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Acute disseminated encephalomyelitis (ADEM) is an immune-mediated acute inflammatory demyelinating disorder, which typically occurs after viral infections or immunisation. We present a case of a man with acute Rickettsia conorii infection whose diagnosis was delayed. He presented with fever, headache, an eschar and an acute paraplegia. The R. conorii IgM serum titre was 1:128. Magnetic resonance imaging showed multifocal lesions in the brain and spinal cord consistent with inflammatory demyelination. The patient responded well to doxycycline and a short course of high-dose corticosteroids. To our knowledge this is the first case of ADEM associated with Mediterranean spotted fever - we found a previous report of ADEM in a child with Rocky Mountain spotted fever, whose diagnosis of rickettsial infection was also delayed. We hypothesise that delayed diagnosis of spotted fever group rickettsial infections could rarely result in ADEM.

We present here the case of a previously healthy 5 year-old boy hospitalized in an intensive care unit due to tonic-clonic seizures focused on the face and right side of the body, and axillary temperature of 37.4°C. Common bacterial and viral etiology was ruled out through studies of cerebrospinal fluid (CSF) samples. Mycoplasma pneumoniae was suspected by a positive immunofluorescence serum test for IgM class antibodies. Finally, with a brain biopsy, M. pneumoniae was confirmed by polymerase chain reaction (PCR) and acute disseminated encephalomyelitis by pathological anatomy. The patient was treated with clarithromycin and had an uneventful evolution. At least to our knowledge, this is the first case in which M. pneumoniae DNA was detected by PCR in a brain biopsy., (Copyright © 2018 Asociación Argentina de Microbiología. Publicado por Elsevier España, S.L.U. All rights reserved.)

Background: A range of different neurological manifestations has been reported in fetuses and adults after Zika virus (ZIKV) infection., Objective: We describe a detection of the ZIKV in the brain tissue from a multiple sclerosis (MS) patient with acute disseminated encephalomyelitis (ADEM)-like event in Rio de Janeiro, Brazil., Methods: Biological samples collected during the hospitalization were tested by serology and molecular diagnostic for various infectious agents. Histopathological analysis was performed using the anti-flavivirus group 4G2 monoclonal antibody, anti-ZIKV non-structural 1 (NS1) monoclonal antibody, and anti-CD4, CD8, and CD11b antibodies., Results: Anti-ZIKV IgM and IgG antibodies were positive in the serum and urine. A brain biopsy showed ZIKV protein in brain cells and T CD8 infiltration in brain tissue., Conclusion: Our data describe the coexistence of a recent central nervous system (CNS) ZIKV infection accompanied by a severe ADEM-like syndrome outcome in a patient with clinical history of MS. A de novo immune response concomitant with ZIKV infection might be involved in the mechanism of the ADEM-like syndrome and response to immunotherapy. The present report reinforces the importance of providing the differential diagnosis of acute episodes of MS exacerbation in an environment prone to ZIKV expression.

We describe a case of a 25-year-old male with a diagnosis of acute disseminated encephalomyelitis (ADEM) following infection with Campylobacter jejuni, which is implicated in various human pathologies regarding the central nervous system (CNS) with acute course like Guillain-Barré syndrome (GBS), Miller-Fisher syndrome (MFS), Bickerstaff's brainstem encephalitis (BEE), acute transverse myelitis (ATM) as well as ADEM. These conditions are caused by cross-reactivity between Campylobacter's epitopes and cells of the CNS that causes an immunomediated inflammatory demyelination of the CNS. In the acute phase, magnetic resonance (MR) can detect pathologic signal intensity at the CNS with areas of pathologic contrast enhancement at cortical and spinal white matter that normalize over time or can be stable. These findings can be associated with edema in parts of the CNS. The lesions typically appear at different times during the disease course and also can have a different evolution. Our purpose therefore was to describe the clinical course and MR findings of this case and perform a critical review of the literature.

