Postinfectious Encephalitis Research Articles

Interferon gamma in acute and subacute encephalitis.

Intrathecal synthesis of interferon gamma was shown in 14 out of 16 samples of cerebrospinal fluid collected in the first days of disease in adults, children, and newborn infants with herpes encephalitis. This synthesis was concomitant with that of interferon alpha and was switched off when the specific antibodies in the central nervous system increased. No endogenous interferon gamma was detected in 11 serum samples or 13 samples of cerebrospinal fluid collected early in the course of the disease from patients with measles encephalitis and rubella encephalitis, or in serum and cerebrospinal fluid samples from seven patients with subacute sclerosing panencephalitis. In serum collected after the 10th day after the onset of neurological symptoms interferon gamma was present at low concentrations in only three out of 11 serum specimens from patients with measles encephalitis or rubella encephalitis. Interferon gamma was present in patients with acute herpes encephalitis and there was active virus replication, but it was not present in postinfectious encephalitis. Possibly the local production of specific antibodies masks the viral antigens and switches off the induction of interferons.

Soluble IL-2 receptors in acute and subacute encephalitis.

Elevated levels of soluble interleukin-2 receptors were present in the serum from patients with acute primary and postinfectious encephalitis and subacute sclerosing panencephalitis. In addition, soluble interleukin-2 receptors were detected in the cerebrospinal fluid from patients with acute primary encephalitis. Their presence in the cerebrospinal fluid was not explained by damage to the blood-brain barrier and our data attest to their local origin. This suggests that it may be possible in certain neurological diseases to detect cerebral T-lymphocyte activation through a specific marker in the cerebrospinal fluid.

Cellular immune responses during complicated and uncomplicated measles virus infections of man

Lymphocytes from patients with measles showed profound and prolonged suppression of proliferative responses to mitogens. The degree of suppression was similar in patients with uncomplicated measles virus infection and in those with pneumonia or postinfectious encephalitis. Despite this suppression, lymphocyte responses to measles antigen and PPD were demonstrated in patients with encephalitis and uncomplicated disease, even early in infection. Most patients with pneumonia did not have demonstrable antigen-specific responses. The proportions of T helper (OKT 4) and T suppressor (OKT 8) cells and functional tests of Con A suppressor cell activity showed no significant difference between control and measles patients but, in contrast to controls, cells from measles patients cultured in the absence of any stimulant significantly suppressed the proliferation of allogeneic responder cells. Nine of 20 supernatant fluids from these cultures possessed a soluble suppressor factor. These studies indicate varied disruptions of immune reactivity during measles.

Immune Response in the CSF in Viral Infections

The local humoral immune response in inflammatory diseases of the central nervous system (CNS) is reflected by an increase in gamma-globulin in the cerebrospinal fluid (CSF) and, more significantly, by the occurrence of oligoclonal gamma-banding. In the detection of local immunoglobulin synthesis, the possibility of changes in the serum gamma-globulin and increased permeability of the blood-CSF barrier to proteins has to be taken into consideration. This chapter evaluates the gamma-globulin reaction in various acute, prolonged, and chronic CNS-infections of viral or presumed viral origin. In addition, the degree of the concomitant blood-CSF barrier disturbance is determined. By stereotyped changes of the CSF-protein spectrum, two pathologic reactions can be defined: the pattern of local immune response, and the pattern of blood-CSF barrier disturbance. The chapter focuses on the local immune response that leads to increase of gamma3-globulin and synthesis of oligoclonal gamma-fractions. In acute aseptic meningitis, minimal or no abnormal gamma-globulin increases are observed. In acute para- and postinfectious encephalitis, however, a marked local humoral immune response may occur. The most striking increases in gamma-globulin can be noticed in herpes simplex virus encephalitis during phases of clinical improvement.

Pathology of viral leukoencephalomyelitis of goats.

The morphologic changes of viral leukoencephalomyelitis of goats (VLG), an afebrile paralytic disease of 2–4 month old kids, were studied in 13 naturally infected goats: 11 during the first 5–22 days of clinical disease and two that survived 8 months and 3 years after onset of clinical signs. Lesions in the early clinical phase of the disease included interstitial pneumonia and widely disseminated myelinoclastic perivascular lesions in the brain and spinal cord. In the central nervous system, hypertrophied and hyperplastic reticulin fibers of the vascular sheath encompassed an inflammatory cell infiltrate composed of lymphocytes, plasma cells, and macrophages. Occasionally, malacia occurred, and several animals had transverse myelitis. Neuronal necrosis and neuronophagia were not features of the disease. Lesions were most frequent in the subpia and subependyma. Pulmonary lesions were not present in goats that survived the initial clinical phase of the disease, but myelin had disappeared from large areas of the spinal cord and from small foci in the brain. Nodular accumulations of mononuclear cells and small perivascular cuffs were also present in the central nervous system. VLG resembles visna in the topographic distribution and myelinoclastic nature of its lesions. Like visna, it bears some resemblance to post-infectious encephalitis of man.

