Presence Of Pleocytosis Research Articles

Tick-borne encephalitis in a dog

Tick-borne encephalitis (TBE) is an infectious disease transmitted by ticks and rarely diagnosed in dogs. The diagnosis of a TBE virus infection in a living animal is based on the simultaneous presence of typical clinical-neurological signs, an acute and rapidly progressive course of the disease, the detection of TBE-specific antibodies (in the cerebrospinal fluid) or virus detection (in blood or cerebrospinal fluid), as well as the presence of pleocytosis in the cerebrospinal fluid. In the case described, the results of the performed tests led to the assumption of the presence of TBE. In addition to hyperthermia and central nervous disorders (ataxia, hyperaesthesia, seizures, changes in behavior) the classic symptoms of clinically overt TBE frequently include neck pain on flexion of the cervical spine. In the case described, a chronic form of the disease with a regeneration period of several months is documented. Treatment is based on symptomatic measures, as there is no specific therapy to date. In contrast to human medicine, there is no vaccine against TBE currently approved for use in the veterinary field. Therefore, tick prophylaxis is the only possibility to prevent TBE in dogs.

Cerebrospinal fluid type I interferon and cytokine profiles in enteroviral meningitis according to the presence or absence of pleocytosis

Enteroviral meningitis is typically diagnosed as the presence of pleocytosis and of viral RNA in cerebrospinal fluid. However, it was recently reported that more than 50% of infants with enteroviral meningitis diagnosed by polymerase chain reaction had no cerebrospinal fluid pleocytosis. This study investigated type I interferon (IFN) and cytokine profiles in the cerebrospinal fluid based on the presence or absence of cerebrospinal fluid pleocytosis in children with enteroviral meningitis. We included 51 enteroviral meningitis patients showing cerebrospinal fluid pleocytosis (pleocytosis group), 31 enteroviral meningitis patients without cerebrospinal fluid pleocytosis (non-pleocytosis group), and 52 controls (control group) and compared cerebrospinal fluid interleukin 6 (IL-6), IL-8, chemokine (C-X-C motif) ligand 10 (CXCL-10), IFN-α, and IFN-β levels. A significant difference was observed in IL-6, IL-8, and CXCL-10 levels across the three groups, with highest values in the pleocytosis patients, followed by those in the non-pleocytosis and control subjects. IFN-α level was higher in the pleocytosis group than in the non-pleocytosis and control groups. Meanwhile, the IFN-β level was higher in the pleocytosis and non-pleocytosis groups than in the control group (34.54 [31.23-38.59] pg/mL vs. 33.21 [31.23-35.21] pg/mL vs. 0.00 [0.00-0.00]pg/mL, respectively; P<0.001). Furthermore, cerebrospinal fluid IFN-β was detected in all patients with enteroviral meningitis, except one (98.8%) regardless of pleocytosis, whereas it was detected in only two (3.8%) control subjects (P<0.001). The cerebrospinal fluid cytokine profiles remarkably differed based on the presence or absence of cerebrospinal fluid pleocytosis. Further investigations are required to determine whether cerebrospinal fluid IFN-β could be used as a surrogate marker of viral meningitis instead of cerebrospinal fluid pleocytosis.

Neurological complications associated with dengue virus infection

Dengue is an arboviral infection caused by the dengue virus. The neurological complications associated with this infection are reviewed. The neurotropic nature of dengue virus has been confirmed in epidemiological studies, case series and histopathological studies. The range of neurological complications is 5.6-14.6%, and they are more frequent in serotypes 1 and 3. Encephalopathy is the most common neurological syndrome (0.5-6%) and its prevalence is higher in children and adolescents. The detection of the viral antigen in brain tissue and the presence of pleocytosis or RNA in cerebrospinal fluid are evidence of the neurotropic nature of dengue virus, which manifests itself in the form of encephalitis. Neurological syndromes during convalescence (disseminated acute cerebellitis, opsoclonus-myoclonus syndrome, mononeuritis, poly-radiculoneuritis and plexitis) appear to be immunomediated. Myelitis can occur during acute dengue virus infection and through an immunomediated mechanism in the convalescence phase. Myalgias, myositis, rhabdomyolysis and hypokalemic paralysis are examples of muscular dysfunction associated with the dengue virus. The incidence of stroke is 0.26%, and may be ischaemic or haemorrhagic. Ophthalmological complications include maculopathy, retinal haemorrhage, optic neuropathy and vitritis. The spectrum of neurological complications from dengue virus is broad. There are no reliable data on its real incidence because most of the studies published to date are isolated series or cases.