An outbreak of a disease characterized by a peculiar spiral movement in farmed greater amberjack, Seriola dumerili (Risso), occurred in Kagoshima Prefecture, Japan, in May 2008, immediately after importing the fish from China. Although neither bacteria nor viruses were detected in routine diagnostic tests, histopathological observations of the affected fish revealed severe inflammation in the tegmentum of the brain including the medulla oblongata and the anterior part of the spinal cord. In addition, a microsporidian parasite was observed in the nerve cell bodies or axons in the inflamed tissues. We identified a microsporidian small subunit rRNA gene (SSU rDNA) from the lesion, and the sequence showed 96.1% identity with that of Spraguea lophii. Subsequent in situ hybridization using probes presumably specific to the SSU rRNA confirmed that the parasite observed in histopathology harboured the identified SSU rRNA. Apparently degenerated microsporidian cells or spores were also frequently observed in tissue sections. Thus, the disease was most probably caused by the infection of a hitherto unknown microsporidian parasite that has a genetic affinity to the genus Spraguea, in the central nervous system of the amberjack., (© 2011 Blackwell Publishing Ltd.)

Introduction: Acute disseminated encephalomyelitis (ADEM) is a monophasic, inflammatory, immune-mediated disorder of the central nervous system. It is particularly difficult to distinguish between ADEM and an initial attack of multiple sclerosis (MS) clinically and based on magnetic resonance imaging (MRI) or cerebrospinal fluid. ADEM is quite rare after malaria infection. Our patient, although diagnosed provisionally of ADEM after mixed malaria infection, had neuroimaging closely simulating MS., Case Report: We report a case of a woman with an adult type 2 diabetes presenting with fever and diagnosed by antigen assay to be suffering from mixed malaria infection (Plasmodium falciparum, Plasmodium vivax). While recovering with artesunate and doxycycline therapy, she developed acute onset bladder retention followed by paraparesis. On examination she had evidence of Upper Motor Neuron (UMN) signs in all the 4 limbs along with truncal sensory loss., Discussion: Her MRI of spine showed T2 hyperintensities suggestive of resolving myelitis. MRI of the brain showed multifocal and confluent areas of demyelination mostly involving the corpus callosum and periventricular region. Lesions, particularly the callosal ones, closely simulated MS. In accordance with the McDonald Criteria and Barkhof's MRI Criteria, this patient did not fit into the diagnosis of MS. Our provisional diagnosis was ADEM.

Objective: To describe 2 patients presenting with severe neurological deficits and extensive lesions on brain magnetic resonance imaging after having experienced Legionella pneumonia., Design: Case reports., Setting: University hospital., Patients: Two patients who developed severe neurological symptoms, including encephalopathic signs, following Legionella infection, with widespread lesions on magnetic resonance imaging compatible with demyelination., Results: After extensive ancillary investigations, a diagnosis of acute disseminating encephalomyelitis was considered most likely. Steroid therapy was initiated in 1 of the patients, followed by plasmapheresis. In both patients, clinical and radiological signs gradually recovered, with only slight residual deficits., Conclusion: In patients presenting with neurological symptoms after an episode of pneumonia, Legionella infection and a subsequent immune-mediated process such as acute disseminating encephalomyelitis should be considered.

Background: Extrapulmonary complications of Mycoplasma pneumoniae infection are rare and dominated by nervous system disorders. Two patients suffering from acute disseminated encephalomyelitis associated with M. Pneumoniae infection are reported., Aim: Report of two new cases, Cases Report: The 2 cases, M. Pneumoniae infection was documented by the positivity of serology, polymerase chain reaction and culture in the respiratory tract. Patient 1 recovered after prolonged mechanical ventilation in the paediatric intensive care unit. He was fully conscious 1 month after admission and able to walk with help 2.5 months after the onset of the disease. The 2nd patient died after 9 days of hospitalisation in the intensive care unit. The death was caused by neurovegetative disorders.