ISOLATION OF INFECTIOUS MEASLES VIRUS IN MEASLES ENCEPHALITIS

A 40-year-old man developed encephalitis 3 days after onset of acute measles. He died 6 weeks later. Histopathological findings were consistent with late type of post-infectious measles encephalitis. Direct inoculation of a homogenate of fresh brain tissue obtained at necropsy into susceptible tissue cultures produced no infectious virus. However, co-cultivation of cells derived from this brain tissue with those of a continuous line of African green monkey kidney tissue culture yielded an infectious virus that was identified as measles.

Fatal mumps meningoencephalitis. Isolation of virus premortem and postmortem.

Mumps virus was recovered from both premortem cerebrospinal fluid and postmortem testicular tissue obtained from an 8-year-old boy with fatal meningoencephalitis. There was histologic evidence of both primary encephalitis with acute invasion of the central nervous system by virus and secondary postinfectious encephalitis with demyelination. With a safe and effective live, attenuated mumps vaccine available, a reappraisal of its place in immunization schedules is urged.

INCLUSION BODIES IN MEASLES ENCEPHALITIS

In 1964, there were 458,083 cases of measles reported by the individual states and territories of the United States through the National Morbidity Reporting System and 300 cases of measles encephalitis. 1 in 1963, a total of 364 deaths were attributed to measles. History has recorded numerous devastating epidemics of measles attacking entire populations of susceptible individuals. In modern civilizations, measles has become accepted as an almost inevitable part of growing up, to the point where a safe and effective vaccine capable of preventing the disease has been accepted slowly for widespread use by the public. This has occurred in spite of the fact that few parents who have suffered through even an uncomplicated case of measles in their own children would deny that it is a severe disease. The most serious complication of measles is encephalitis, generally classified as a postinfectious encephalitis. The frequency of clinical encephalitis complicating measles

Current status of diagnosis and therapy of encephalitis.

Encephalitis is a primary inflammatory process in the brain, with resulting disturbance of brain function. For clinical purposes, the disease can be said to be infectious or postinfectious. For the most part, the infectious encephalitides are caused by intracellular parasites: viruses and, less commonly, rickettsiae. The great epidemic of encephalitis in the 1920's (the so-called von Economo's type of encephalitis) is believed to belong in the virus infection group, although no agent was ever isolated.1All of the bacterial, mycotic, treponemal, and parasitic meningitides can cause an associated encephalitis in the underlying brain, but these are generally classified with the meningitides. The postinfectious encephalitides are believed to represent damage to the nervous system as a part of an allergic response to a preceding infection, usually viral. The entity of postvaccinal encephalitis, similar clinically and pathologically to postinfectious encephalitis, is an occasional complication of vaccination with a virus vaccine (i.

Phosphatases and phospholipases in the central nervous system. A study in normal states and in experimentally induced disseminated allergic encephalomyelitis.

Experimentally produced disseminated allergic encephalomyelitis closely resembles certain spontaneously occurring demyelinating diseases in humans for which no etiologic agent has been discovered. 1 These include the postinfectious encephalitides and the encephalomyelitis which sometimes follows rabies and smallpox vaccinations. These conditions present the same clinical symptoms and identical histopathological manifestations. The pathogenesis of multiple sclerosis may be primarily a biochemical derangement of the central myelin. 2 The breakdown process is usually restricted to segments of myelin sheaths within the central nervous system. This has suggested that the hypothetical biochemical lesion occurs in myelin segments, in axons, or in the oligodendrocytes, but not primarily in the neuron bodies. It may be that the demyelination is related to an enzyme concerned with the physiology of conduction rather than with any of the lipases. 3 The limitations of microscopic histochemistry are twofold: ( a ) It is not quantitative, although the methods proposed by Coujard, 4

Mumps encephalitis: Pathology and pathogenesis

Summary 1. The literature concerning the pathology of mumps encephalitis has been reviewed. 2. Two cases of fatal mumps meningoencephalitis with histopathological studies have been reported. 3. The fundamental lesion was a perivascular demyelinization similar to that seen in other postinfectious encephalitides. 4. It is suggested that the encephalitis may be due to the virus of the associated disease.

Public-health aspects of the virus encephalitides.

