Pathologic and immunohistochemical findings in an outbreak of systemic toxoplasmosis in a mob of red kangaroos

Toxoplasma gondii is a zoonotic protozoan pathogen that infects many endothermic vertebrates, including humans; the domestic cat and other felids serve as the definitive host. Macropodids are considered highly susceptible to toxoplasmosis. Here, we describe the clinical, pathologic, and immunohistochemical findings of an outbreak of systemic toxoplasmosis in a mob of 11 red kangaroos (Macropus rufus), with high morbidity (73%) and mortality (100%) rates. Affected animals had either severe and rapidly deteriorating clinical conditions or sudden death, which was correlated with widespread necrotizing lesions in multiple organs and intralesional T. gondii organisms identified via MIC3-specific immunohistochemistry and confirmed by REP529-specific rtPCR. Quantification of parasites demonstrated the highest parasite density in pulmonary parenchyma compared with other tissues. Our study highlights the continued importance of this severe condition in Australian marsupials.     

Flash flood simulation and valve behavior of Mytilus galloprovincialis measured with Hall sensors

Mussels close their shell as a protective strategy and the quantification of this behavioral marker may represent an alarm signal when they are exposed to environmental stressors. In the present study, we investigated the ability of the Mediterranean mussel Mytilus galloprovincialis to recover and then the resilience or inertia of valve activity after a pulsing exposition to diverse levels of salinity (5, 10, 20, and 35 PSU as reference value). The trial simulated an event of drastic and sudden reduction of seawater salinity thus mimicking an event of flash flood from intense rain. Valve gaping and movements were measured in continuous cycle for 10 days using a customized magneto-electric device which uses Hall sensors. Results showed that under normal conditions of salinity (35 PSU), the general pattern of valve movements was a continuously open state with sporadic spikes indicating a closing motion. At salinity of 5, PSU mussels reacted by closing their valves, leading to a 77% mortality on the 4th day. At salinity of 10, PSU animals were observed with closed valves for the entire duration of the exposure and no mortality occurred, they showed a significant reduction in the valve activity once the reference value of salinity was re-established. In contrast, salinity of 20 PSU did not trigger a significant behavioral response. Interestingly, there no define rhythms of valve movements were recorded during salinity challenges.     

MAGNETIC RESONANCE IMAGING FINDINGS IN THE EQUINE DEEP DIGITAL FLEXOR TENDON AND DISTAL SESAMOID BONE IN ADVANCED NAVICULAR DISEASE—AN EX VIVO STUDY

We describe the abnormal magnetic resonance (MR) imaging findings in the deep digital flexor tendon (DDFT) and distal sesamoid bone in horses with radiographic changes compatible with navicular syndrome. Thirteen postmortem specimens were examined using a 1.5-T magnetic field, with spin echo (SE) T1-weighted, turbo SE (TSE) proton density-weighted (with and without fat saturation), and fat saturation TSE T2-weighted sequences. The limbs were then dissected to compare the MR findings with the gross assessment and histologic examination of the DDFT and distal sesamoid bones. Tendonous abnormalities were detected by MR imaging in 12 DDFTs and confirmed at necropsy. Most tendon lesions were located at the level of the distal sesamoid bone and the proximal recess of the podotrochlear bursa. Tendon lesions were classified based on their MR imaging features as core lesions, dorsal lesions, dorsal abrasions, and parasagittal splits. Areas of increased MR signal in the DDFTs were characterized by tendon fiber disturbance and lack of continuity of the collagen fibers, foci of edema, hemorrhages, and formation of lakes containing eosinophilic plasma-like material or amphophilic material of low density. Bone marrow signal alterations in the distal sesamoid bone were seen in all digits. Two main phenomena were responsible for the abnormal signal, respectively, in T1-weighted (decreased signal) and in T2-weighted fat-suppressed images (increased signal): a decrease in the fat marrow content in the trabecular spaces and an increase in the fluid content. Histologic examination revealed foci of bone marrow edema, hemorrhage, necrosis, and fibrosis. Cyst formation and trabecular abnormalities (disorganization, thinning, remodelling) were also observed in areas of abnormal signal intensity. Increased bone density because of trabecular thickening induced a decrease in signal in all sequences.     