We report the case of a 17-year-old male on long-term steroid therapy for minimal lesion glomerulopathy who, after an upper respiratory infection, presented with Haemophilus influenzae type b meningitis. Twenty-four hours later he developed depression of consciousness which progressed to coma and left hemiparesis. Brain magnetic resonance imaging (MRI) revealed multiple lesions (hyperintense on T2 and slightly hypointense on Tl) involving mainly white matter suggestive of inflammation. MRI features were compatible with acute disseminated encephalomyelitis (ADEM), although a differential diagnosis included cerebritis or vasculitis, secondary to bacterial meningitis. The patient was treated with high-dose steroids which resulted in a gradual improvement followed by complete clinical recovery. We propose a diagnosis of ADEM was the best diagnosis because of the radiological features and response to steroids. The occurrence of ADEM associated with acute meningitis, however rare, represents an important diagnostic challenge for the clinician.

We report an unusual case concerning encephalitis following Mycoplasma pneumonia. This interpretation corner case showed an unusual pattern of lesion distribution, resembling primary nervous system angiitis. The distribution of the lesions according to the perivascular spaces suggests a predominant leptomeningeal infiltration.

Myelitis is one of the most severe central nervous system complications seen in association with Mycoplasma pneumoniae infections and both acute transverse myelitis (ATM) as well as acute disseminated encephalomyelitis (ADEM) have been observed. We reviewed all available literature on cases of Mycoplasma spp. associated ATM as well as ADEM with dominant spinal cord pathology and classified those cases according to the strength of evidence implicating M. pneumoniae as the cause. A wide range of data on diagnosis, epidemiology, immunopathogenesis, clinical picture, laboratory diagnosis, neuroimaging and treatment for this rare entity is presented. The use of highly sensitive and specific molecular diagnostic techniques may assist in clearly elucidating the role of M. pneumoniae in ATM/ADEM syndromes in the near future. Immunomodulating therapies may have a role in treating such cases.

A 4-year-old male presented with acute disseminated encephalomyelitis with seizures and transient amaurosis after initial symptoms of a flulike febrile infection 1 week earlier. Immunoglobulin M type antibody titers against Mycoplasma pneumoniae were significantly increased in serum and cerebrospinal fluid. The patient improved appreciably on immunosuppressive therapy with immunoglobulin. This patient exemplifies a rare case of acute disseminated encephalomyelitis presenting with bilateral transient amaurosis as a complication of M. pneumoniae infection. Aydin A, Atasever S, Cakmakci H. Acute disseminated encephalomyelitis presenting with bilateral transient amaurosis.

Purpose of Review: Autoimmune disease has long been intertwined with investigations of infectious causes. Antibodies that are formed against an infectious agent can, through the process of molecular mimicry, also recognize healthy cells. When this occurs, the immune system erroneously destroys the healthy cells causing autoimmune disease in addition to appropriately destroying the offending infectious agent and attenuating the infectious process. The first infectious agent shown to cause a post-infectious autoimmune disorder in the central nervous system was Streptococcus pyogenes in Sydenham's chorea. The present review summarizes the most recent published findings of central nervous system diseases that have evidence of a post-streptococcal autoimmune etiology., Recent Findings: Sydenham's chorea and other central nervous system illnesses that are hypothesized to have a post-streptococcal autoimmune etiology appear to arise from targeted dysfunction of the basal ganglia. PANDAS (pediatric autoimmune disorders associated with streptococcal infections) is the acronym applied to a subgroup of children with obsessive-compulsive disorder or tic disorders occurring in association with streptococcal infections. In addition, there are recent reports of dystonia, chorea encephalopathy, and dystonic choreoathetosis occurring as sequelae of streptococcal infection. Investigators have begun to isolate and describe antistreptococcal-antineuronal antibodies as well as possible genetic markers in patients who are susceptible to these illnesses., Summary: Clinical and research findings in both immunology and neuropsychiatry have established the existence of post-streptococcal neuropsychiatric disorders and are beginning to shed light on possible pathobiologic processes.

