Failure of monovalent and polyvalent rabies vaccines to induce anti-rabies IgG in dogs as measured using an indirect ELISA

We aimed to investigate the efficacy of current practice of rabies vaccination in dogs of Bangladesh. Pet dogs (n=20) visited Teaching Veterinary Hospital of Chattogram Veterinary and Animal Sciences University were injected with commercially available monovalent or polyvalent vaccines containing inactivated adjuvanted rabies virus. Group of dogs were administered with single dose of monovalent (n=5) or polyvalent (n=5) rabies vaccine. Separate group of animals were injected with a second dose (monovalent n=5, polyvalent n=5) 14-days after the primary injection. Blood samples were collected at day-28 after the initial injection. Baseline sera were collected before starting injections. Indirect enzyme-linked immunosorbent assay was performed with sera samples to detect anti-rabies IgG. We were unable to detect any anti-rabies IgG titer in the dogs vaccinated with either monovalent or polyvalent vaccines irrespective of frequency of vaccination. The results indicate that the current commercial rabies vaccines are doubtful in generating protective antibody titer in dogs of this area. The results predict public health risk and demand for extensive investigation of vaccine quality and transportation

Determination of the role of group G Streptococcus in the pathogenesis of rheumatic heart disease using a rat model

Acute rheumatic fever and rheumatic heart disease (ARF/RHD) have long been described as autoimmune sequelae of Streptococcus pyogenes or group A streptococcal (GAS) infection characterised by inflammatory changes to heart, joint, brain, blood vessel and skin tissue. In ARF/RHD both antibody and T-cell responses against immunodominant GAS virulence factors including M-proteins, cross-react with host tissue proteins. The M-protein antibodies activate heart endothelial cells by upregulation of adhesion molecules such as VCAM-1 and ICAM-1 to trigger an inflammatory response. Repeat exposure to GAS perpetuates the autoimmune process leading to permanent cardiac damage. However, in some ARF/RHD endemic regions, throat carriage of GAS is low but carriage of the related Streptococcus dysgalactiae subspecies equisimilis (SDSE), also known as β-haemolytic groups C and G streptococci (GCS/GGS) is high. As SDSE also express M-protein, it has been postulated that streptococci other than GAS may have the potential to initiate or exacerbate ARF/RHD. Further investigation of this hypothesis was limited due to the unavailability of an appropriate experimental model for this uniquely human disease. Using an animal model initially developed to investigate S. pyogenes associated ARF/RHD, we have now discovered that GGS does indeed cause both myocarditis and valvulitis, hallmarks of ARF/RHD. We injected Lewis rats with whole-killed GGS or GGS M-protein Stg480 with or without whole-killed GAS and GAS rM5 protein to induce carditis. Carditis development was determined by electrocardiographic and echocardiographic examination of rats, and histological examination after heart retrieval. Antibody and T-cell reactivity to M-proteins and antibody cross-reactivity to host cardiac myosin and collagen I has been demonstrated. Remarkably the histological, immunological and functional changes in the hearts of rats exposed to GGS are identical to those exposed to GAS. Furthermore, antibody cross-reactivity to cardiac myosin was comparable in both GGS and GAS exposed animals providing additional evidence that GGS can induce and/or exacerbate ARF/RHD. The results provide further evidence that the heterologous GAS and GGS antigen combinations are equally as effective as homologous antigens at inducing heart pathology, heart conduction and valve abnormalities and potentially autoreactive immune responses. The role of GAS and GGS M-protein specific antibodies and T-cells in upregulation of VCAM-1 and ICAM-1 has been investigated in vitro using cultured rat aortic endothelial cells, and in vivo in tissue sections taken from Lewis rats immunised with GAS and GGS M-proteins. Upregulation of VCAM-1 and ICAM-1 was observed in an endothelial cell line stimulated with antibodies and/or T-cells, and in heart sections of rats injected with GAS and GGS M-proteins. Using a Transwell cell culture system, we observed that T-cells from M-protein immunised animals migrated through the endothelial monolayer. Furthermore, we observed the development of carditis in Lewis rats following injection of serum and/or splenocytes from rats previously immunised with GAS rM5 protein. Our findings suggest that group G Streptococcus (GGS) and its M-protein has the potential to induce autoimmune mediated carditis in the Lewis rat model of RHD. The data provides further direct evidence that M-protein specific lymphocytes and antibodies facilitate migration of inflammatory cells to the heart and likely contribute to heart pathology in this animal model as well in human RHD

