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Despite being important conservation tools, tourism and research may cause transmission of pathogens to wild great apes. Investigating respiratory disease outbreaks in wild bonobos, we identified human respiratory syncytial virus and Streptococcus pneumoniae as causative agents. A One Health approach to disease control should become part of great ape programs.

Habituation of wild great apes for tourism and research has had a significant positive effect on the conservation of these species. However, risks associated with such activities have been identified, specifically the transmission of human respiratory viruses to wild great apes, causing high morbidity and, occasionally, mortality. Here, we investigate the source of bacterial-viral co-infections in wild and captive chimpanzee communities in the course of several respiratory disease outbreaks. Molecular analyses showed that human respiratory syncytial viruses (HRSV) and human metapneumoviruses (HMPV) were involved in the etiology of the disease. In addition our analysis provide evidence for coinfection with Streptococcus (S.) pneumoniae. Characterisation of isolates from wild chimpanzees point towards a human origin of these bacteria. Transmission of these bacteria is of concern because - in contrast to HRSV and HMPV - S. pneumoniae can become part of the nasopharyngeal flora, contributing to the severity of respiratory disease progression. Furthermore these bacteria have the potential to spread to other individuals in the community and ultimately into the population. Targeted vaccination programs could be used to vaccinate habituated great apes but also human populations around great ape habitats, bringing health benefits to both humans and wild great apes.

The type and potency of an immune response provoked during vaccination will determine ultimate success in disease prevention. The basis for this response will be the design and implementation of antigen presentation to the immune system. Whereas direct antigen administration will elicit some form of immunological response, a more sophisticated approach would couple the antigen of interest to a vector capable of broad delivery formats and designed for heightened response. New antigens associated with pneumococcal disease virulence were used to test the delivery and adjuvant capabilities of a hybrid biological-biomaterial vector consisting of a bacterial core electrostatically coated with a cationic polymer. The hybrid design provides (i) passive and active targeting of antigen-presenting cells, (ii) natural and multicomponent adjuvant properties, (iii) dual intracellular delivery mechanisms, and (iv) a simple formulation mechanism. In addition, the hybrid format enables device-specific, or in situ, antigen production and consolidation via localization within the bacterial component of the vector. This capability eliminates the need for dedicated antigen production and purification before vaccination efforts while leveraging the aforementioned features of the overall delivery device. We present the first disease-specific utilization of the vector toward pneumococcal disease highlighted by improved immune responses and protective capabilities when tested against traditional vaccine formulations and a range of clinically relevant Streptococcus pneumoniae strains. More broadly, the results point to similar levels of success with other diseases that would benefit from the production, delivery, and efficacy capabilities offered by the hybrid vector.

Background: Streptococcus pneumoniae, a Gram-positive bacterium carried in the human nasopharynx, is an important human pathogen causing mild diseases such as otitis media and sinusitis as well as severe diseases including pneumonia, meningitis and sepsis. There is a strong resemblance between the anatomy, immunology and physiology of the pig and human species. Furthermore, there are striking similarities between S. suis pathogenesis in piglets and S. pneumoniae pathogenesis in humans. Therefore, we investigated the use of piglets as a model for pneumococcal colonization and invasive disease., Results: Intravenous inoculation of piglets with an invasive pneumococcal isolate led to bacteraemia during 5 days, showing clear bacterial replication in the first two days. Bacteraemia was frequently associated with fever and septic arthritis. Moreover, intranasal inoculation of piglets with a nasopharyngeal isolate led to colonization for at least six consecutive days., Conclusions: This demonstrates that central aspects of human pneumococcal infections can be modelled in piglets enabling the use of this model for studies on colonization and transmission but also on development of vaccines and host-directed therapies. Moreover this is the first example of an animal model inducing high levels of pneumococcal septic arthritis.

Bacterial cell wall hydrolases are essential for peptidoglycan turnover and crucial to preserve cell shape. The d,d-carboxypeptidase DacA and l,d-carboxypeptidase DacB of Streptococcus pneumoniae function in a sequential manner. Here, we determined the structure of the surface-exposed lipoprotein DacB. The crystal structure of DacB, radically different to that of DacA, contains a mononuclear Zn(2+) catalytic centre located in the middle of a large and fully exposed groove. Two different conformations were found presenting a different arrangement of the active site topology. The critical residues for catalysis and substrate specificity were identified. Loss-of-function of DacA and DacB altered the cell shape and this was consistent with a modified peptidoglycan peptide composition in dac mutants. Contrary, an lgt mutant lacking lipoprotein diacylglyceryl transferase activity required for proper lipoprotein maturation retained l,d-carboxypeptidase activity and showed an intact murein sacculus. In addition we demonstrated pathophysiological effects of disabled DacA or DacB activities. Real-time bioimaging of intranasal infected mice indicated a substantial attenuation of ΔdacB and ΔdacAΔdacB pneumococci, while ΔdacA had no significant effect. In addition, uptake of these mutants by professional phagocytes was enhanced, while the adherence to lung epithelial cells was decreased. Thus, structural and functional studies suggest DacA and DacB as optimal drug targets., (© 2014 John Wiley & Sons Ltd.)

