Lyme disease is a multisystem disorder transmitted through the Ixodes tick and is most commonly diagnosed in northeastern and mid-Atlantic states, Wisconsin, and Minnesota, though its disease borders are expanding in the setting of climate change. Approximately 10%-15% of untreated Lyme disease cases will develop neurologic manifestations of Lyme neuroborreliosis (LNB). Due to varying presentations, LNB presents diagnostic challenges and is associated with a delay to treatment. We discuss three cases of LNB admitted to our referral center in a traditionally low-incidence state to highlight clinical pearls in LNB diagnosis. Three patients from low-incidence areas with prior diagnostic evaluations presented in August with neurologic manifestations of radiculoneuritis, cranial neuropathies, and/or lymphocytic meningitis. MRI findings included cranial nerve, nerve root, and leptomeningeal enhancement leading to broad differential diagnoses. Lumbar puncture demonstrated lymphocytic pleocytosis (range 85-753 cells/uL) and elevated protein (87-318 mg/dL). Each patient tested positive for Lyme on two-tiered serum testing and was diagnosed with LNB. All three cases were associated with a delay to health care presentation (mean 20 days) and a delay to diagnosis and treatment (mean 54 days) due to under-recognition and ongoing evaluation. With the geographic expansion of Lyme disease, increasing awareness of LNB manifestations and acquiring detailed travel histories in low-incidence areas is crucial to prompt delivery of care. Clinicians should be aware of two-tiered serum diagnostic requirements and use adjunctive studies such as lumbar puncture and MRI to eliminate other diagnoses. Treatment with an appropriate course of antibiotics leads to robust improvement in neurological symptoms.

BACKGROUND: Streptococcus intermedius is a member of the S. anginosus group and is part of the normal oral microbiota. It can cause pyogenic infections in various organs, primarily in the head and neck area, including brain abscesses and meningitis. However, ventriculitis due to periodontitis has not been reported previously.
METHODS: A 64-year-old male was admitted to the hospital with a headache, fever and later imbalance, blurred vision, and general slowness. Neurological examination revealed nuchal rigidity and general clumsiness. Meningitis was suspected, and the patient was treated with dexamethasone, ceftriaxone and acyclovir. A brain computer tomography (CT) scan was normal, and cerebrospinal fluid (CSF) Gram staining and bacterial cultures remained negative, so the antibacterial treatment was discontinued. Nine days after admission, the patient\'s condition deteriorated. The antibacterial treatment was restarted, and a brain magnetic resonance imaging revealed ventriculitis. A subsequent CT scan showed hydrocephalus, so a ventriculostomy was performed. In CSF Gram staining, chains of gram-positive cocci were observed. Bacterial cultures remained negative, but a bacterial PCR detected Streptococcus intermedius. An orthopantomography revealed advanced periodontal destruction in several teeth and periapical abscesses, which were subsequently operated on. The patient was discharged in good condition after one month.
CONCLUSIONS: Poor dental health can lead to life-threatening infections in the central nervous system, even in a completely healthy individual. Primary bacterial ventriculitis is a diagnostic challenge, which may result in delayed treatment and increased mortality.

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OBJECTIVE: Diagnosing and treating postoperative central nervous system infections (PCNSIs) remains challenging due to the low detection rate and time-consuming nature of traditional methods for identifying microorganisms in cerebrospinal fluid. Metagenomic next-generation sequencing (mNGS) technology provides a rapid and comprehensive understanding of microbial composition in PCNSIs by swiftly sequencing and analyzing the microbial genome. The current study aimed to assess the economic impact of using mNGS versus traditional bacterial culture-directed PCNSIs diagnosis and therapy in post-neurosurgical patients from Beijing Tiantan Hospital. mNGS is a relatively expensive test item, and whether it has the corresponding health-economic significance in the clinical application of diagnosing intracranial infection has not been studied clearly. Therefore, the investigators hope to explore the clinical application value of mNGS detection in PCNSIs after neurosurgery.

