Mild Clinical Disease Research Articles

Comparison of clinical and histopathological findings in patients with lupus nephritis having IgG deposits versus patients without IgG deposits in renal biopsies

Introduction: Up to 10% of lupus nephritis (LN) do not show IgG deposition of immunofluorescence (IF). Our rationale is to find out whether there is any significant difference in clinical presentation and histopathological findings in both groups of patients. Objectives: To compare clinical and histopathological findings in patients with LN having IgG deposits versus patients without IgG deposits in renal biopsies. Patients and Methods: Two groups of IgG positive and IgG negative were made and their details were recorded. Data were analyzed by SPSS 20. Fischer’s exact test was applied to determine significance of above mentioned clinical and laboratory findings with/without IgG deposits in renal biopsies. Results: Fischer’s exact test results’ for all variables was as follows; M: F ratio was 0.5, edema 0.10, deranged RFT 0.3, hematuria 0.10, proteinuria 0.4, anti-double stranded DNA antibody 0.3 and anti-nuclear antibody 0.5. The P values of LN were class II 0.003, class III 0.8 and class IV 0.3. These findings show that groups with no IgG deposits on IF, present with milder clinical disease. Conclusion: There was a marginal significant P value for hematuria, edema and LN class II, pointing towards the fact that relatively milder disease in IgG negative group as compared to IgG positive group.

Characterization of Fitzroy River Virus and Serologic Evidence of Human and Animal Infection.

In northern Western Australia in 2011 and 2012, surveillance detected a novel arbovirus in mosquitoes. Genetic and phenotypic analyses confirmed that the new flavivirus, named Fitzroy River virus, is related to Sepik virus and Wesselsbron virus, in the yellow fever virus group. Most (81%) isolates came from Aedes normanensis mosquitoes, providing circumstantial evidence of the probable vector. In cell culture, Fitzroy River virus replicated in mosquito (C6/36), mammalian (Vero, PSEK, and BSR), and avian (DF-1) cells. It also infected intraperitoneally inoculated weanling mice and caused mild clinical disease in 3 intracranially inoculated mice. Specific neutralizing antibodies were detected in sentinel horses (12.6%), cattle (6.6%), and chickens (0.5%) in the Northern Territory of Australia and in a subset of humans (0.8%) from northern Western Australia.

Acute heaptozoonosis caused by <em>Hepatozoon canis</em> in dogs in Sri Lanka

Canine hepatozoonosis caused by H. canis is usually recognized as a mild clinical disease characterized by mild anaemia and lethargy. Complicated clinical manifestations of H. Canis infection have been occasionally observed in dogs. This clinical communication describes acute hepatozoonosis in five dogs characterized by neurological symptoms, ataxia or paresis, emaciation and anaemia.

A Case of Cocaine-induced Toxic Leukoencephalopathy With Severe Radiologic but Mild Clinical Disease

Objective: To present a case of toxic leukoencephalopathy secondary to cocaine use presenting as mild clinical disease with mainly neurobehavioral symptoms, but relatively severe radiologic disease. Background: The term leukoencephalopathy was first used to describe cerebral white matter changes seen in children with leukemia, but is now used to refer to any of a group of diseases affecting the white substance of the brain. Toxic leukoencephalopathy may be caused by exposure to a wide variety of agents, including cranial irradiation, therapeutic agents, drugs of abuse and environmental toxins. Cocaine-induced toxic leukoencephalopathy is a relatively rare phenomenon with unknown prevalence. Case Presentation: We describe a case of cocaine-induced toxic leukoencephalopathy in a 55-year-old man presenting with confusion, inattention, abulia, and apathy. Infectious work-up and cerebrospinal fluid studies were unremarkable except for a mild elevation of cerebrospinal fluid protein. Magnetic resonance imaging of the brain showing extensive bilateral symmetric leukoencephalopathy is provided, along with a brief discussion of this entity of white matter disease. Conclusions: Cocaine use can manifest as diffuse symmetric white matter changes on magnetic resonance imaging of the brain as well as changes in the basal ganglia and globus pallidus. In the absence of other laboratory and historical abnormalities and in the setting of neurobehavioral disabilities and previous drugs use, it is important to consider cocaine-induced leukoencephalopathy as a differential.