VIRUS encephalitides are best discussed in three groups: virus encephalitides caused by familiar viruses not ordinarily encephalitogenic; suspected, primary virus infections; and primary virus infections.Virus encephalitides can be caused by ordinarily nonencephalitigenic viruses, which are those of herpes simplex, measles, lymphogranuloma venereum, mumps and infectious mononucleosis (probably due to a virus). Although secondary or post-infectious encephalitis has not as yet been shown to be caused by a virus, the illness occurs within a few days to a few weeks after various virus infections, such as measles, mumps, influenza, chicken pox, vaccinia, smallpox and infectious hepatitis and after vaccination against . . .

POSTINFECTIOUS ENCEPHALOMYELITIS

Recent years have seen increased interest in postinfectious and postvaccinal encephalitis and realization of the prevalence of bromide poisoning. A case is presented in which these conditions occurred simultaneously. <h3>REPORT OF A CASE</h3> W. W., a 9 year old white boy, was first seen Aug. 2, 1939. The chief complaint was "jerking and twitching" of six weeks' duration. <i>History.</i>—Fifteen weeks earlier he had contracted measles and was moderately ill. He stayed in bed one week but was out of school two weeks longer because of excruciating headaches, which started about a week after the onset of measles. The headaches were severe enough to make him stop whatever he was doing and run to lie down. They occurred every day or two and lasted from three hours to a day. There was occasional nonprojectile emesis. He received pills (nature unknown) for the pain but obtained no relief. After two weeks,

Hormone Treatment of Prostatic Hypertrophy

<h3>Objective:</h3> To report a case of Post-Malaria Neurological Syndrome presenting in the US in a returning Peace Corps volunteer <h3>Background:</h3> Post-Malaria Neurological Syndrome (PMNS) is a rare post-infectious encephalitis which occurs 4 to 60 days after recovery from severe <i>falciparum</i> malaria. There is a proclivity for non-immune travelers visiting endemic areas. <h3>Design/Methods:</h3> A 24-year-old man presented with acute onset fever, impaired consciousness, tremors and generalized tonic-clonic seizures. One month prior he had successfully completed treatment for P. <i>falciparum</i> malaria contracted while working in Togo, Africa. On exam temperature was 38.0 C. He exhibited neck rigidity with Kernig’s and Brudzinski’s signs. Glasgow Coma Scale was 6. There was generalized hyper-reflexia. Babinski signs were absent. Peripheral WBC 15.3, Neutrophils 76%. Cerebrospinal fluid (CSF) analysis: WBC 65, lymphocytes 91%, protein 65, Glucose 64. Four malaria smears, DNA PCR and malaria antigen were negative. CSF infectious panel was also negative. Patient received empiric antibiotics with no improvement. After initiation of high dose glucocorticoids he demonstrated rapid improvement with complete recovery in seven days. <h3>Results:</h3> PMNS must be distinguished from relapse of malaria or cerebral malaria (CM). CM is an encephalopathy occurring during acute malaria infection where parasitemia and other manifestations of malaria such as acidosis, hemolysis, renal and hepatic failure are also present. In PMNS, there is a disease-free interval between treated malaria and the onset of neurological symptoms, parasitemia is absent and other organ systems are not involved. MRI abnormalities consist of increased T2-weighted signal in periventricular area, internal capsule, pons, thalamus and corona radiata. It is usually self-limited, lasting 2–14 days, and requires no specific treatment. Steroids may play a role in severe cases. <h3>Conclusions:</h3> It is prudent to consider and distinguish the diagnosis of Post Malaria Neurological Syndrome in a patient who presents with new onset neurological symptoms with recent malaria infection in the background. <b>Disclosure:</b> Dr. Waseem has nothing to disclose. Dr. Singh has nothing to disclose. Dr. Bradshaw has received research support from Cytokinetics, Catalyst.

ACUTE, TOXIC (NONSUPPURATIVE) ENCEPHALITIS IN CHILDREN

In the present study are recorded the clinicopathologic observations in five cases which may generally be classified as acute, toxic, non-suppurative encephalitis. The first three cases presented a rather unusual, though characteristic pathologic picture in the form of acute and peracute processes of liquefaction. In the last two cases, the pathologic changes were less characteristic and corresponded largely with the condition ordinarily described in toxic, noninflammatory lesions of the brain. The clinical features in cases 1 and 4 were discussed by Beverly,1who, however, did not give a detailed pathologic description. Nonsuppurative encephalitis has been known to occur: (1) as hemorrhagic encephalitis of the Struempell and Leichtenstern2type; (2) as postinfectious encephalitis, a sequel both to the exanthematous diseases and to influenza, as described by Oppenheim,3Abt4and others; (3) as epidemic encephalitis. But in recent years, a series of cases has been reported by various