Objective: To describe a case of Pasteurella multocida meningitis associated with acute disseminated encephalomyelitis (ADEM)., Case Report: A 33-year-old woman employed in a dog pound presented herself to hospital with fever and meningismus and was found to have culture positive Pasteurella multocida meningitis. Despite appropriate antibiotic treatment her clinical course was characterized by a persistent fever and worsening encephalopathy, which prompted further neurological investigation. Spinal fluid exam and serial MRI scans as well as her one-year clinical course were found to be compatible with ADEM., Conclusion: Persistent fever and worsening encephalopathy in meningitis may indicate a para-infectious immune process such as ADEM, and may serve as indications for further neurological investigation.

Objective: To describe the epidemiologic, clinical, neuroimaging, and laboratory features; treatment; and outcome in a cohort of children with acute disseminated encephalomyelitis (ADEM)., Methods: A 6-year retrospective chart review of children with the diagnosis of ADEM was conducted., Results: Eighteen cases were identified. Sixteen patients (88%) presented in either winter or spring. Thirteen children (72%) had a recent upper respiratory tract illness. Patients presented most often with motor deficits (77%) and secondly with altered consciousness (45%). Spinal fluid abnormalities occurred in 70%. Despite rigorous microbiologic testing, a definite microbiologic diagnosis was established only in 1 child with Epstein-Barr virus disease and probable or possible diagnoses in 3 children with Bartonella henselae, Mycoplasma pneumoniae, or rotavirus disease. Brain magnetic resonance imaging identified lesions in the cerebral cortex in 80%, in subcortical white matter in 93%, in periventricular white matter in 60%, in deep gray matter in 47%, and in brainstem in 47% of patients. Eleven patients (61%) were treated with corticosteroids, and 2 were treated with intravenous immunoglobulins. All patients survived. Three patients (17%) had long-term neurologic sequelae., Conclusions: Epidemiologic evidence from this study suggests an infectious cause for ADEM. The agent is most likely a difficult-to-diagnose winter/spring respiratory virus. Magnetic resonance imaging was the neuroimaging study of choice for establishing the diagnosis and for following the course of the disease. Prognosis for survival and outcome was excellent. Recurrent episodes of ADEM must be differentiated from multiple sclerosis.

Introduction: Mycoplasma pneumoniae infection has been associated with severe central nervous system diseases. The pathogenesis of these disorders is unknown and the treatment uncertain., Case Reports: The authors present three cases of central nervous system diseases: acute transverse myelitis, cerebellitis and encephalomyelitis associated with M. pneumoniae infection., Conclusions: M. pneumoniae infection should be considered in all cases of severe acute central nervous system symptomatology.

We experienced the case of a boy suffering from acute disseminated encephalomyelitis and concomitant acute glomerulonephritis. The multiple lesions observed on MR images, which located mainly in the cortical gray matter, quickly responded to methyl prednisolone pulse therapy. Renal biopsy confirmed the diagnosis of poststreptococcal acute glomerulonephritis. Streptococcus pyogenes was identified by pharyngeal culture, and the infection was serologically confirmed. We speculated that S. pyogenes infection was coincidentally involved in both diseases.

Multiphasic disseminated encephalomyelitis (MDEM) is a rare peculiar diagnosis which is defined as acute demyelinating central nervous system disease with relapses occurring only within 4 weeks of initial manifestation. This report describes the case of a 6-year-old boy with MDEM diagnosed by clinical findings and magnetic resonance imaging. The disease had a biphasic evolution, and with a second course of high-dose corticosteroids a complete recovery without further relapse was obtained during the following 18 months. Serological evidence of streptococcal infection as specific trigger for MDEM was given. Thus this report raises the question whether an additional penicillin prophylaxis could be valuable for prevention of streptococcus-associated MDEM relapses.