Butyrylcholinesterase activity in dairy cows naturally infected by Dictyocaulus viviparous and treated with eprinomectin

The aim of this study was to evaluate the activity of butyrylcholinesterase (BChE) in dairy cows naturally infected by Dictyocaulus viviparus and treated with eprinomectin. Among 22 serum samples, 10 were of animals with mild clinical disease and 12 with severe clinical disease. The samples were collect on days 0 (day of diagnosis) and 10 post-treatment (a single dose of eprinomectin [360 μg/kg, topically]). We evaluated the activity of BChE, alanine aminotransferase (ALT), aminotransferase andaspartate (AST), and gamma-glutamyl transferase (GGT) in serum. There was no significant difference between groups with different degrees of clinical disease (mild and severe) for the activity of BChE (p > 0.05). However, when considering the treatment (before and after), a significant difference was identified in the activity of BChE (p 0.05), was found. Based on these results, we can conclude that the treatment D. viviparus leads to a decrease of BChE activity, probably due to decrease in the inflammatory response in response to clinical improvement.

Extracellular microvesicle microRNAs in children with sickle cell anaemia with divergent clinical phenotypes.

Sickle cell anaemia (SCA) is the most frequent genetic haemoglobinopathy, which exhibits a highly variable clinical course characterized by hyper-coagulable and pro-inflammatory states, as well as endothelial dysfunction. Extracellular microvesicles are released into biological fluids and play a role in modifying the functional phenotype of target cells. We hypothesized that potential differences in plasma-derived extracellular microvesicles (EV) function and cargo from SCA patients may underlie divergent clinical trajectories. Plasma EV from SCA patients with mild, intermediate and severe clinical disease course were isolated, and primary endothelial cell cultures were exposed. Endothelial cell activation, monocyte adhesion, barrier disruption and exosome cargo (microRNA microarrays) were assessed. EV disrupted the endothelial barrier and induced expression of adhesion molecules and monocyte adhesion in a SCA severity-dependent manner compared to healthy children. Microarray approaches identified a restricted signature of exosomal microRNAs that readily distinguished severe from mild SCA, as well as from healthy children. The microRNA candidates were further validated using quantitative real time polymerase chain reaction assays, and revealed putative gene targets. Circulating exosomal microRNAs may play important roles in predicting the clinical course of SCA, and in delineation of individually tailored, mechanistically-based clinical treatment approaches of SCA patients in the near future.

Middle East respiratory syndrome: A new global threat.

The outbreak of Middle East respiratory syndrome (MERS) is reported from Saudi Arabia and the Republic of Korea. It is a respiratory disease caused by coronavirus. Camels are considered as a source for MERS transmission in humans, although the exact source is unknown. Human-to-human transmission is reported in the community with droplet and contact spread being the possible modes. Most patients without any underlying diseases remain asymptomatic or develop mild clinical disease, but some patients require critical care for mechanical ventilation, dialysis and other organ support. MERS is a disease with pandemic potential and awareness, and surveillance can prevent such further outbreaks.

C-Reactive Protein in Stable Cystic Fibrosis: An Additional Indicator of Clinical Disease Activity and Risk of Future Pulmonary Exacerbations.

IntroductionIn stable adult cystic fibrosis (CF) patients, we assessed the role of baseline high sensitivity C-reactive protein (hs-CRP) on CF clinical variables and frequency of intravenous (IV) treated pulmonary exacerbations (PExs) 1-year post-baseline.MethodsWe recruited 51 clinically stable CF patients from our Adult CF Center. We incorporated collected parameters into Matouk CF clinical score and CF questionnaire-revised quality of life score (QOL). We used the clinical minus complications subscores as a clinical disease activity score (CDAS). We dichotomized our patients according to the cohort median baseline hs-CRP of 5.2 mg/L.ResultsPatients in the high hs-CRP group (≥ 5.2 mg/L) demonstrated worse CDAS (r=0.67, p=0.0001) and QOL scores (r=0.57, p=0.0017) at a given FEV1% predicted. In both hs-CRP groups, prior-year IV-treated PExs and baseline CDASs were significant predictors of future IV-treated PExs. Interestingly, the association between baseline CDAS and future PExs frequency was more robust in the high compared to the low hs-CRP group (r=−0.88, p<0.0001, r=−0.48, p=0.017, respectively) with a steeper regression slope (p=0.001). In addition, a significant interaction was demonstrated between elevated baseline hs-CRP levels and CDASs for the prediction of increased risk of future PExs (p=0.02). This interaction provided an additional indicator of clinical disease activity and added another dimension to the prior year PExs frequency phenotype to identify patients at increased risk for future PExs.ConclusionStable CF patients with elevated baseline hs-CRP (≥ 5.2 mg/L) demonstrated worse clinical disease activity and QOL scores at a given level of disease severity (FEV1% predicted). Elevated baseline hs-CRP values combined with clinical disease activity scores are associated with increased risk for future IV-treated PExs even in those with mild clinical disease activity scores.

