Pheno- and genotypic characterization and identification of novel subtypes of Peste des Petits Ruminants virus in domestic and captive wild goats in Northern Iraq.

BACKGROUND: Peste des Petits Ruminants (PPR) is an acute or peracute contagious transboundary viral disease that mainly affects caprine and ovine and causes significant economic impact in developing countries. After two PPR virus outbreaks in 2011 and 2014, an investigation, from August 2015 to September 2016, was carried out in Northern Iraq when an increased morbidity and mortality rates were reported in the domestic and captive wild goats. In the present study, ten domestic goat farms and seven captive wild goat herds located in seven geographical areas of Northern Iraq were clinically, pathologically, serologically and genotypically characterized to determine the prevalence and potential cause of PPR virus outbreak. RESULTS: The outbreak occurred with rate of morbidity (26.1%) and mortality (11.1%) in domestic goat farms as compared to captive wild goat herds where relatively high mortality (42.9%) and low morbidity (10.9%) rates were recorded. Based on the clinical symptoms (mucopurulent nasal discharges, ulceration and erosion of oral mucosa, profuse watery diarrhea) and necropsy (hemorrhage and congestion on mucous membranes of the colon and rectum with zebra stripes lesions) results, overall, the serological test findings revealed a high frequency (47.9%) of positive samples for anti-PPRV nucleoprotein antibodies. Furthermore, the nucleoprotein (N) gene was detected in 63.2 and 89.1% of samples using conventional and reverse transcription real-time quantitative PCR assays. A phylogenetic analysis of N gene amino acid sequences clustered with the reference strain revealed lineage IV similar to the strains isolated in 2011 and 2014, respectively. However, two sub-types of lineage IV (I and II), significantly distinct from the previous strains, were also observed. CONCLUSION: The phylogenetic analysis suggests that movements of goats are possible cause and one of the important factors responsible for the spread of virus across the region. The study results would help in improving farm management practices by establishing a PPR virus eradication program using regular monitoring and vaccination program to control and mitigate the risk of re-emergence of PPR virus infection in domestic and captive wild goats in Iraq.

Outbreak of Peste des Petits Ruminants among Critically Endangered Mongolian Saiga and Other Wild Ungulates, Mongolia, 2016-2017.

The 2016-2017 introduction of peste des petits ruminants virus (PPRV) into livestock in Mongolia was followed by mass mortality of the critically endangered Mongolian saiga antelope and other rare wild ungulates. To assess the nature and population effects of this outbreak among wild ungulates, we collected clinical, histopathologic, epidemiologic, and ecological evidence. Molecular characterization confirmed that the causative agent was PPRV lineage IV. The spatiotemporal patterns of cases among wildlife were similar to those among livestock affected by the PPRV outbreak, suggesting spillover of virus from livestock at multiple locations and time points and subsequent spread among wild ungulates. Estimates of saiga abundance suggested a population decline of 80%, raising substantial concerns for the species' survival. Consideration of the entire ungulate community (wild and domestic) is essential for elucidating the epidemiology of PPRV in Mongolia, addressing the threats to wild ungulate conservation, and achieving global PPRV eradication.

Neuropathology mediated through caspase dependent extrinsic pathway in goat kids naturally infected with PPRV.

Peste des petits ruminant (PPR), a highly contagious viral disease of small ruminants, is characterized by erosive stomatitis and pneumo-enteritis. However, its neurovirulence potential as observed with other morbilliviruses has not been fully investigated. The present study describes the neuropathological alterations induced by PPR virus through apoptotic pathway. A total number of 12 carcasses of local breed goat kids of either sex were received for postmortem examination. The clinical history was described as symptoms of mucopurulent nasal discharge, high to low grade fever, erosive stomatitis, dyspnoea and profuse watery diarrhoea followed by mortality of 35 goat kids within a week. The pathoanatomical lesions and immunohistochemical demonstration of PPRV antigen in lungs, intestine, spleen and lymph nodes confirmed PPR disease in goats. Grossly, five brain specimens showed moderate to severe leptomeningeal congestion during necropsy. Microscopically, brain sections showed leptomeningitis and nonsuppurative encephalitis characterized by vascular congestion, haemorrhages in the parenchyma, perivascular cuffing with mild to moderate mononuclear cells (mainly lymphocytes and few macrophages), focal to diffuse microgliosis, neuronal degeneration, satellitosis and neuronophagia. Immunolabelling of viral antigen was observed in the cytoplasm of neurons and glial cells. The RT-PCR amplification of N gene fragment also confirmed the presence of PPRV in the brain. The strong immunoreactivity of Caspase-3, Caspase-8 and comparatively lower expression of caspase-9 along with the absence of any reactivity for Apaf-1 antigen in the brain sections indicated the role of caspase dependent extrinsic pathway in inducing neuropathological changes. The presence of apoptotic neurons in the brain by TUNEL assay further confirmed the apoptosis and strong immunoreactivity of iNOS in neurons which suggested the generation of oxidative stress, that might have induced the apoptosis. The overall findings confirm the neurovirulence potential of PPR virus, via the extrinsic pathway of apoptosis, in natural cases of PPR disease in goat kids.