A combination of kanamycin and cefalexin was licensed in Europe in 2008 to treat bovine clinical mastitis. Preliminary broth and disk clinical breakpoints for this antibiotic combination have been proposed for Staphylococcus aureus, Streptococcus dysgalactiae, Streptococcus uberis, and Escherichia coli. This study indicates that these proposed breakpoints also hold for coagulase-negative staphylococci (CNS), a group of bacteria frequently isolated in milk samples from cows with clinical mastitis. The data show that clinical bovine mastitis isolates of CNS from Europe have a high degree of susceptibility to the kanamycin/cefalexin combination, with minimal resistance to either agent alone. The use of the available kanamycin and cefalexin combination disk for testing the susceptibility of bovine mastitis isolates of Staph. aureus, Strep. uberis, Strep. dysgalactiae, and E. coli is also reliable for use in the testing of CNS, as disk results correlated with broth minimum inhibitory concentrations. The study reports, for the first time, the approved Clinical Laboratory Standards Institute quality control ranges for the kanamycin/cefalexin combination and wild-type cutoff values for major bacterial pathogens implicated in bovine mastitis., (Copyright © 2012 American Dairy Science Association. Published by Elsevier Inc. All rights reserved.)

In wild chimpanzees in the Taï National Park, Côte d'Ivoire, sudden deaths which were preceded by respiratory problems had been observed since 1999. Two new clones of Streptococcus pneumoniae were identified in deceased apes on the basis of multilocus sequence typing analysis and ply, lytA, and pbp2x sequences. The findings suggest that virulent S. pneumoniae occurs in populations of wild chimpanzees with the potential to cause infections similar to those observed in humans.

An approximately 2-month-old, reproductively intact female Domestic Shorthair kitten was presented to the Mississippi Veterinary Research and Diagnostic Laboratory with a history of possible trauma to the left shoulder region while playing with children, and was found dead the following day. Marked swelling, with subcutaneous edema and hemorrhages, was observed in the left forelimb. Severe pleocellular, but largely suppurative cellulitis, fasciitis, and interstitial myositis with edema were observed microscopically in sections from the affected limb. Massive numbers of gram-positive diplococci also were observed. Other pathologic changes included moderate interstitial pneumonia, mild cholangitis, lymph node hemorrhage, gastrointestinal nematodiasis, mild enteritis, and mild interstitial nephritis. Bacteriologic culture identified Streptococcus pneumoniae as the causative agent, which was confirmed by polymerase chain reaction amplification of the pneumolysin gene from chromosomal DNA of the isolate.

Although often considered a strict human pathogen, Streptococcus pneumoniae has been reported to infect and cause pneumonia in horses, although the pathology appears restricted compared to that of human infections. Here we report on the molecular characterization of a group of S. pneumoniae isolates obtained from horses in England and Ireland. Despite being obtained from geographically distinct locations, the isolates were found to represent a tight clonal group, virtually identical to each other but genetically distinguishable from more than 120 divergent isolates of human S. pneumoniae. A comprehensive analysis of known pneumococcal virulence determinants was undertaken in an attempt to understand the pathogenicity of equine pneumococci. Surprisingly, equine isolates appear to lack activities associated with both the hemolytic cytotoxin pneumolysin, often considered a major virulence factor of pneumococci, and the major autolysin gene lytA, also considered an important virulence factor. In support of phenotypic data, molecular studies demonstrated a deletion of parts of the coding sequences of both lytA and ply genes in equine pneumococci. The implications of these findings for the evolution and pathogenicity of equine S. pneumoniae are discussed.

A retrospective study of extrapulmonary disease in 17 guinea pigs with Streptococcus pneumoniae infection showed the most common to be either chronic active or acute fibrinopurulent pericarditis, pleuritis or peritonitis, or all three. In periparturient females the uterus was commonly affected. Hepatic and adrenal necrosis, splenitis, otitis media, encephalitis, lymphadenitis and ovarian abscesses also occurred. There were gram-positive diplococci in all lesions and Strep. pneumoniae, most often type 19, was cultured from tissues of 11 guinea pigs.

Type 19 pneumococcus was isolated only in anaerobic cultures from tissue fluids of guinea-pigs suffering from exudative pericarditis and pleuropneumonia. The organism was pathogenic to mice even after 40 subcultures. Further study showed it to be carboxyphilic rather than anaerobic. The necessity of specifying various atmospheric conditions in the diagnostic bacteriological isolation routine is emphasized.

Guineapig antibodies to Streptococcus pneumoniae (SPN) serotype 19F were detected by an enzyme-linked immunosorbent assay using a simple procedure. In experimentally infected hosts, antibody was detectable as early as 2 to 3 weeks after infection, and high titres were maintained for a long period. Antibodies higher than 1:64 were regarded as specific. In a field study, high antibody titres were shown in SPN enzootic colonies in contrast to negative or low antibody titres in a majority of the animals from non-enzootic and SPF colonies.

An acute respiratory disease in a colony of Wistar-derived rats is described. The infection, due to Diplococcus pneumoniae type 16, has apparently not been described previously in the rat. Rigid sanitary measures and treatment with penicillin were effective in controlling the disease.

An acute respiratory disease, due to Diplococcus pneumoniae type 3, affecting Wistar and Sprague-Dawley rats is described. The infection was experimentally transmitted to Sprague-Dawley rats. The zoonotic potential of the condition dictated euthanasia of affected animals and instigation of rigid sanitary measures.