Measurement of Systemic Mitochondrial Function in Advanced Primary Open-Angle Glaucoma and Leber Hereditary Optic Neuropathy.

Primary Open Angle Glaucoma (POAG) is a common neurodegenerative disease characterized by the selective and gradual loss of retinal ganglion cells (RGCs). Aging and increased intraocular pressure (IOP) are glaucoma risk factors; nevertheless patients deteriorate at all levels of IOP, implying other causative factors. Recent evidence presents mitochondrial oxidative phosphorylation (OXPHOS) complex-I impairments in POAG. Leber Hereditary Optic Neuropathy (LHON) patients suffer specific and rapid loss of RGCs, predominantly in young adult males, due to complex-I mutations in the mitochondrial genome. This study directly compares the degree of OXPHOS impairment in POAG and LHON patients, testing the hypothesis that the milder clinical disease in POAG is due to a milder complex-I impairment. To assess overall mitochondrial capacity, cells can be forced to produce ATP primarily from mitochondrial OXPHOS by switching the media carbon source to galactose. Under these conditions POAG lymphoblasts grew 1.47 times slower than controls, whilst LHON lymphoblasts demonstrated a greater degree of growth impairment (2.35 times slower). Complex-I enzyme specific activity was reduced by 18% in POAG lymphoblasts and by 29% in LHON lymphoblasts. We also assessed complex-I ATP synthesis, which was 19% decreased in POAG patients and 17% decreased in LHON patients. This study demonstrates both POAG and LHON lymphoblasts have impaired complex-I, and in the majority of aspects the functional defects in POAG were milder than LHON, which could reflect the milder disease development of POAG. This new evidence places POAG in the spectrum of mitochondrial optic neuropathies and raises the possibility for new therapeutic targets aimed at improving mitochondrial function.

Identifying HIV-infected children who may benefit from early initiation of antiretrovirals

In resource-limited settings lacking laboratory testing, clinical staging criteria may not identify all human immuno- deficiency virus (HIV)-infected children who could benefit from antiretroviral therapy (ART). A retrospective analysis was conducted to identify clinical markers in children that could predict rapid progression and need for earlier ART. Pediatric HIV- infected patients receiving care at an outpatient clinic at the Kilimanjaro Christian Medical Centre (KCMC) in Moshi, Tanzania from November 2004-March 2006 were enrolled. Medical records were retrospectively reviewed for sociodemographic data, growth parameters, and medical information. Bivariable analysis was performed to identify predictors of clinical progression. Of 162 patients enrolled, 69 initially presented with mild clinical HIV disease and this analysis focuses on progression within this group. Twenty-one of those 69 progressed clinically to WHO Stage 3/4 during the 18 months of follow-up; 19 progressed within 2-9 months and two additional children were found to have progressed by the 9-18 months visit. Median (range) age at presentation among 69 patients with mild disease was 6.1 years (0.1-13.7 years), and 32 (46%) were female. Fourteen (20% of 69) patients were on ART at their first visit or started ART within the next 2 months (early ART), and an additional 20 (29% of 69) patients started ART in the following 2-18 months. Of initial visit clinical and laboratory criteria, lymphadenopathy (P = 0.046), chronic upper respiratory infections (P = 0.010), lower height-for-age z-score (P = 0.007), lower weight-for-age z-score ( P< 0.001), and CD4% (P = 0.016) were associated with clinical progression. Fewer patients receiving early ART progressed, as compared to patients receiving late ART (P = 0.004). Almost one third of children with clinically mild HIV disease progressed to Stage 3/4 disease within 2-18 months. In settings lacking CD4 cell counts, current guidelines would not have identified the majority of these children for treatment. Improved clinical criteria and low-tech modalities such as point-of-care CD4 testing may help improve identification of children for ART initiation.

Risk of infection and associated influenza-like disease among abattoir workers due to two Leptospira species.