Varicella-zoster meningoencephalitis — Case report

Introduction: Encephalitis is defined as inflammation of the brain parenchyma and meningoencephalitis when there is meningeal involvement. A viral etiology is the most common and the diagnostic method of choice is the polymerase chain reaction (PCR) of viral nucleic acids in cerebrospinal fluid (CSF). Herpes simplex virus is the leading cause of encephalitis and varicella-zoster virus (VZV) a less common cause, particularly in immunocompetent individuals. Case report: Woman, 67 years old, retired nurse, brought to the emergency room by disorientation. Physical examination: slowed, disoriented, incoherent and repetitive speech; subfebrile (T-37, 2 °C); no meningeal signs or skin lesions were identified. Laboratory tests revealed leukocytosis (10.5 × 10 ^9/L) with neutrophilia (86.9%). Computed tomography and magnetic resonance imaging (MRI) of the brain were performed and there were no lesions on brain parenchyma. Lumbar puncture (LP): 5 leukocytes/mm3; erythrocytes 2327/mm3; glucose: 80 mg/dl, and protein 26.7 mg/dl. Blood, cerebrospinal fluid cultures and capsular antigens were collected. The patient had clinical worsening at 48 h with fever (T-38, 7 °C), agitation, seizures, left hemiparesis and meningeal signs. LP was repeated: leukocytes 40/mm (98% of polymorphonuclear cells), glucose: 113 mg/dl, and protein: 30.4 mg/dl. CSF cultures were repeated and viral PCR in cerebrospinal fluid was requested. Human immunodeficiency virus testing was negative. Empirically ceftriaxone, ampicillin and acyclovir 10 mg/Kg ev, 8/8 h was established. Electroencephalography revealed severe cortical structural damage in the left hemisphere. MRI of the brain was repeated and showed no lesions. Microbiological study was negative and VZV PCR in CSF was positive. She completed 21 days of acyclovir. The patient had a good clinical and neurologic outcome with resolution of all the symptoms. Conclusion: VZV meningoencephalitis. The case stands out for infection of the central nervous system by VZV in an immunocompetent patient, along with the importance of a high clinical suspicion of viral encephalitis even in the presence of pleocytosis with a predominance of polymorphonuclear cells in the early phase of infection. The suspicion of encephalitis is critical in the decision of early antiviral therapy to prevent neurological sequelae.

Increased Recognition of Powassan Encephalitis in the United States, 1999–2005

Powassan virus (POWV) disease is a rare human disease caused by a tick-borne encephalitis group flavivirus maintained in a transmission cycle between Ixodes cookei and other ixodid ticks and small and medium-sized mammals. During 1958-1998, only 27 POWV disease cases (mostly Powassan encephalitis) were reported from eastern Canada and the northeastern United States (average, 0.7 cases per year). During 1999-2005, nine cases (described herein) of serologically confirmed POWV disease were reported in the United States (average, 1.3 cases per year): four from Maine, two from New York, and one each from Michigan, Vermont, and Wisconsin. The Michigan and Wisconsin cases are the first ever reported from the north-central United States. Of these nine patients, 5 (56%) were men, the median age was 69 years (range: 25-91 years), and 6 (67%) had onset during May-July. All but one patient developed encephalitis with acute onset of profound muscle weakness, confusion, and other severe neurologic signs. In one case, no neurologic symptoms were present but the presence of pleocytosis, an elevated cerebrospinal fluid (CSF) protein concentration, and POWV-specific immunoglobulin M in CSF suggested neuroinvasion. All patients recovered from their acute disease, but most had long-term neurologic sequelae. Periresidential ecologic investigations were performed in three cases, including tests of local mammals and ticks for evidence of POWV infection. Woodchucks (Marmota monax), striped skunks (Mephitis mephitis), and a raccoon (Procyon lotor) collected at two of the Maine case-patients' residences had neutralizing antibody titers to POWV. I. cookei were found on woodchucks and skunks and questing in grassy areas of one of these residences; all were negative for POWV. Although POWV disease is rare, it is probably under-recognized, and it causes significant morbidity, and thus is an additional tick-borne emerging infectious disease entity. Because no vaccine or specific therapy is available, the basis of prevention is personal protection from ticks (or "tick hygiene") and reduced exposure to peridomestic wild mammals.