Brucellosis is one of the most common zoonosis worldwide, affecting 500 000 people, annually. Neurobrucellosis incidence is approximately 4%, and it is almost always heterogeneous. As there are no typical clinical features, its diagnosis is frequently misdiagnosing by other infections.
Neurobrucellosis picture includes meningitis, meningoencephalitis, encephalitis, cranial neuropathies, intracranial hypertension, sinus thrombosis, hemorrhages radiculitis, peripheral neuropathy, myelitis, and psychiatric manifestations. The diagnosis should be based on symptoms and signs suggestive of neurobrucellosis, not explained by other neurological disease, cerebrospinal fluid analysis, a positive Brucella serology or culture, and a response to specific antibiotics, with a significant improvement of cerebrospinal fluid parameters.
Neurobrucellosis can be insidious, and despite its global distribution, it is still unrecognized and frequently goes unreported. The understanding of the current epidemiology is necessary for eradication of the disease in humans, as well as the disease control in animals and prevention based on occupational hygiene and food hygiene.

Neuroretinitis due to Bartonella henselae infection is a rare cause of vision loss in children. Two pediatric cases of acute unilateral vision loss accompanied by edema of the optic nerve on fundoscopic examination are presented. Severe causes of vision loss were excluded. During the course of the disease, macular stellate exudates emerged on control fundoscopic examinations, and diagnosis of neuroretinitis was made. A causative agent was confirmed by serologic examination, as high titers of IgM and IgG antibodies to Bartonella henselae were detected. Both patients significantly recovered after oral antibiotic treatment.

Brucellosis is an endemic disease in Saudi Arabia, which can present with variable clinical manifestations. It is a zoonotic disease transmitted from animals to humans. Brucellosis is a multisystemic disease that can present with any system involvement; and neurobrucellosis is a serious complication, sometimes leading to permanent neurological deficit, if treatment is not started promptly. Herein, we present a 6-year boy with neurobrucellosis, who developed demyelination of cerebral white matter and presented with fever and seizures. Key Words: Neurobrucellosis, Demyelination, White matter.

The present report describes outbreaks of Streptococcus gallolyticus subsp. pasteurianus in young geese flocks in Austria. The flocks, comprising 160-1450 goslings of 2-3 wk of age, experienced increased mortalities The clinical signs were characterized by severe central nervous symptoms, namely leg paddling and torticollis. The postmortem investigation revealed hepatitis, splenitis, and a low amount of liquid fluid in the coelomic cavity. Livers were of fragile texture, with white necrotic areas. The latter were also found in spleens. No macroscopic lesions were seen in brains. Bacteriologic investigation followed by bacterial identification by matrix-assisted laser desorption time-of-flight mass spectrometry and phylogenetic analysis of the partial 16S rRNA region revealed the presence in heart, liver, spleen, and brain of S. gallolyticus subsp. pasteurianus. Histologic investigation revealed multifocal necrosis in liver and spleen samples together with infiltration of mononuclear cells and heterophilic granulocytes. Furthermore, in the lesions, coccoid bacteria could be identified. No histopathologic changes were observed in brain samples from goslings, except in one bird in which accumulation of coccoid bacteria in blood vessels of the brain samples was present. Antibiotic sensitivity tests revealed identical profiles for all strains, which were susceptible to penicillins, cephalosporins, chloramphenicol, imipenem, and tylosin. However, resistance was found against quinolones, aminoglycosides, tetracycline, and trimethoprim-sulfamethoxazole, which are commonly used to treat infections with gram-positive bacteria.
Reporte de caso—Brotes de Streptococcus gallolyticus subsp. pasteurianus en gansitos caracterizados por síntomas nerviosos centrales. El presente informe describe brotes de Streptococcus gallolyticus subsp. pasteurianus en parvadas de gansos jóvenes en Austria. Las bandadas, que comprendían entre 160 a 1450 gansos de 2 a 3 semanas de edad, experimentaron aumento de la mortalidad. Los signos clínicos se caracterizaron por síntomas severos del sistema nervioso central, incluyendo, movimientos de pataleo y tortícolis. La investigación post mórtem reveló hepatitis, esplenitis y la presencia de líquido en la cavidad celómica en poca cantidad. Los hígados presentaron textura frágil, con áreas necróticas blancas. Estos últimos también se encontraron en bazos. No se observaron lesiones macroscópicas en el cerebro. La investigación bacteriológica seguida de la identificación bacteriana mediante espectrometría de masas MALDI-TOF y el análisis filogenético de la región parcial de ARNr 16S revelaron la presencia en el corazón, el hígado, el bazo y en el cerebro de S. gallolyticus subsp. pasteurianus. La investigación histológica reveló necrosis multifocal en muestras de hígado y bazo junto con infiltración de células mononucleares y granulocitos heterófilos. Además, en las lesiones se pudieron identificar bacterias de morfología cocoide. No se observaron cambios histopatológicos en muestras de cerebro de los gansitos, excepto en un ave en la que se observó acumulación de bacterias cocoides en los vasos sanguíneos de las muestras de cerebro. Las pruebas de sensibilidad a los antibióticos revelaron perfiles idénticos para todas las cepas, que eran susceptibles a penicilinas, cefalosporinas, cloranfenicol, imipenem y tilosina. Sin embargo, se encontró resistencia contra quinolonas, aminoglucósidos, tetraciclina y trimetoprim-sulfametoxazol, que se usan comúnmente para tratar infecciones con bacterias grampositivas.