The aims of this study were to determine the annual incidence of infection with Leptospira interrogans serovar Pomona and/or Leptospira borgpetersenii serovar Hardjo and its association with influenza-like illness (ILI) in meat workers in New Zealand. Sera were collected twice, 50-61 weeks apart, from 592 workers at eight abattoirs slaughtering sheep (n=4), cattle (n=2) and deer (n=2), and tested by the microscopic agglutination test for Hardjo and Pomona. Forty-nine (8·3%) participants either seroconverted or had at least a twofold increased serological titre against either serovar. The worker infection risk was higher in sheep abattoirs (11·9%) than in abattoirs processing deer (0%) or cattle (1·2%) (P<0·01). The annualized risk of mild (ILI) or severe clinical disease attributable to the two Leptospira serovars was 2·7%. This study has demonstrated that meat workers are at substantial risk of infection and clinical disease, suggesting further investigation of infection sources and preventive measures are warranted.

EHV‐5 Associated with Respiratory Disease in a Survey of Alpha‐ and Gammaherpesviruses in 409 Australian Horses

Reasons for performing studyTo determine the prevalence of EHV‐1, ‐2, ‐4 and ‐5 in respiratory samples from a large number of horses using quantitative PCR methods. Samples from horses with, and without mild signs of respiratory disease provided an opportunity to examine associations with single or multiple herpesviral infections.ObjectivesTo determine any correlation between quantitative detection of these equine herpesviruses and mild clinical respiratory disease in horses.MethodsNasal swabs were taken from horses with, and without, clinical respiratory disease. Nucleic acid was extracted from all swabs prior to PCR testing for EHV‐1, ‐2, ‐4 and ‐5. Clinical signs of respiratory disease included coughing, fever (temperature &gt;38.5°C) or nasal discharge.ResultsOf the 409 horses, 250 (61%) were clinically normal, 121 (30%) presented with clinical signs consistent with mild respiratory disease and 38 (9%) horses had no traceable clinical history. One‐fifth (83/409) of horses sampled were infected with EHV‐2 and almost two‐thirds 249/409 (60.9%) with EHV‐5. Infection with EHV‐5 was significantly associated with mild respiratory disease (85/121; 70.2%) compared to nondiseased horses (137/249; 55%) P = 0.005. The proportion of EHV‐2 infected horses, however, did not differ significantly between those in the diseased (18/121) and nondiseased (61/250) groups. Too few horses were detected with alphaherpesviruses to determine any association with clinical signs of disease. Mean nasal shedding loads of herpesviruses were not significantly different between diseased and nondiseased horses.ConclusionsThere was a significant association between horses displaying clinical signs of mild respiratory disease and infection with EHV‐5, however, no such association was evident for neither horses with EHV‐2 nor the alphaherpesviruses EHV‐1 and ‐4. The clinical significance of respiratory gammaherpesvirus infections in horses remains yet to be determined; however, these findings add to the mounting body of evidence incriminating EHV‐5 in association with equine respiratory disease.Acknowledgements: The authors are grateful to veterinarians and animal health staff who took samples. Garry Anderson provided valued and erudite statistical assistance.Ethical animal research: Ethical committee oversight not currently required by this congress: the study was performed on archived material collected for the Victorian Department of Environment and Primary Industries’ Equine Influenza surveillance programme. Explicit owner informed consent for participation in this study was not stated. Sources of funding: Special Virology Fund at the University of Melbourne and the Chief Veterinary Officer's unit DEPI Victoria. Competing interests: None.

Natural Immunity of Sheep and Lambs Against the Schmallenberg Virus Infection.

Since the first reports of the Schmallenberg disease (SBD) outbreaks in late 2011, the disease has spread across Europe, affecting cattle and sheep farms. While Schmallenberg virus (SBV) causes a mild clinical disease in adults, infection of pregnant females may lead to the production of typical congenital malformations (CMFs) in their offspring. It is speculated that the immunity acquired after a SBV infection is effective in preventing further infections. However, this has not been proven in naturally infected sheep, especially if they are pregnant when reinfected. The aim of this study was to monitor the natural immunity in SBV-infected sheep. Twenty-four ewes from the only Spanish farm with a SBV OIE-notified outbreak were sampled. Subsequently, nine pregnant ewes were inoculated with SBV infectious plasma under controlled conditions. Six of them were euthanized before delivery, and their fetuses were inspected for lesions indicative for the SBV infection. The three remaining ewes were allowed to deliver one lamb each. Inoculation of the lambs was scheduled at approx. 3months after birth. All samples were analyzed for viral RNA by RT-PCR, and for antibodies by an indirect ELISA and a virus neutralization test (VNT). The majority of the 24ewes showed a serological reaction against SBV. The three ewes that were allowed to lamb down demonstrated variable degrees of seroconversion which corresponded to the levels of immune reaction observed in their lambs. Moreover, no viral RNA was detected, no lesions were observed in the fetuses, and no clinical signs were detected in the inoculated animals. These findings suggest that the immunity acquired by sheep following a natural SBV infection could be sufficient to stop SBV reinfection. However, vaccination could be a valuable tool to control SBV infections and associated economic losses as it affords a more uniform and predictable protection at the flock/herd level.