Data on Growth, survivability, water quality and hemato-biochemical indices of Nile Tilapia (Oreochromis niloticus) fry fed with selected marine microalgae

Data of this article describes growth, survival rate, water quality and hemato-biochemical indices of Nile Tilapia (Oreochromis niloticus) fry. To collect the data, the Nile Tilapia fry was reared in 30 L glass aquarium (18 fish/ tank) for 56-days under controlled environmental condition. Feed was prepared with 25 and 50% replacement of commercial fish meal with Nannochloropsis sp. and Tetraselmis sp. microalgae, while no replacement was made for control feed. Initial and final body weight of fish was recorded to find the data of growth rate; survival rate was calculated from the initial and final live individuals recorded during the experiment; physico-chemical parameters were analyzed to collect water quality data; hemato-biochemical indices were collected using hematology analyzer and photometry. The data on growth, survival rate and hemato-biochemical indices were statistically significant (p < 0.05). Therefore, these data might contribute to the selection of marine microalgae to improve the water quality during fish farming which could enhance the growth and survivability of fish. In addition, the data of hemato-biochemical indices represent that feeding selected marine microalgae might result in the production of healthy and disease-free fish

Bovine Brucellosis: An Epidemiological Study at Chittagong, Bangladesh

An epidemiological survey was conducted to identify probable risk factors and prevalence of brucellosis in commercial and backyard dairy cows at Chittagong, Bangladesh. A total of 500 milk samples were collected (250 commercial and 250 backyards) for Milk Ring Test (MRT). The MRT positive cows were subjected to sera collection and Rose Bengal Plate Test (RBPT) and indirect ELISA were done for confirmatory diagnosis. The overall seroprevalence of brucellosis in cattle was 5% (7.6% in commercial and 2.4% in backyard). Significantly higher (P<0.05) prevalence was found in the zero grazing (5.74%), pregnant cows (7.53%) and cows with history of retained placenta (7.89%) or abortion (5.88%) or both (11.76%) than non-pregnant (2.68%) and without any reproductive disorder (4.44%). A total of 420 farm attendants and owners were interviewed where 93.55 and 99.08% commercial and backyard personnel were found to have no knowledge of brucellosis and 9.67 and 87.77% consumed raw milk and yogurt respectively were highly vulnerable to zoonotic brucellosis. The results showed that brucellosis is widely distributed locally, underscoring the need for further studies including biovar determination

Requirements for a Robust Animal Model to Investigate the Disease Mechanism of Autoimmune Complications Associated With ARF/RHD

The pathogenesis of Acute Rheumatic Fever/Rheumatic Heart Disease (ARF/RHD) and associated neurobehavioral complications including Sydenham's chorea (SC) is complex. Disease complications triggered by Group A streptococcal (GAS) infection are confined to human and determining the early events leading to pathology requires a robust animal model that reflects the hallmark features of the disease. However, modeling these conditions in a laboratory animal, of a uniquely human disease is challenging. Animal models including cattle, sheep, pig, dog, cat, guinea pigs rats and mice have been used extensively to dissect molecular mechanisms of the autoimmune inflammatory responses in ARF/RHD. Despite the characteristic limitations of some animal models, several rodent models have significantly contributed to better understanding of the fundamental mechanisms underpinning features of ARF/RHD. In the Lewis rat autoimmune valvulitis model the development of myocarditis and valvulitis with the infiltration of mononuclear cells along with generation of antibodies that cross-react with cardiac tissue proteins following exposure to GAS antigens were found to be similar to ARF/RHD. We have recently shown that Lewis rats injected with recombinant GAS antigens simultaneously developed cardiac and neurobehavioral changes. Since ARF/RHD is multifactorial in origin, an animal model which exhibit the characteristics of several of the cardinal diagnostic criteria observed in ARF/RHD, would be advantageous to determine the early immune responses to facilitate biomarker discovery as well as provide a suitable model to evaluate treatment options, safety and efficacy of vaccine candidates. This review focuses on some of the common small animals and their advantages and limitations