A 17-year-old boy presented with a severe form of an acute disseminated encephalomyelitis (ADEM) with hemiparesis and coma after initial symptoms of a flu-like febrile infection 1 week previously. Titers against Mycoplasma pneumoniae were significantly increased in serum and cerebrospinal fluid (CSF). Detection of M. pneumoniae was achieved in the initial CSF sample using M. pneumoniae-specific PCR. The patient improved significantly on antimicrobial therapy with erythromycin and immunosupressive therapy with immunoglobulins and corticosteroids. This case report demonstrates a well-documented course of a central nervous system (CNS) infection resulting in the ADEM syndrome.

Introduction: Disseminated acute encephalomyelitis is a monophasic demyelinating disease which progresses rapidly and is often fatal. It is an autoimmune condition, mediated by T lymphocytes, in which the immune response is directed against the myelin antigens., Clinical Case: We describe the clinical, radiological and neuropathological findings in the case of a 31 year old woman who, ten days after complaining of a clinical condition of upper respiratory tract inflammation, presented with unilateral focal neurological signs, subsequent rapid deterioration of consciousness and death. On autopsy the neuropathological characteristics of disseminated acute encephalomyelitis were seen., Conclusions: The relative rarity of this condition at the present time makes clinical diagnosis difficult. The differential diagnosis with other conditions may be difficult also. Thus, this disease often leads to a neuropathological diagnosis.

Inflammatory demyelinating diseases are a common cause of neurologic disability in young adults, and usually the cause is unknown. We describe a case of acute disseminated encephalomyelitis (ADEM) associated with Chlamydia pneumoniae infection. An 18-year-old previously healthy women, with a one-week history of coryzal illness, was admitted because of progressive headache, dizziness, and a left-sided hemiparesis. MR imaging of the brain and brainstem showed typical signs of ADEM. The diagnosis was established by PCR Chlamydia pneumoniae DNA positivity in a tracheal swab and by increasing titres of Chlamydia IgM antibody. The patient was treated with doxycycline and steroids and recovered completely. Apart from therapeutic implications, this case may contribute to our understanding of demyelinating diseases of the central nervous system.

Objective: After implicating Streptococcus pyogenes as causing acute disseminated encephalomyelitis (ADEM) in a child, we wanted to prove that in vivo activation of autoreactive T lymphocytes by superantigens of this Streptococcus contributed to the dramatic demyelination., Background: ADEM is a demyelinating disorder of the CNS sharing many similarities with MS. Demyelination in MS is considered to be the result of an autoimmune process mediated by autoreactive T lymphocytes with specificity for myelin antigens., Methods: Phenotypic analysis and proliferation assays on blood monocytes, as well as isolation of myelin basic protein (MBP)-reactive T-cell lines/clones; and TCR repertorium analysis by PCR-ELISA and cytokine production., Results: 1) The blood T-cell receptor (TCR) repertoire was compatible with in vivo expansion induced by S. pyogenes exotoxins. 2) TCR expression analysis indicated clonal expansion of CD8+ MBP-reactive T cells, suggesting in vivo activation. MBP-reactive T cells showed crossreactivity to S. pyogenes supernatant and exotoxins. 3) Cytokine mRNA quantification of the mononuclear cells revealed a Th2-biased profile., Conclusion: In vivo exposure to S. pyogenes may have induced activation of pathogenic myelin reactive T cells, contributing to the dramatic inflammatory demyelination.

Although acute disseminated encephalomyelitis has been observed after a variety of viral infections and an occasional bacterial infection, it has not been reported in association with rickettsial infections. Reported is a 7-year-old male with magnetic resonance images and clinical manifestations suggestive of acute disseminated encephalomyelitis after a tick bite and serologically proven Rocky Mountain spotted fever.

We report the case of a 35-year-old woman who developed headache and psychosis and gradually became comatose within 3 weeks after a flu-like infection. MRI revealed bifrontal demyelination consistent with acute disseminating encephalomyelitis (ADEM). Two different cerebrospinal fluid samples were positively tested for Legionella cincinnatiensis by direct sequencing of a PCR-amplified Legionella-specific fragment. This result made it possible to interpret the initial symptoms as Pontiac fever. We think it most likely that this is a case of ADEM following the very rare situation of a systemic infection with L. cincinnatiensis. A review of the literature on Legionella-associated encephalopathy suggests that some of these cases may also have had ADEM.

