Co-infection with Trypanosoma congolense and Trypanosoma brucei is a significant risk factor for cerebral trypanosomosis in the equid population of the Gambia.

Trypanosomosis is a major cause of morbidity and mortality in working equids in The Gambia. Recently, a progressive, severe neurological syndrome characterised by a diffuse lymphoplasmacytic meningoencephalitis has been identified and associated with Trypanosoma brucei infection of the central nervous system. The pathogenesis of cerebral trypanosomosis is unclear and the clinical syndrome not well described. This observational cross-sectional study aimed to identify host and parasite related risk factors associated with the development of cerebral trypanosomosis and to describe the neurological syndrome associated with cerebral trypanosomosis. History, signalment, clinical and laboratory parameters were collected from 326 horses and donkeys presented to The Gambia Horse and Donkey Trust. Neurological derangements in affected animals were described. Species-specific polymerase chain reaction (PCR) for Trypanosoma congolense, Trypanosoma vivax and Trypanosoma brucei was performed. The associations between signalment, clinical and laboratory parameters and PCR results were assessed using multivariable logistic regression. The overall prevalence of trypanosomosis was 50 %, with infections dominated by T. congolense (44.1 %) and a lower intensity of T. brucei (7.4 %) and T. vivax (6.5 %). Overall, 54.8 % of neurological cases were PCR positive for trypanosomosis. Within the neurological sub-population prevalence remained similar to the whole population for T. congolense (48.4 %) and T. vivax (6.5 %); whilst the prevalence increased markedly for T. brucei (32.3 %). Co-infections were identified in 32.3 % of neurological cases. Donkeys typically presented with progressive cerebral dysfunction and cranial nerve deficits, whereas in horses a progressive spinal ataxia was predominant. Mortality in affected animals was high (82.4 %). The final multivariable model identified a significant association between body condition score ≤2 (OR 11.4; 95 % CI 4.6-27.9; P = <0.001), and T. congolense and T. brucei. coinfection (OR 20.6; 95 % CI 1.71-244.1; P = 0.016) with the presence of neurological deficits. This study has provided clinically relevant information confirming the link between T. brucei and neurological disease outbreak in the equid population of The Gambia, and crucially identified co-infection with T. brucei and T. congolense as a major risk factor for the development of neurological trypanosomosis. Further research is required to identify the epidemiology of co-infection in equidae of The Gambia, so that cerebral trypanosomosis can be better prevented in this vulnerable population.

Prevalence of acute kidney injury in a population of hospitalized horses.

BACKGROUND: Hospital-acquired acute kidney injury (AKI) in humans and dogs increases morbidity and nonsurvival. Azotemia at presentation has been associated with a poor outcome in horses; however, prevalence and consequences of hospital-acquired AKI are unreported. HYPOTHESIS/OBJECTIVES: To evaluate the prevalence of AKI in hospitalized horses, risk factors associated with AKI, and the effect of AKI on short-term survival. We hypothesized that the prevalence of AKI in horses is similar to that reported in other domestic mammalian species and would be associated with nonsurvival. ANIMALS: Adult horses hospitalized for >2 days from which a minimum of 2 measurements of serum creatinine concentration were available. METHODS: Retrospective cohort study. Clinical records were reviewed and horses grouped according to their baseline serum creatinine concentration and change in serum creatinine concentration from baseline. The associations between signalment, diagnosis, and treatment variables, and the presence of azotemia or AKI were assessed using multinomial logistic regression. The relationship between these conditions and survival to discharge was evaluated. RESULTS: Three hundred twenty-five horses were included; 4.3% (14/325) had azotemia at baseline and 14.8% (48/325) developed AKI. There were no significant associations between investigated risk factors and development of AKI. The presence of azotemia and AKI did not significantly affect survival to discharge (P = .08 and .81, respectively). CONCLUSIONS AND CLINICAL IMPORTANCE: The prevalence of AKI in this population of hospitalized horses is similar to that reported in dogs and humans; however, in this study population, there was less impact on morbidity and short-term survival.

Characterization of lethal inhalational infection with Francisella tularensis in the common marmoset (Callithrix jacchus).

The intracellular Gram-negative pathogen Francisella tularensis is the causative agent of tularaemia and is prevalent in many countries in the northern hemisphere. To determine whether the common marmoset (Callithrix jacchus) would be a suitable non-human primate model of inhalational tularaemia, a pathophysiology study was undertaken. Ten animals were challenged with approximately 10(2) c.f.u. F. tularensis strain SCHU S4 (F. tularensis subsp. tularensis). To look for trends in the infection, pairs of animals were sacrificed at 24 h intervals between 0 and 96 h post-challenge and blood and organs were assessed for bacteriology, pathology and haematological and immunological parameters. The first indication of infection was a raised core temperature at 3 days post-challenge. This coincided with a number of other factors: a rapid increase in the number of bacteria isolated from all organs, more pronounced gross pathology and histopathology, and an increase in the immunological response. As the disease progressed, higher bacterial and cytokine levels were detected. More extensive pathology was observed, with multifocal lesions seen in the lungs, liver and spleen. Disease progression in the common marmoset appears to be consistent with human clinical and pathological features of tularaemia, indicating that this may be a suitable animal model for the investigation of novel medical interventions such as vaccines or therapeutics.

The cationic peptide magainin II is antimicrobial for Burkholderia cepacia-complex strains.

This study was undertaken to determine the antibacterial activity of eight cationic antimicrobial peptides towards strains of genomovars I-V of the Burkholderia cepacia complex (Bcc) in time-kill assays. All but one of the peptides failed to show activity against the panel of test strains. The exception was magainin II, a 23 aa peptide isolated from the epidermis of the African clawed frog, Xenopus laevis, which exhibited significant bactericidal activity for Bcc genomovars most frequently associated with lung infection of patients with cystic fibrosis. In vitro studies indicated that magainin II protected a human bronchial epithelial cell line (BEAS-2B) from killing by Bcc and suggest that this peptide may have therapeutic potential against these organisms.

Establishment of lethal inhalational infection with Francisella tularensis (tularaemia) in the common marmoset (Callithrix jacchus).

Susceptibility and lethality studies of inhalational tularaemia were undertaken using the common marmoset (Callithrix jacchus) to determine its suitability as a non-human primate model. Pairs of marmosets were exposed to varying challenge doses of Francisella tularensis by the airborne route and monitored for up to 14 days postchallenge (p.c.). Lethal infection was achieved following a retained dose of less than 10 bacterial colony-forming units (CFU). However, precise LD(50) determination was not possible. The model was characterized using a target challenge dose of approximately 100 CFU. Increased core body temperature was the first indicator of disease, at approximately 2.5 days p.c. Overt clinical signs were first observed 12-18 h after the temperature increase. Significantly decreased activity was observed after approximately 3 days. All animals succumbed to infection between 4.5 and 7 days p.c. At postmortem examination, gross pathology was evident in the liver, spleen and lungs of all animals and high bacterial numbers were detected in all the organs assessed. Bacteraemia was demonstrated in all animals postmortem. Histopathological observations included severe suppurative bronchopneumonia, severe multifocal pyogranulomatous hepatitis, splenitis and lymphadenitis. Tularaemia disease progression in the common marmoset therefore appears to be consistent with the disease seen in humans and other animal models. The common marmoset may therefore be considered a suitable model for further studies of inhalational tularaemia.