Group G Streptococcus has the potential to cause Rheumatic Fever and Rheumatic Heart Disease

Rheumatic Fever (RF) and Rheumatic Heart Disease (RHD) are caused by autoimmune responses triggered by Group A Streptococcus (GAS). Both T lymphocytes and antibodies generated against GAS are known to cross-react with the host tissue proteins. M proteins of GAS share structural homology with human cardiac proteins. Streptococcus dysgalactiae subspecies equisimilis (SDSE; Group G Streptococcus, GGS) possess many of the same GAS characteristics. GGS is known to possess virulence factors similar to those of GAS, however the role of GGS in RF/RHD has not been studied. In this study, the rheumatogenic potential of GGS in the development of RHD was investigated using a rat autoimmune valvulitis (RAV) model. Lewis rats were immunised with either whole killed GAS or GGS or M proteins derived from GAS or GGS. Rats immunised with GAS and GGS showed cross-reactive antibody and T cell responses to cardiac myosin and collagen I. Histology of heart tissues revealed multiple foci of inflammation within mitral valves and myocardium with fibrosis throughout the valves and myocardium. Significantly prolonged P-R intervals were demonstrated in electrocardiographic examination of hearts of both GAS and GGS immunised rats. These results highlight the possibility of SDSE/GGS triggering and/or potentiating the development of RF/RHD

Two-shots of immunization effectively induce protective IgG against canine parvo-viral infection

Regardless of good hygiene and management, a significant number of dogs are lost every year due to deadly attack of parvo virus. The immunization schedules recommended by the World Small Animal Veterinary Association (WSAVA) do not have exclusive suggestions on dogs living in Bangladesh. The WSAVA Vaccination Guidelines Group (VGG) suggested that vaccination recommendations that apply to a developed country may not be appropriate for a developing country. Due to inadequate sero-monitoring, emergence and re-emergence of Parvo viral infection following immunization is a common event. Therefore, the current study is designed to establish a definite guideline for Parvo viral immunization in dogs. We immunized group of dogs with commercially available parvo virus vaccine Nobivac Dog®, and a second dose was injected 14-days following the initial dose. Sera samples were collected before starting injections and 7-day following 1st and 2nd dose of vaccinations. We performed Enzyme Linked Immunosorbent Assay (ELISA) to detect protective serum IgG titer against the canine parvo virus type 2 antigen. Demographic data of the participated animals was compared to the status of antibody titer. Findings of this study revealed that two-shots of immunizations with a booster injection of 2-3 weeks apart from the primary immunization is essential to develop positive titer. The purebred female dogs of older than three-months had higher IgG when compared to local, crossbred, male and younger dogs. The results will provide valuable information to establish National Guidelines for Immunizations in Dogs of Bangladesh for effective prevention and control of this deadly disease

Determination of the role of group G Streptococcus in the pathogenesis of rheumatic heart disease using a rat model