Structure-Guided Identification of a Nonhuman Morbillivirus with Zoonotic Potential.

Morbilliviruses infect a broad range of mammalian hosts, including ruminants, carnivores, and humans. The recent eradication of rinderpest virus (RPV) and the active campaigns for eradication of the human-specific measles virus (MeV) have raised significant concerns that the remaining morbilliviruses may emerge in so-called vacated ecological niches. Seeking to assess the zoonotic potential of nonhuman morbilliviruses within human populations, we found that peste des petits ruminants virus (PPRV)-the small-ruminant morbillivirus-is restricted at the point of entry into human cells due to deficient interactions with human SLAMF1-the immune cell receptor for morbilliviruses. Using a structure-guided approach, we characterized a single amino acid change, mapping to the receptor-binding domain in the PPRV hemagglutinin (H) protein, which overcomes this restriction. The same mutation allowed escape from some cross-protective, human patient, anti-MeV antibodies, raising concerns that PPRV is a pathogen with zoonotic potential. Analysis of natural variation within human and ovine SLAMF1 also identified polymorphisms that could correlate with disease resistance. Finally, the mechanistic nature of the PPRV restriction was also investigated, identifying charge incompatibility and steric hindrance between PPRV H and human SLAMF1 proteins. Importantly, this research was performed entirely using surrogate virus entry assays, negating the requirement for in situ derivation of a human-tropic PPRV and illustrating alternative strategies for identifying gain-of-function mutations in viral pathogens.IMPORTANCE A significant proportion of viral pandemics occur following zoonotic transmission events, where animal-associated viruses jump species into human populations. In order to provide forewarnings of the emergence of these viruses, it is necessary to develop a better understanding of what determines virus host range, often at the genetic and structural levels. In this study, we demonstrated that the small-ruminant morbillivirus, a close relative of measles, is unable to use human receptors to enter cells; however, a change of a single amino acid in the virus is sufficient to overcome this restriction. This information will be important for monitoring this virus's evolution in the field. Of note, this study was undertaken in vitro, without generation of a fully infectious virus with this phenotype.

Pathological and molecular characterisation of peste des petits ruminants in Nubian ibex (Capra nubiana) in Israel.

Peste des petits ruminants (PPR) is a devastating disease that generally affects sheep and goats, mostly in Asia, the Middle East and Africa. The disease has been declared a target for global eradication. Despite its high prevalence in domestic flocks and its high seroprevalence among wildlife, it is rarely reported as a fulminant disease in wild ruminant species (with the exception of Central Asia). In this report, we describe a severe PPR outbreak in a zoo herd of Nubian ibex (Capra nubiana), causing the deaths of 2/3 of the herd. The clinical onset was acute with morbid animals exhibiting lethargy and watery-to-bloody diarrhea and death usually within 48 h. The most consistent gross pathologic findings were hemorrhagic abomasitis and enteritis. Oral lesions and pulmonary lesions were rare. Histology revealed necrohemorrhagic enteritis and abomasitis with myriad nuclear and cytoplasmic viral inclusion bodies. Molecular examinations confirmed the diagnosis of PPR and determined that the causative agent belongs to lineage IV. Further molecular examination showed that the virus belongs to the Asian clade of lineage IV and is closely related to a virus described in Turkey.

Peste des petits ruminants pathogenesis on experimental infected goats by the Moroccan 2015 isolate.

