encephalitis caused by Toxoplasma gondii was diagnosed in ten patients in Belgium, the U.S.A., and Canada. None had underlying conditions usually associated with toxoplasmosis. Three had evidence of extraneural infection at necropsy. Nine patients died. Only two of the patients had a history of homosexuality, and one was a heroin addict. Five were Haitian, and four of them had lived in North America for 2-5 years. Eight of the patients had pronounced lymphopenia. Diagnosis of toxoplasmosis was hampered by a lack of suspicion that Toxoplasma could be the agent causing necrotising encephalitis in the non-immunocompromised host, the protean manifestations of the encephalitis, and a lack of a specific antibody response. The large number of cases appearing in western Europe and North America emphasise the necessity of including toxoplasmosis in the differential diagnosis of encephalitis of unknown aetiology.

A disease outbreak characterized by torticollis, incoordination, and depression was seen in a commercial broiler operation in California. Listeria monocytogenes was isolated from brain tissue with some degree of difficulty, and only after culturing directly from the brain stem. No evidence of concurrent disease was found, and the source of the outbreak was undetermined.

Clinical cases of Murray Valley Encephalitis in southeast Australia have tended to occur in summer and autumn following extended periods of above average rainfall over most of eastern and northern Australia. The Southern Oscillation, an important mode of climatic fluctuations over the Indian and Pacific Oceans, is closely related to eastern and northern Australian rainfall. The Southern Oscillation has been used previously to develop methods for predicting rainfall fluctuations over Australia and their biological and economic impacts. The relationship, therefore, between the Southern Oscillation and Murray Valley Encephalitis in southeast Australia was examined. Darwin atmospheric pressure, an index of the Southern Oscillation, was found to be well below average during the autumn, winter and spring preceding the occurrence of Murray Valley Encephalitis. It is suggested that this relationship can be used to provide a simple, objective early warning system.

Caprine arthritis-encephalitis virus (CAEV) was isolated by explant cultures of carpal synovial membrane, udder, lymph-nodes, lung and choroid plexus from six goats in two different herds with histories of arthritis-encephalitis. The virus was also isolated from milk, heparinized blood and carpal synovial fluid, using secondary goat synovial membrane cells. Virus identification was made by means of cytopathology, agar gel immunodiffusion test, immunofluorescence, in vitro host range and electron microscopy. Efficacy of different virus isolation procedures from live and necropsied animals are discussed.