C6‐peptide serology as diagnostic tool in neuroborreliosis

The aim of this study was to evaluate the usefulness of borrelia serology (Quick ELISA C6 Borrelia assay kit) as a diagnostic tool in cases of suspected neuroborreliosis. A retrospective patient material consisting of 124 paired serum and cerebrospinal fluid samples with a positive anti-borrelia antibody index (AI) using the IDEIA Lyme Neuroborreliosis test was compared with 124 AI-negative matched control subjects. The patients were divided into four groups based on presence of pleocytosis and age above or below 12 years. The presence of positive C6 serology in AI-positive patients with pleocytosis was 89% (83/93), significantly different (p<0.01) from in patients without pleocytosis (58%, 18/31). In AI-positive patients aged > or =12 years with pleocytosis, 94% (51/54) had a positive C6 serology. Of AI-positive patients with a symptom duration of more than 30 days, 93% (27/29) were positive by the C6 test. We conclude that the C6 serum test, together with clinical evaluation, is a powerful diagnostic tool in adult (> or =12 years) European patients with suspected neuroborreliosis with a symptom duration of more than 30 days. Patients with suspected neuroborreliosis and positive C6 results should be further investigated by lumbar puncture for definite diagnosis.

Neuroborreliose: klinisches Spektrum, Diagnose und Therapie

Borreliosis is a tick-borne disease which is endemic in many states of Europe and the USA. It manifests itself with a broad clinical spectrum, mainly involving skin, nervous system, heart and joints. The neurological manifestations were first recognised in the early twenties of the last century in a patient with meningoradiculitis after erythema migrans following a tick bite. This was later called Garin-Bujadoux-Bannwarth's syndrome. The clinical spectrum of well-documented neuroborreliosis includes lymphocytic meningitis, cranial neuropathy, motoric or sensoric meningoradiculitis and mononeuritis multiplex as manifestations of early dissemination. In addition, peripheral neuropathy and chronic encephalomyelitis are observed in late disseminated disease. Meningitis is characterised by subtle clinical symptoms. Stiff neck and cephalea are the leading symptoms which can, however, even be lacking in PCR-proven Borrelia meningitis. Unfortunately, PCR has a low sensitivity (<50%) in patients with lymphocytic meningitis presenting with a classical case history and positive Borrelia antibodies. The most frequent cranial neuropathy is facial palsy. In endemic regions it is caused by Borrelia burgdorferi as frequently as by the Varicella-Zoster virus. The diagnosis of Borrelia meningitis or cranial neuropathy requires a typical history (tick bite and/or erythema migrans) together with a positive serology confirmed by Western blotting. Meningoradiculitis is a classical manifestation of early dissemination of Borrelia burgdorferi in the central nervous system. Key symptoms are dysaesthesia, distressing migrating pain and occasionally peripheral nerve paresis. Chronic encephalomyelitis is characterised by spastic paraparesis, bladder dysfunction, ataxia, cephalea, fatigue, malaise, sleep disturbance and cognitive impairment. Due to the high Borrelia burgdorferi seroprevalence in Switzerland (14.7%), positive serum antibodies indicate only previous infection, but not disease. Only the evidence of intrathecal specific antibody response proves meningitis, radiculitis and chronic encephalomyelitis. PCR-testing does not resolve the diagnostic dilemma because the sensitivity is as low as 40% in early meningitis and 20% in chronic encephalomyelitis. Polyneuropathy is a late manifestation which usually occurs together with acrodermatitis atrophicans. Treatment of borreliosis is well established. Cranial neuropathy is treated with doxycycline or amoxicillin during 14-21 days. A diagnostic lumbar puncture is not required because there are no data about the need of different treatments according to the absence or presence of pleocytosis. Patients with symptomatic meningitis, meningoradiculitis or polyneuropathy require an iv-treatment with ceftriaxone or cefotaxime (14-28 days). In patients with chronic meningoencephalitis, still symptomatic after previous treatment, there is no benefit of prolonged antibiotic treatment. In a placebo-controlled study with a sequential iv/oral treatment with ceftriaxone and doxycycline during 90 days, no benefit at all was observed in the antibiotic treated patients.

Penicillin concentrations in cerebrospinal fluid and serum after intramuscular, intravenous, and oral administration to syphilitic patients

Penicillin concentration in serum and cerebrospinal fluid (CSF) were estimated in 19 syphilitic patients given three different regimens: Penicillin G, 10 MIU i.v. three times a day (3 patients); procaine penicillin, 600 000 IU i.m. (11 patients); and penicillin V, 1.2 MIU by mouth four times a day (5 patients). Intravenous administration of penicillin G resulted in a penicillin concentration in CSF of 0.3-0.5 micrograms/ml; In contrast, procaine penicillin, i.m. and penicillin V by mouth did not result in any measurable CSF concentration, even in the presence of pleocytosis and/or barrier lesion. Penicillin V by mouth gave considerably higher serum concentrations than procaine penicillin intramuscular, however. In the light of these results, and reported treatment failures in neurosyphilis and demonstration of viable Treponema pallidum after treatment, we propose that neurosyphilis should be treated with high intravenous doses of penicillin to ensure treponemicidal concentrations in the central nervous system.