Acute rheumatic fever and rheumatic heart disease (ARF/RHD) have long been described as autoimmune sequelae of Streptococcus pyogenes or group A streptococcal (GAS) infection characterised by inflammatory changes to heart, joint, brain, blood vessel and skin tissue. In ARF/RHD both antibody and T-cell responses against immunodominant GAS virulence factors including M-proteins, cross-react with host tissue proteins. The M-protein antibodies activate heart endothelial cells by upregulation of adhesion molecules such as VCAM-1 and ICAM-1 to trigger an inflammatory response. Repeat exposure to GAS perpetuates the autoimmune process leading to permanent cardiac damage. However, in some ARF/RHD endemic regions, throat carriage of GAS is low but carriage of the related Streptococcus dysgalactiae subspecies equisimilis (SDSE), also known as β-haemolytic groups C and G streptococci (GCS/GGS) is high. As SDSE also express M-protein, it has been postulated that streptococci other than GAS may have the potential to initiate or exacerbate ARF/RHD. Further investigation of this hypothesis was limited due to the unavailability of an appropriate experimental model for this uniquely human disease. Using an animal model initially developed to investigate S. pyogenes associated ARF/RHD, we have now discovered that GGS does indeed cause both myocarditis and valvulitis, hallmarks of ARF/RHD. We injected Lewis rats with whole-killed GGS or GGS M-protein Stg480 with or without whole-killed GAS and GAS rM5 protein to induce carditis. Carditis development was determined by electrocardiographic and echocardiographic examination of rats, and histological examination after heart retrieval. Antibody and T-cell reactivity to M-proteins and antibody cross-reactivity to host cardiac myosin and collagen I has been demonstrated. Remarkably the histological, immunological and functional changes in the hearts of rats exposed to GGS are identical to those exposed to GAS. Furthermore, antibody cross-reactivity to cardiac myosin was comparable in both GGS and GAS exposed animals providing additional evidence that GGS can induce and/or exacerbate ARF/RHD. The results provide further evidence that the heterologous GAS and GGS antigen combinations are equally as effective as homologous antigens at inducing heart pathology, heart conduction and valve abnormalities and potentially autoreactive immune responses. The role of GAS and GGS M-protein specific antibodies and T-cells in upregulation of VCAM-1 and ICAM-1 has been investigated in vitro using cultured rat aortic endothelial cells, and in vivo in tissue sections taken from Lewis rats immunised with GAS and GGS M-proteins. Upregulation of VCAM-1 and ICAM-1 was observed in an endothelial cell line stimulated with antibodies and/or T-cells, and in heart sections of rats injected with GAS and GGS M-proteins. Using a Transwell cell culture system, we observed that T-cells from M-protein immunised animals migrated through the endothelial monolayer. Furthermore, we observed the development of carditis in Lewis rats following injection of serum and/or splenocytes from rats previously immunised with GAS rM5 protein. Our findings suggest that group G Streptococcus (GGS) and its M-protein has the potential to induce autoimmune mediated carditis in the Lewis rat model of RHD. The data provides further direct evidence that M-protein specific lymphocytes and antibodies facilitate migration of inflammatory cells to the heart and likely contribute to heart pathology in this animal model as well in human RHD

Meloxicam is the primary choice of analgesic for dogs and cats; a cross-sectional clinical study in Bangladesh

A cross-sectional clinical survey was conducted on 262 veterinarian participants practicing in the Bangladesh with the aim to current practice of pain management in dogs and cats. The veterinarians were interviewed physically or online communication with a structured questionnaire. Demographic data of the veterinarians revealed that majority of them are young male and freshly graduated who use their academic knowledge during practice. Findings of the study also demonstrated that meloxicam is the primary choice of pain management in dogs 66.79% and cats 52.67%. Ketoprofen is the second most choice in both orthopedic and muscular injuries. Among the steroids and opioids categories, dexamethasone and tramadol are recorded respectively as first choice. Dexamethasone is the primary choice where pain is the worst. Usual duration of analgesic therapy recorded is less than three-days. In most cases, veterinarians suggest H2 blockers in association with meloxicam and ketoprofen to reduce adverse effects. Side effects following analgesic therapy observed are vomition and diarrhea. The current study reviewed the present scenario of analgesics use in dogs and cats in Bangladesh. Further studies are required involving more participants, detailed information on cases, and response to analgesic therapy