BACKGROUND: Peste des petits ruminants (PPR) is a viral disease of major economic importance on small ruminants. Goats are usually known to be more susceptible to the disease. Infection chronology, virus circulation, and the disease early detection need to be better understood. This study evaluates the tissue tropism and pathogenesis of PPR following experimental infection of goats using a lineage IV virus, the most dominant in the world originated from Asia. PPRV infection was experimentally induced in 4 six-month-old goats by intra-nasal and intravenous route of cell virus suspension and from infectious mashed tissue. The clinical signs were observed and goats were euthanized at predetermined clinical score level for post-mortem examinations and PPRV detection by RT-PCR. Clinical signs of infection were present, pyrexia, serous-mucopurulent nasal discharges, coughing, diarrhea and asthenia, for both cell virus suspension and infectious mashed tissue. PPRV genome was highly detected in swabs and tissues with clinical signs dominated by pulmonary attack and digestive symptoms secondary. RESULTS: Results of this study indicates that PPRV is an invasive infection in animals that in a short period, less than 10 days, invade all vital organs. On live animals, early diagnostic may be easily done on lacrimal and rectal swabs. CONCLUSION: The experimental PPRV-infection model using the cell virus suspension is suitable for vaccine evaluation as a standard model.

Pathophysiology of peste des petits ruminants in sheep (Dorper & Kajli) and goats (Boer & Beetal).

Peste des petits ruminants (PPR), an economically important viral transboundary disease of small ruminants is not only prevalent in Pakistan but also in other countries where people rely on agriculture and animal products. The present study was aimed at describing the pathology and antigen localization in natural PPR infections in local (Kajli sheep; Beetal goats) as well as imported small ruminant breeds (Dorper sheep; Australian Boer goat). Morbidity and mortality rates were significantly (P < 0.001) higher in indigenous Kajli sheep (75.37 and 32.80%) and Beetal goats (81.10 and 37.24%) as compared to Dorper sheep (6.99 and 1.48%) and Australian Boer goat (5.01 and 2.23%). Affected animals exhibited high fever, severe diarrhea, abdominal pain, respiratory distress and nodular lesions on lips and nostrils. Thick mucous discharge was oozing out from nostrils. On necropsy, lungs were congested and pneumonic, with nodular and cystic appearance. Intestines were hemorrhagic with zebra stripping. Characteristic histopathological lesions of PPR were noted in intestines, lymphoid organs and lungs. In GI tract, stunting and blunting of villi, necrotic enteritis, and infiltration of mononuclear cells in duodenum, jejunum and ileum. Small intestines exhibited diffuse edema of the submucosa along with proliferation of fibrocytes leading to thickened submucosa which has not been reported previously. Lymphoid organs showed partial to complete destruction of lymphoid follicles. Lesions of the respiratory tract included depictive of bronchopneumonia, severe congestion of trachea and apical lobe of lungs with deposition of fibrinous materials. Histopathological lesions of respiratory tract were severe and characteristic of broncho-interstitial pneumonia, bronchopneumonia, interstitial pneumonia and fibrinous pneumonia. The alveoli were filled with edematous fluid mixed with fibrinous exudate, numerous alveolar macrophages, mononuclear cells along with thickened interalveolar septa and presence of intranuclear eosinophilic inclusion bodies. One-Step RT-PCR using NP3 and NP4 primers confirmed a PPR virus of 352 bp size in spleen, lungs and mesenteric and brachial lymph node samples. It was concluded that morbidity and mortality due to PPR were significantly higher in indigenous breeds of sheep and goat as compared to imported sheep and goat breeds. PPR has rendered various lesions in GI and respiratory tract which are characteristic in nature for the diagnosis of the disease under field condition.

Expression kinetics of ISG15, IRF3, IFNγ, IL10, IL2 and IL4 genes vis-a-vis virus shedding, tissue tropism and antibody dynamics in PPRV vaccinated, challenged, infected sheep and goats.