Dynamics of porcine circovirus type 2 infection in a herd of pigs with postweaning multisystemic wasting syndrome

OBJECTIVE: To determine the pattern of infection for porcine circovirus type 2 (PCV2) in a herd of pigs with postweaning multisystemic wasting syndrome (PMWS). ANIMALS: 29 sows and 250 pigs. PROCEDURE: Blood samples were collected from all 3-, 7-, and 12-week old pigs and 59 pigs at 28 weeks of age. Pigs that died during the study were necropsied. Porcine parvovirus and PCV2 antibodies were assayed. A polymerase chain reaction (PCR) was used to detect PCV2 genome in serum of selected pigs. RESULTS: The PMWS started when pigs were 8 weeks old, with a prevalence of 30% in 8- to 10-week-old pigs. Eighty-three pigs died during the period between 3 and 12 weeks of age. Microscopic lesions consistent with PMWS were observed, and PCV2 nucleic acid was detected (50 of 68 pigs). Antibodies to PCV2 decreased from 3 to 7 weeks of age, increased at 12 weeks of age, and were maintained until 28 weeks of age. One sow had a positive result for PCR of serum. Nine, 37 and 8 pigs had PCV2 genome in serum obtained at 7, 12, and 28 weeks of age, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: Infection with PCV2 coincided with severe clinical signs; however, infected 28-week-old pigs did not have evidence of disease. Immunity declined over time in young pigs. A long duration of PCV2 viremia was apparent in a high percentage of infected pigs, which may affect transmission and persistence of the virus in a herd.     

Mutation and virulence assessment of chromosomal genes of Rhodococcus equi 103

Rhodococcus equi can cause severe or fatal pneumonia in foals as well as in immunocompromised animals and humans. Its ability to persist in macrophages is fundamental to how it causes disease, but the basis of this is poorly understood. To examine further the general application of a recently developed system of targeted gene mutation and to assess the importance of different genes in resistance to innate immune defenses, we disrupted the genes encoding high-temperature requirement A (htrA), nitrate reductase (narG), peptidase D (pepD), phosphoribosylaminoimidazole-succinocarboxamide synthase (purC), and superoxide dismutase (sodC) in strain 103 of R. equi using a double-crossover homologous recombination approach. Virulence testing by clearance after intravenous injection in mice showed that the htrA and narG mutants were fully attenuated, the purC and sodC mutants were unchanged, and the pepD mutant was slightly attenuated. Complementation with the pREM shuttle plasmid restored the virulence of the htrA and pepD mutants but not that of the narG mutant. A single-crossover mutation approach was simpler and faster than the double-crossover homologous recombination technique and was used to obtain mutations in 6 other genes potentially involved in virulence (clpB, fadD8, fbpB, glnA1, regX3, and sigF). These mutants were not attenuated in the mouse clearance assay. We were not able to obtain mutants for genesfurA, galE, and sigE using the single-crossover mutation approach. In summary, the targeted-mutation system had general applicability but was not always completely successful, perhaps because some genes are essential under the growth conditions used or because the success of mutation depends on the target genes.     

Molecular evidence of Leishmania spp. in spider monkeys (Ateles geoffroyi) from The Tuxtlas Biosphere Reserve,Veracruz, Mexico

Veterinary Research Communications - The black-handed spider monkey (Ateles geoffroyi) is a platyrrhine primate distributed in southern Mexico, Central America, and part of South America. Two...     

Susceptibility to and transmission of H5N1 and H7N1 highly pathogenic avian influenza viruses in bank voles (Myodes glareolus)

The study of influenza type A (IA) infections in wild mammals populations is a critical gap in our knowledge of how IA viruses evolve in novel hosts that could be in close contact with avian reservoir species and other wild animals. The aim of this study was to evaluate the susceptibility to infection, the nasal shedding and the transmissibility of the H7N1 and H5N1 highly pathogenic avian influenza (HPAI) viruses in the bank vole (Myodes glareolus), a wild rodent common throughout Europe and Asia. Two out of 24 H5N1-infected voles displayed evident respiratory distress, while H7N1-infected voles remained asymptomatic. Viable virus was isolated from nasal washes collected from animals infected with both HPAI viruses, and extra-pulmonary infection was confirmed in both experimental groups. Histopathological lesions were evident in the respiratory tract of infected animals, although immunohistochemistry positivity was only detected in lungs and trachea of two H7N1-infected voles. Both HPAI viruses were transmitted by direct contact, and seroconversion was confirmed in 50% and 12.5% of the asymptomatic sentinels in the H7N1 and H5N1 groups, respectively. Interestingly, viable virus was isolated from lungs and nasal washes collected from contact sentinels of both groups. The present study demonstrated that two non-rodent adapted HPAI viruses caused asymptomatic infection in bank voles, which shed high amounts of the viruses and were able to infect contact voles. Further investigations are needed to determine whether bank voles could be involved as silent hosts in the transmission of HPAI viruses to other mammals and domestic poultry.