Treatment considerations of cervical spondylotic myelopathy.

Cervical spondylotic myelopathy (CSM) is the leading cause of myelopathy in patients over age 50 years. Despite advances, CSM remains a clinical diagnosis and its natural history remains unclear. The treatment of CSM is controversial, especially in patients with mild or moderate clinical disease without rapid progression of symptoms. Herein, we begin with a clinical vignette followed by a brief description of the clinical problems. We discuss evaluation, treatment, and recommendations for the treatment of CSM. Emphasis is drawn to areas of uncertainty and present level of evidence for the treatment modalities of CSM.

Bovine viral diarrhoea virus ('pestivirus') in Australia: to control or not to control?

Acute infection with bovine viral diarrhoea virus (BVDV) usually causes only mild clinical disease in cattle, but infection of animals of breeding age can result in immune suppression (resulting in an increased incidence and severity of secondary disease) and decreased reproductive performance. If infection occurs during pregnancy, the virus may cross the placenta and either cause abortion, establish immunotolerance and persistent infection (PI) in the fetus or cause congenital deformities. These outcomes depend on the stage of pregnancy at the time of infection. BVDV is recognised as a disease of significant financial impact in a number of countries. As a result, national and regional BVDV control programs are now in place in several regions around the world. In Europe, these programs largely rely on the identification and removal of the PI animals, whereas vaccination has tended to be the chosen method of control in the United States. BVDV is endemic in Australian cattle populations, with more than 80% of herds surveyed showing some level of exposure to the pathogen. The cost to the national industry is estimated to be AUD57.9 million annually. This review identifies and discusses the challenges to BVDV control in Australia, including farmer attitudes, herd size, sheep as a potential reservoir host and diagnostic capabilities. We conclude that systematic BVDV control in Australia is, or soon will be, an option; however, detailed cost-benefit analyses will need to be undertaken.

Mutations in RSPH1 Cause Primary Ciliary Dyskinesia with a Unique Clinical and Ciliary Phenotype

Primary ciliary dyskinesia (PCD) is a genetically heterogeneous recessive disorder of motile cilia, but the genetic cause is not defined for all patients with PCD. To identify disease-causing mutations in novel genes, we performed exome sequencing, follow-up characterization, mutation scanning, and genotype-phenotype studies in patients with PCD. Whole-exome sequencing was performed using NimbleGen capture and Illumina HiSeq sequencing. Sanger-based sequencing was used for mutation scanning, validation, and segregation analysis. We performed exome sequencing on an affected sib-pair with normal ultrastructure in more than 85% of cilia. A homozygous splice-site mutation was detected in RSPH1 in both siblings; parents were carriers. Screening RSPH1 in 413 unrelated probands, including 325 with PCD and 88 with idiopathic bronchiectasis, revealed biallelic loss-of-function mutations in nine additional probands. Five affected siblings of probands in RSPH1 families harbored the familial mutations. The 16 individuals with RSPH1 mutations had some features of PCD; however, nasal nitric oxide levels were higher than in patients with PCD with other gene mutations (98.3 vs. 20.7 nl/min; P < 0.0003). Additionally, individuals with RSPH1 mutations had a lower prevalence (8 of 16) of neonatal respiratory distress, and later onset of daily wet cough than typical for PCD, and better lung function (FEV1), compared with 75 age- and sex-matched PCD cases (73.0 vs. 61.8, FEV1 % predicted; P = 0.043). Cilia from individuals with RSPH1 mutations had normal beat frequency (6.1 ± Hz at 25°C), but an abnormal, circular beat pattern. The milder clinical disease and higher nasal nitric oxide in individuals with biallelic mutations in RSPH1 provides evidence of a unique genotype-phenotype relationship in PCD, and suggests that mutations in RSPH1 may be associated with residual ciliary function.