Here, we studied the in vivo expression of Th1 (IL2 and IFN gamma) and Th2 (IL4 and IL10) - cytokines and antiviral molecules - IRF3 and ISG15 in peripheral blood mononuclear cells in relation to antigen and antibody dynamics under Peste des petits ruminants virus (PPRV) vaccination, infection and challenge in both sheep and goats. Vaccinated goats were seropositive by 9 days post vaccination (dpv) while in sheep idiosyncratic response was observed between 9 and 14 dpv for different animals. Expression of PPRV N gene was not detected in PBMCs of vaccinated and vaccinated challenged groups of both species, but was detected in unvaccinated infected PBMCs at 9 and 14 days post infection. The higher viral load at 9 dpi coincided with the peak clinical signs of the disease. The peak in viral replication at 9 dpi correlated with significant expression of antiviral molecules IRF3, ISG15 and IFN gamma in both the species. With the progression of disease, the decrease in N gene expression also correlated with the decrease in expression of IRF3, ISG15 and IFN gamma. In the unvaccinated infected animals ISG15, IRF3, IFN gamma and IL10 expression was higher than vaccinated animals. The IFN gamma expression predominated over IL4 in both vaccinated and infected animals with the infected exhibiting a stronger Th1 response. The persistent upregulation of this antiviral molecular signature - ISG15 and IRF3 even after 2 weeks post vaccination, presumably reflects the ongoing stimulation of innate immune cells.

Investigating peste des petits ruminants (PPR) in naturally infected goats and sheep in Anseba Region, Eritrea, by reverse transcription polymerase chain reaction (RT-PCR).

The impact of peste des petits ruminants (PPR) virus was investigated by reverse transcription polymerase chain reaction (RT-PCR) on different samples obtained from non-vaccinated diseased and necropsied sheep and goats showing PPR-like symptoms. The disease picture was typical and sheep were observed to be less susceptible. Nasal and rectal swabs, whole blood and pathological tissue samples from the lungs, intestine, and mesenteric lymph nodes were used for this study. The results of RT-PCR indicated that from a total of 32 samples collected, 12 (41%) were positive by this method. Out of those collected samples, 29 were from goats and 3 were from sheep. Nasal and rectal swabs and blood samples were superior in detection of the PPR virus compared to other tissue samples.

Sequence analysis of peste des petits ruminants virus from ibexes in Xinjiang, China.

Peste des petits ruminants (PPR) is an infectious disease caused by peste des petits ruminants virus (PPRV). While PPR mainly affects domestic goats and sheep, it also affects wild ungulates such as ibex, blue sheep, and gazelle, although there are few reports regarding PPRV infection in wild animals. Between January 2015 and February 2015, it was found for the first time that wild ibexes died from PPRV infection in Bazhou, Xinjiang, China, where a total of 38 ibexes (including young and adult ibexes) were found to have died abnormally from PPR-related issues. First, we tested for the presence of the F gene of PPRV by RT-PCR. Then, we compared the sequence of the isolated F gene from the ibex strain, termed PPRV Xinjiang/Ibex/2015, with those previously identified from small domestic ruminants from local areas near where the reported isolate was collected as well as those from other regions. The current sequence was phylogenetically classified as a lineage IV virus, and shared a high level of sequence identity (99.7%) with a previously described Xinjiang PPRV isolate.

Syndromic surveillance of peste des petits ruminants and other animal diseases in Koinadugu district, Sierra Leone, 2011-2012.

PURPOSE: The purpose of this study was to conduct syndromic surveillance for important veterinary diseases in Koinadugu district, Northern Province, Sierra Leone. METHODS: This study examined all veterinary syndromic surveillance reports submitted to the district veterinary office from January 2011 through December 2012. RESULTS: In total, 5679 case reports were submitted, including 2394 fatalities. The most common syndrome reported was consistent with peste de petits ruminants (PPR) in goats (n = 1649). PPR cases were reported from eight of 11 chiefdoms in the district, with a 42 per 1000 reported incidence rate and a 48 % case fatality rate. Other syndromes reported were consistent with trypanosomiasis in cattle (n = 1402), Newcastle disease in poultry (n = 911), black quarter in cattle (n = 691), and haemorrhagic septicaemia in cattle (n = 542). CONCLUSIONS: Expanded use of the PPR virus vaccine may be required to help control the spread of the infection. Improved community-based prevention efforts may be effective for better control of trypanosomiasis and all these conditions.

Natural peste des petits ruminants virus infection in Black Bengal goats: virological, pathological and immunohistochemical investigation.