The case of a 2 1/2 year old Swiss Braunvieh heifer suffering from an acute disseminated mycotic encephalitis caused by a Mucorales spp. infection is presented. Clinical signs and analysis of cerebrospinal fluid (increased protein concentration and pleocytosis) were typical for an acute encephalitis, probably due to a listeriosis. The histological examination of the brain revealed an acute disseminated thrombo-embolic encephalomyelitis due to a fungi infection, morphologically consistent with Mucorales spp. The occurrence of bovine cerebral mucormycosis is rare and therefore the veterinarian should become aware of a case which was clinically not distinguishable from a listeriosis.

The virulence of a yellow fever (YF) virus (P-16065) isolated from a fatal case of vaccine-associated viral encephalitis was investigated. P-16065 appeared identical to its parent vaccine virus (17D-204 USA, lot 6145) when examined with monoclonal antibodies except that YF wild type-specific MAb S24 recognized P-16065 but not 17D-204 USA 6145. Thus, a mutation of at least one epitope on the envelope (E) protein had occurred. Unlike 17D-204 USA 6145 and other 17D vaccine viruses, P-16065 was neuroinvasive and virulent for mice after intranasal inoculation, and neurovirulent for monkeys after intracerebral inoculation. The E protein of P-16065 differed from 17D-204 USA by two amino acids at positions 155 and 303. Changes at amino acid position 155 are found in other YF vaccine viruses that are not neurovirulent, and it is therefore postulated that the change at position 303 is involved in the alteration of the phenotype of P-16065 and may be important for virulence of YF virus.

Four isolates of measles virus (Gag, Il, Buk and Shed) were obtained from suspensions of mononuclear cells from patients at the active stage of the disease. Vero cells were used for the virus isolation. All the isolates caused in the infected cell culture the appearance of symplasts of differently sized, star- or spindle-shaped multinuclear cells. The specificity of cytopathic effect was proved by the adsorption of monkey erythrocytes on the surface of cells infected by virus. The isolates were identified in virus neutralization (VN) and haemagglutination inhibition (HI) tests with different immune preparations: measles-globulin (standard), hyperimmune sera to rubella and mumps viruses, Sch. Zonne and Sch. Flexneria, as well as with conjugates of sera from measles patients and those vaccinated with live measles vaccine (LMV) L-16.

Results of virological examination of 239 samples taken from 84 children with neurological complications after smallpox vaccination are described. In postvaccinal encephalitis, vaccinia virus was isolated from blood, cerebrospinal fluid and pharyngeal secretions of 23 out of 40 children (57.5%) as well as from autopsy specimens sampled between 10-35 days after vaccination. During the acute period of disease, virus was detected in 17 out of 31 (54.2%) cerebrospinal fluid specimens. In 3 postvaccinal encephalitis cases the virus was present in brain and in a case of encephalomyelitis--in the spinal cord. These results confirmed the participation of vaccinia virus in the pathogenesis of postvaccinal encephalitis. The pathogenicity of vaccinia virus may be manifested only under a changed reactivity of the vaccinated host.

The results of 10-year virological and immunological studies in patients with postvaccination encephalitis (PVE) developing after smallpox vaccination are analysed. Vaccinia virus was isolated from 23 (59%) out of 39 children in the acute stage of PVE and for a long period in the protracted course of the disease in 14 out of 24 from the cerebrospinal fluid in 15 out of 33 from the blood, in 8 out of 24 from the throat and in 4 out of 5 from the brain or spinal cord tissue. Examinations of 56 serum specimens from 36 children with PVE revealed considerable variations in the levels of virus-neutralizing antibodies (VNA): 6 had no VNA, while 10 children showed low titres (10-20). No cases of agammaglobulinemia were observed. Instances of defective immune response were found which was manifested by a delay in increasing levels of IgM and IgG in response to vaccination. Two children were shown to have a defective cellular immunity. It is concluded that vaccinia virus participates in the pathogenesis of PVE; realization of the pathogenic properties of the virus requires the proper conditions, the main of which appears to consist in the immunodeficient state. The analysis of the appurtenance of 342 children to blood groups of the ABO system did not confirm the dependence of the development of postvaccination complications upon the presence in the blood of the vaccinees of the A antigen or immunological advantages of persons having alpha-isoantibodies.