The present report describes an outbreak of Pullorum disease in a young layer parent stock in Austria. The flock, which comprised 14,220 Lohmann brown layer chickens, experienced high mortality from the first week of life, reaching a total of 1905 chickens in the fifth week, when the flock was depopulated. Clinical signs included uneven size of the chicks, pasty vents, apathy, and diminished water and feed intake, with some birds presenting central nervous system signs such as tremors and torticollis. The postmortem investigation of 43 birds, of ages 1 to 4 weeks, revealed retained yolk sacs filled with caseous exudate, purulent airsacculitis, hepatitis with whitish pinpoint coalescing necrotic foci, splenitis with splenomegaly, hemorrhagic-mucoid enteritis in the small intestine, fibrinous typhlitis, nephromegaly, and urate deposits in the ureters and cloaca. Inflammation and/or necrosis were identified in liver, spleen, kidney, small intestine, and heart by histopathology. However, no histopathologic lesions were observed in the brain. Salmonella enterica was isolated from heart, liver, spleen, and brain in pure culture. Group-specific serotyping determined the presence of group D, with S. enterica subspecies enterica serovar Gallinarum being confirmed based on the Kauffmann-White scheme. A duplex PCR further identified S. enterica subspecies enterica serovar Gallinarum biovar Pullorum as the responsible agent for the outbreak. Subsequently, the grandparent flocks, from which the affected flock originated, were tested and found to be negative for Salmonella Pullorum, with no other progenies from the same grandparents developing disease. Although the source of the pathogen could not be identified, such findings highlight the importance of \"old\" pathogens such as Salmonella Pullorum causing sudden high mortality in chicks, even in a highly controlled environment.
Reporte de caso—Brote de pulorosis en una parvada de reproductores de postura jóvenes en Austria que presentó signos del sistema nervioso central. El presente reporte describe un brote de pulorosis en un lote de reproductoras de postura jóvenes en Austria. La parvada, que comprendió 14,220 gallinas de postura Lohmann, experimentó alta mortalidad desde la primera semana de vida, alcanzando un total de 1905 gallinas en la quinta semana, cuando la parvada se despobló. Los signos clínicos incluyeron tamaño desigual de pollito, empastamiento de la cloaca, apatía y disminución del consumo de agua y alimento, y algunas aves presentaron signos del sistema nervioso central como temblores y tortícolis. La investigación post mórtem de 43 aves, de 1 a 4 semanas de edad, reveló sacos vitelinos retenidos llenos de exudado caseoso, aerosaculitis purulenta, hepatitis con focos necróticos coalescentes blanquecinos, esplenitis con esplenomegalia, enteritis hemorrágica-mucoide en el intestino delgado, tiflitis fibrinosa, nefromegalia y depósitos de uratos en los uréteres y cloaca. Se identificaron inflamación y/o necrosis en hígado, bazo, riñón, intestino delgado y corazón mediante histopatología. Sin embargo, no se observaron lesiones histopatológicas en el cerebro. Se aisló Salmonella enterica de corazón, hígado, bazo y cerebro en cultivo puro. La serotipificación específica de grupo determinó la presencia del grupo D, con S entérica subespecie enterica serovar Gallinarum que se confirmó según el esquema de Kauffmann-White. Un método dúplex de PCR identificó S. enterica subspecie enterica serovar Pullorum como el agente responsable del brote. Posteriormente, las parvadas de abuelas, de las que se originó la parvada afectada, fueron analizadas y resultaron negativas para Salmonella Pullorum, sin que ninguna otra progenie de los mismos abuelos desarrollara la enfermedad. Aunque no se pudo identificar la fuente del patógeno, tales hallazgos resaltan la importancia de patógenos “viejos” como Salmonella Pullorum que causan una alta mortalidad repentina en los pollitos, incluso en un ambiente altamente controlado.