BACKGROUND: Peste des Petits Ruminants (PPR), also known as Goat Plague, occurs in goats, sheep and related species. It is caused by a morbillivirus in the family Paramyxoviridae. In Bangladesh PPR is endemic and it causes serious economic losses. Pathology of PPR has been reported in different goat and sheep breeds from natural and experimental infections. Field results are better indicators of pathogenicity of the circulating virus. The severity of the disease varies with species, breed and immune status of the host. Pathological investigations of natural outbreaks of PPR in Balck Bengal goats are very limited. The current investigation was aimed at describing pathology and antigen localization in natural PPR infections in Black Bengal goats. RESULTS: A total of 28 outbreaks were investigated clinically and virologically. Average flock morbidity and mortality were 75% and 59%, respectively, with case fatality rate of 74%. Necropsy was conducted on 21 goats from 15 outbreaks. The major gross lesions were congestion of gastrointestinal tract, pneumonia, engorged spleen, and oedematous lymphnodes. Histopathological examination revealed severe enteritis with denudation of intestinal epithelium, severe broncho-interstitial pneumonia with macrophages within lung alveoli and extensive haemorrhages with depletion of lymphoid cells and infiltration of macrophages in the sinuses of spleen. In lymph nodes, the cortical nodules were replaced by wide sinusoids with severe depletion of lymphocytes, infiltration of mononuclear cells and some giant cells in sub-capsular areas and medullary sinuses. PPR virus antigen was found in pneumocytes and alveolar macrophages in lungs. Viral RNA could be detected by RT-PCR in 69 out of 84 nasal swab, 59 out of 84 blood and 21 out of 21 lymph node samples. Sequence analyses revealed closeness of Bangladeshi strains with other recent Asian isolates. CONCLUSION: Natural outbreaks of PPR in Black Bengal goats in Bangladesh resulted in 75% and 59% flock morbidity and mortality, respectively, with a case fatality rate of 74%. The striking histo-morphologic diagnosis of PPR was acute pneumonia and severe gastro-enteritis. A detailed experimental pathological study on Black Bengal goats infected with recent isolates is required.

Epidemiological and pathomorphologic investigation of peste des petits ruminants in Western Algeria: A comprehensive study of clinical and histopathological findings.

Background: This study delves into the epidemiology and pathomorphologic characteristics of peste des petits ruminants (PPR) in western Algeria, a viral disease that constantly threatens small animals in Africa, the Middle East, and Asia. Aim: The purpose of this investigation was to evaluate the epidemiology of PPR in western Algeria and to understand the pathomorphological lesions in naturally infected small ruminants. Methods: An online survey conducted via google forms and shared with veterinarians in the wilaya of Tiaret, provided insights into the prevalence and clinical manifestations of PPR.A comprehensive examination of organs was conducted and representative tissue samples from the lungs, trachea, thymus, spleen, liver, kidney, heart, tongue, stomach, different parts of the small and large intestine, and mesenteric lymph nodes were collected and the specimen was fixed in a 10% neutral buffer formalin solution. Results: Among 2,200 small ruminants managed by expert veterinarians, 192 small ruminants exhibited clinical signs compatible with PPR, and 79 dead animals. Among the 31 sick young small ruminants, eight were confirmed to be infected with the PPR virus. Necropsies of affected animals revealed significant gross lesions in organs such as the lungs, intestines, spleen, and lymph nodes. Histopathological analysis further illuminated the severity of lesions, including interstitial pneumonia, syncytial cell formation, and severe gastroenteritis. Conclusion: The study's comprehensive approach, encompassing epidemiological data, necropsy findings, and histopathological insights, contributes valuable knowledge for understanding and managing PPR outbreaks.The pathological lesions observed in this study exhibited consistency with those previously documented in experimental studies, thereby providing support for the diagnosis based on clinical signs and disease history.

Unveiling of the Co-Infection of Peste des Petits Ruminants Virus and Caprine Enterovirus in Goat Herds with Severe Diarrhea in China.