Considerable variations were found in the content of virus neutralizing antibodies (VNA) to smallpox in 35 children with postvaccinal encephalitis (PVE) which developed after vaccination against smallpox: the titre of VNA was high in 7 children, negligible in 14, and in 6 children VNA were not present 3-4 weeks after vaccination. Dependence of the production of VNA on the peculiarities of individual development and premorbid state of the patients as well as on serotherapy was analysed; the role of the inhibitory effect of immunoglobulin on the process of antibody formation was excluded. No correlation was found between the isolation of vaccinia virus from the blood, liquor and throat of the children suffering from PVE (virus was isolated from 17 children) and the level of VNA. The content of immunoglobulins A, M and G in PVE patients did not essentially differ from the corresponding age norm, though the increase in IgM and IgG in response to vaccination was absent or considerably delayed in most children. Importance of the obtained results for understanding the pathogenesis of PVE is discussed.

Properties of 6 isolates of vaccinia virus isolated from the brain and cerebrospinal fluid in postvaccination encephalitis were studied in comparison with 2 production strains of vaccinia virus with which the children had been vaccinated. Significant differences were found between the strains isolated in postvaccination encephalitis and reference virus strains. The plaques produced by the isolates from brain and CSF were larger (and in some isolates had a hemorrhagic pattern). The isolates were highly pathogenic for chick embryos, reproduced more actively in cells of the chorioallantoic membrane of chick embryos at higher temperature of incubation (40 degrees C), more intensively accumulated in the liver and brain of chick embryos at 37 degrees C and 40 degrees C, produced more intensive lesions and necroses in rabbit skin. The isolates were markedly thermostable at 56 degrees C and insensitive to interferon. It is suggested that the increased pathogenicity of the virus is manifested in the presence of altered immune responsiveness of the host.

In a previously well child with no evidence of pre-existing immunologic defect a fatal encephalitis developed 10 days after administration of measles vaccine. There was pathologic evidence of an early viral encephalitis characterized by perivascular mononulcear infiltrates. Although the virus was not recovered, the diagnosis of a measles virus infection and encephalitis is supported by the postmortem findings of Warthin-Finkeldey cells in lymphoid tissues, an intranuclear inclusion in the brain and histologic changes of encephalitis.

In the province of Voyvodina 18 cases of post-vaccinal encephalitis have been recorded, three of which were fatal.The estimated morbidity rate was 0.6 per 10(5) after revaccination, and 3.9 per 10(5) after primary vaccination. The virological studies described, as well as other findings referred to in this report, are consistent with the possibility of an autoimmune aetiology of the post-vaccinal encephalitis cases observed.

The virological examination of 1365 samples taken from 469 children vaccinated against smallpox revealed considerable differences in the frequency and the time of vaccinia virus detection in different clinical forms of postvaccinal pathology as compared with uncomplicated vaccinal process. During the postvaccinal period taking its normal course vaccinia virus was isolated from 7.3% of children only from the pharynx till day 8 following vaccination. In generalized and creeping vaccinia the virus was isolated from 71.4% of children, in postvaccinal encephalitis from 57.1% of children, in vaccinal angina frove-mentioned complications vaccinia virus was detected in the samples obtained from the patients till days 24, 35, 15 and 24 respectively. The etiopathogenetic role of vaccinia virus in a number of postvaccinal complications is discussed.