Outbreaks of Streptococcus gallolyticus subsp. pasteurianus in Goslings Characterized by Central Nervous Symptoms.

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 caso­Brotes 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.

An Outbreak of Pullorum Disease in a Young Layer Parent Flock in Austria Presented with Central Nervous System Signs.

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 caso­Brote 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.

Testing for Bartonella ssp. DNA in cerebrospinal fluid of dogs with inflammatory central nervous system disease.

BACKGROUND: Neurobartonellosis occurs in people. The role these organisms might play in inflammatory brain disease of dogs is unclear. HYPOTHESIS/OBJECTIVES: That Bartonella spp. DNA would be amplified more commonly from the CSF of dogs with inflammatory disease compared to those with noninflammatory disease. To report the prevalence of Bartonella spp. in dogs with and without inflammatory CNS disease with a commercially available PCR assay. ANIMALS: Cerebrospinal fluid (CSF) samples from 172 dogs from either Washington State University or Colorado State University. METHODS: Retrospective study. A search was performed of all medical records from dogs with CSF samples submitted to CSU's Center for Companion Animal Studies or Veterinary Diagnostic Laboratory from CSU or WSU for Toxoplasma or Neospora PCR assay. Increased CSF nucleated cell counts and an adequate volume of CSF must have been present to evaluate Bartonella spp. by PCR assay. RESULTS: Inflammatory CNS disease was confirmed in 65 dogs, none of which were positive for Bartonella spp. DNA. Of the other 107 dogs, one was positive for B. henselae DNA. The CSF from this dog contained red blood cells. CONCLUSIONS AND CLINICAL IMPORTANCE: Failure to amplify Bartonella spp. DNA from the CSF of the dogs with inflammatory disease suggests the organism was not involved in the etiology of the disease, the organism was in the CNS tissues but not in the CSF, or the organism was present but in quantities undetectable by this PCR assay. The combination of PCR and culture is the most sensitive way to detect Bartonella spp. and the use of that technique should be considered in future studies.

Genetic Separation of Listeria monocytogenes Causing Central Nervous System Infections in Animals.

Listeria monocytogenes is a foodborne pathogen that causes abortion, septicemia, gastroenteritis and central nervous system (CNS) infections in ruminants and humans. L. monocytogenes strains mainly belong to two distinct phylogenetic groups, named lineages I and II. In general, clinical cases in humans and animals, in particular CNS infections, are caused by lineage I strains, while most of the environmental and food strains belong to lineage II. Little is known about why lineage I is more virulent than lineage II, even though various molecular factors and mechanisms associated with pathogenesis are known. In this study, we have used a variety of whole genome sequence analyses and comparative genomic tools in order to find characteristics that distinguish lineage I from lineage II strains and CNS infection strains from non-CNS strains. We analyzed 225 strains and identified single nucleotide variants between lineages I and II, as well as differences in the gene content. Using a novel approach based on Reads Per Kilobase per Million Mapped (RPKM), we identified 167 genes predominantly absent in lineage II but present in lineage I. These genes are mostly encoding for membrane-associated proteins. Additionally, we found 77 genes that are largely absent in the non-CNS associated strains, while 39 genes are especially lacking in our defined "non-clinical" group. Based on the RPKM analysis and the metadata linked to the L. monocytogenes strains, we identified 6 genes potentially associated with CNS cases, which include a transcriptional regulator, an ABC transporter and a non-coding RNA. Although there is not a clear separation between pathogenic and non-pathogenic strains based on phylogenetic lineages, the presence of the genes identified in our study reveals potential pathogenesis traits in ruminant L. monocytogenes strains. Ultimately, the differences that we have found in our study will help steer future studies in understanding the virulence mechanisms of the most pathogenic L. monocytogenes strains.

Listeria monocytogenes infection in ruminants: Is there a link to the environment, food and human health? A review.

Listeria (L.) monocytogenes is widely distributed in the environment, but also has the ability to cause serious invasive disease in ruminants and humans. This review provides an overview of listeriosis in ruminants and discusses our insufficient understanding of reservoirs and possible cycling ofL. monocytogenes between animal and human hosts, food and the environment. It indicates gaps in our knowledge of the role of genetic subtypes in L. monocytogenes ecology and virulence as well as risk factors, in vivo diagnostics and pathogenesis of listeriosis in ruminants. Filling these gaps will contribute to improving the control of L. monocytogenes and enhancing disease prevention. As the prevalence of listeriosis in ruminants in Switzerland is likely to be underestimated, propositions concerning improvement options for surveillance of listeriosis in ruminants are provided.

Central nervous system infection with Staphylococcus intermedius secondary to retrobulbar abscessation in a dog.

In this report, we describe a case of retrobulbar abscessation in a dog that was initially diagnosed as masticatory myositis and treated with immunosuppressive doses of corticosteroids. Secondary bacterial infection of the central nervous system (CNS) occurred and was definitively diagnosed by the analysis and culture of the cerebrospinal fluid. This is the first time that retrobulbar infection has been definitively shown to result in secondary bacterial infection of the CNS in the dog and highlights the importance of ruling out infectious causes of retrobulbar disease before assuming and treating for an immune-mediated etiology.

[The incidence of bacterial CNS infections in roe deer (Capreolus capreolus), red deer (Cervus elaphus) and chamois (Rupicapra rupicapra) in Bavaria]. / Zum Vorkommen bakterieller ZNS-Infektionen beim Rehwild (Capreolus capreolus), Rotwild (Cervus elaphus) und Gamswild (Rupicapra rupicapra) in Bayern.

Brain samples of 849 wild ruminants (654 roe deer, 189 red deer and 6 chamois) from Bavaria were examined for the occurrence of encephalopathies caused by bacteria, using cultural, serological and genetic methods. In addition, 87 brain samples were investigated histologically for clarification of the pathogenetic relevance of specific microorganisms. Using conventional bacteriological methods, 464 different bacteria were isolated. 229 of them could be differentiated to the genus level and 235 to the species level. Totally, 35 different bacteria species were isolated, most frequently Micrococcus spp., Bacillus spp. and E. coli. Listeria spp. were detected in 43 brain samples (37 from roe deer, 5 from red deer and 1 from chamois). Sixteen strains were identified as L. innocua, 14 as L. monocytogenes, 9 as L. seeligeri and 4 as L. grayi. Serological investigations of L. monocytogenes showed that 9 strains belong to serotype 1/2a and five to 4b. Analysis of the geographical distribution of the Listeria findings indicate a statistically significant (p<0.011) regional aggregation in Unterfranken (prevalence for roe deer: 12.2%, versus 4.5% in Oberbayern-Schwaben, 6.1% in Niederbayern-Oberpfalz and 0% in Oberfranken-Mittelfranken). The histological investigation (HE staining) of 87 tissue samples contaminated with encephalitis relevant bacteria showed inflammation of different severity (mild meningitis and choroiditis (n = 26) to moderate (meningo)encephalitis (n = 13)) in 41 cases.