Here, we report the discovery of two viruses associated with a disease characterized by severe diarrhea on a large-scale goat farm in Jilin province. Electron Microscopy observations revealed two kinds of virus particles with the sizes of 150-210 nm and 20-30 nm, respectively. Detection of 276 fecal specimens from the diseased herds showed the extensive infection of peste des petits ruminants virus (63.77%, 176/276) and caprine enterovirus (76.81%, 212/276), with a co-infection rate of 57.97% (160/276). These results were partially validated with RT-PCR, where all five PPRV-positive and CEV-positive specimens yielded the expected size of fragments, respectively, while no fragments were amplified from PPRV-negative and CEV-negative specimens. Moreover, corresponding PPRV and CEV fragments were amplified in PPRV and CEV double-positive specimens. Histopathological examinations revealed severe microscopic lesions such as degeneration, necrosis, and detachment of epithelial cells in the bronchioles and intestine. An immunohistochemistry assay detected PPRV antigens in bronchioles, cartilage tissue, intestine, and lymph nodes. Simultaneously, caprine enterovirus antigens were detected in lung, kidney, and intestinal tissues from the goats infected by the peste des petits ruminants virus. These results demonstrated the co-infection of peste des petits ruminants virus with caprine enterovirus in goats, revealing the tissue tropism for these two viruses, thus laying a basis for the future diagnosis, prevention, and epidemiological survey for these two virus infections.

Investigation of the Clinical and Diagnostic Aspects of Peste des Petits Ruminants (PPR) in Sheep from the Southern Region of Iraq.

In the southern region of Iraq, Peste des petits ruminants (PPR) has been identified and diagnosed. The study was done on (300) local sheep breeds of varying ages and sexes exhibiting PPR symptoms, while (25), healthy sheep breeds served as the control group. Additionally, the diagnosis of PPRV was confirmed by PCR. Infected sheep exhibit a variety of clinical symptoms. However, DNA sequencing was used to detect genetic links and genetic variation, and the results revealed a closed genetic relationship with the NCBI BLAST PPRV India isolate (GU014574.1) at total genetic variation (0.02-0.01%). Results indicate a large rise in PCV and ESR in conjunction with leukocytopenia and lymphocytopenia, a significant difference in clotting factor indices, and a significant increase in ALT, AST, and CK. In addition, there was a substantial variation in acute phase response. Postmortem examinations revealed various erosive lesions on the upper and lower gums, severe hemorrhagic enteritis, particularly of the small intestine, and obvious congestion of the lungs. Histopathological changes revealed an obvious flattening of the intestinal mucosa as well as an enlargement of the villi. In addition to a granuloma in the sub-mucosa, chronic inflammatory cells, primarily lymphocytes, were seen invading the mucosa. It has been determined that the sickness was circulating in the southern region of Iraq and severely afflicted sheep, which might result in significant economic losses owing to the detrimental effects of the virus that causes the disease on the various bodily parts.

A reliable and reproducible experimental challenge model for peste des petits ruminants virus.

Experimental challenge protocols that consistently reproduce clinical signs of peste des petits ruminants in Alpine goats infected with a tissue culture-passaged peste des petits ruminants virus are described. The protocols can be used to carry out quality-controlled vaccine efficacy and pathogenesis studies under experimental conditions.

Coagulation profile, haematological and biochemical changes in kids naturally infected with peste des petits ruminants.

The aim of this study was to examine the coagulation profile in peste des petits ruminant (PPR) in kids. Five kids from a group of 150 animals (72 goats and 78 kids) were brought to the Veterinary Medical Teaching Hospital from a farm in Burdur province (Turkey) with nasal and ocular discharges and diarrhea. Fifteen goats and 41 kids had died due to diarrhea and three kids were presented to the Department of Pathology for diagnosis. Blood samples were taken from 12 ill animals (infected group) for haematological and biochemical analysis. In addition, five healthy kids were examined from another healthy flock (control group). Leukocyte and lymphocyte numbers of infected group showed significant declinations in comparison to control group (≤0.001). Haemorrhages in all organs of digestive system and small haemorrhagic areas in liver were caused to decrease in erythrocyte and haematocrit values (p ≤ 0.001) in infected group. Concentrations of blood urea nitrogen (BUN) (p ≤ 0.01) and creatinine (p ≤ 0.001) in infected group were significantly higher than control group. Compared to control group, significant increases were determined in serum concentrations of alkaline phosphatase (ALP) (p ≤ 0.01), aspartate aminotransferase (AST) (p ≤ 0.001) and alanine aminotransferase (ALT) (p ≤ 0.001) in the infected group. No significant differences were observed between the infected and control groups for serum gamma glutamyl-transferase (GGT) concentration value. In our study, thrombocytopenia (p ≤ 0.001) together with prolonged activated partial thromboplastin time (APTT; p ≤ 0.01) and prothrombin time (PT; p ≤ 0.001) may show that disseminated intravascular coagulopathy which can occur in kids with PPR.

A study on transmission of Peste des petits ruminants virus between dromedary camels and small ruminants.

INTRODUCTION: In recent years Peste des petits ruminants (PPR) disease caused several epidemics in a wide range of susceptible hosts. The ability of the peste des petits ruminants virus (PPRV) to cross the species barrier necessitates further research, particularly on disease circulation and cross-species transmission between typical and atypical hosts to guide and facilitate the eradication program anticipated by the Food and Agriculture Organization (FAO) and the World Organization for Animal Health (OIE) in 2030. The aim of this study is to explore the role of dromedary camels as transmitters for PPR. METHODOLOGY: Four experiments were carried out on clinically healthy seronegative camels, sheep and goats. In experiment I, the animals were inoculated with a PPR- positive suspension of camel pneumonic lung homogenate. In the other three experiments either sheep and goats were inoculated and after three days were housed with camels or vice versa. RESULTS: Marked clinical signs suggestive of PPR were seen in sheep and goats while camels showed mild infection. Severe clinical signs of PPR were seen in sheep and goats when kept with inoculated camels. Postmortem examination revealed PPR lesions in all inoculated animals including camels. CONCLUSIONS: This study showed that dromedary camels infected with PPRV can transmit the disease to sheep and goats, even when they developed mild clinical signs.

Evidence of peste des petits ruminants virus (PPRV) infection in Sindh Ibex (Capra aegagrus blythi) in Pakistan as confirmed by detection of antigen and antibody.

An outbreak resulting in mortality in Sindh Ibex (Capra aegagrus blythi) was investigated. There was a history of about 36 deaths (both young and adult) during the period of 1 month. Disease appeared in a generalized form, affecting the respiratory and digestive systems. Major lesions were respiratory distress, pustules on and in the mouth, ocular-nasal discharges, and severe diarrhea. The most significant lesion was the oculonasal discharges and diarrhea. Deaths were mainly due to blindness, anorexia, diarrhea, and respiratory arrest. Both adult (mortality = 21) and young (mortality = 15) animals were affected with the disease. Peste des petits ruminants virus (PPRV) antigen was detected in the spleen, lung, lymph node, and swab samples by immunocapture enzyme-linked immunosorbent assay. Spleen and lung samples were also tested and found positive for the presence of F-gene of PPRV by polymerase chain reaction. Thirteen of 20 serum samples from nearby sheep and goats were found positive for antibodies to PPRV. The disease threatened the huge population of ibex in the wild life park, which was spread over a large area, but vaccination of the domestic population of sheep and goats in the surrounding villages appeared to control the disease.

A Mouse Model of PPRV Infection for Elucidating Protective and Pathological Roles of Immune Cells.

The study was aimed at developing an accessible laboratory animal model to elucidate protective and pathological roles of immune mediators during Peste des petits ruminants virus (PPRV) infection. It is because of the critical roles of type I IFNs in anti-viral defense, we assessed the susceptibility of IFN receptor knock out (IFNR KO) mice to PPRV infection. IFNR KO mice were exceedingly susceptible to the infection but WT animals efficiently controlled PPRV. Accordingly, the PPRV infected IFNR KO mice gradually reduced their body weights and succumbed to the infection within 10 days irrespective of the dose and route of infection. The lower infecting doses predominantly induced immunopathological lesions. The viral antigens as well as the replicating PPRV were abundantly present in most of the critical organs such as brain, lungs, heart and kidneys of IFNR KO mice infected with high dose of the virus. Neutrophils and macrophages transported the replicating virus to central nervous system (CNS) and contributed to pathology while the elevated NK and T cell responses directly correlated with the resolution of PPRV infection in WT animals. Using an array of fluorescently labeled H-2Kb tetramers, we discovered four immunogenic epitopes of PPRV. The PPRV-peptides interacted well with H-2Kb in acellular and cellular assay as well as expanded the virus-specific CD8+ T cells in immunized or infected mice. Adoptively transferred CD8+ T cells helped control PPRV in infected mice. Our study therefore established and employed a mouse model for investigating the pathogenesis of PPRV. The model could be useful for elucidating the contribution of immune cells in disease progression as well as to test anti-viral agents.