An international survey on the interpretation of pigmentation using the C class of the Clinical, Etiological, Anatomical, Pathophysiological Classification

Skin changes over the gaiter area like pigmentation, lipodermatosclerosis and eczema are a clinical sign of advanced chronic venous disorder. This is documented as C4 in the Clinical, Etiological, Anatomical, Pathophysio logical (CEAP) classification. The hypothesis was that there is great variability whether skin changes are recorded as early or advanced disease. The aim was to evaluate different patterns of skin changes by delegates at 3 international venous conferences. Seven high-definition, A4-sized, color photographs were taken of untreated legs with skin changes from patients attending a public hospital venous clinic. They all had venous disease confirmed on duplex with deep or superficial vein reflux &gt;0.5 s. The photographs were displayed and a questionnaire was provided. Delegates familiar with CEAP were asked to choose from 3 C class options for each photograph. The responses were summarized by grouping them into mild (C0-3) and severe (C4-6). A total of 117 delegates completed the questionnaire from 30 countries. A percentage of 60 had practiced phlebology &gt;10 years. The percentages of responders scoring mild (C0-3) and severe disease (C4-6) were: mild/severe=3/96 (photo 1), 65/33 (photo 2), 31/67 (photo 3), 56/34 (photo 4), 74/21 (photo 5), 89/10 (photo 6) and 37/59 (photo 7). The median percentage measure of agreement was 36.8 [95% confidence interval (CI): 24.8- 48.9]. The range was 23.2 (95% CI: 10.5-36.0) to 94.8 (95% CI: 90.7-98.9), P&lt;0.001/image, Fisher exact test). This indicates a significant difference of opinion between the appearances of mild and severe clinical disease. Clinical decisions using the C class as a sign of advanced disease may be unreliable if used alone for recording severity, grouping patients or rationing treatment.

Evidence of vertical transmission of lumpy skin disease virus in Rhipicephalus decoloratus ticks

Lumpy skin disease (LSD) is an economically important acute or sub-acute disease of cattle that occurs across Africa and in the Middle East. The aim of this study was to assess whether Rhipicephalus decoloratus ticks were able to transmit lumpy skin disease virus (LSDV) transovarially. Uninfected, laboratory-bred R. decoloratus larvae were placed to feed on experimentally infected “donor” cattle. After completion of the life cycle on donor animals, fully engorged adult female ticks were harvested and allowed to lay eggs. Larvae that hatched from these eggs were then transferred to feed on uninfected “recipient” cattle. The latter became viraemic and showed mild clinical disease with characteristic skin lesions and markedly enlarged precrural and subscapular lymph nodes. This is the first report of transovarial transmission of poxviruses by R. decoloratus ticks, and the importance of this mode of transmission in the spread of LSDV in endemic settings requires further investigation.

Understanding and Managing Atopic Dermatitis in Adult Patients

Atopic dermatitis (AD) in adults is an important dermatologic disease. Even in patients in whom the clinical presentation is mild, the burden of disease can be considerable. Relatively little has been published on adult AD compared to the body of literature devoted to AD in children, although adults with severe AD are greatly affected by the disease. Even when AD is a mild clinical disease in adults, the psychosocial and economic burden of the disease can be profound. Patients are likely to find it useful if these nondermatologic comorbidities of AD are addressed by health care providers in clinical encounters. The treatment options for AD in adults are the same as those for children with AD, with some modifications.

Natural infection with peste des petits ruminants virus: A pre and post vaccinal assessment following an outbreak scenario

Peste des petits ruminants virus (PPRV) infection was confirmed in a herd of goats (n=55) at an organised farm in Islamabad, Pakistan. PPRV infection was confirmed using both antigen- and antibody-based detection methods, haemagglutination (HA) tests and molecular methods. Animals that survived natural infection developed a typical serological response and virus antigen was detected in fecal matter. Following determination of serological response to infection animals were grouped and either vaccinated or left unvaccinated: group 1 animals succumbed to infection (n=5) and samples were analysed for PPRV antigen; group 2 animals developed clinical disease (n=10) and were divided into 2 groups, half being vaccinated (group 2a) whilst the remainder were unvaccinated (group 2b); group 3 (n=15) animals included those that developed only very mild clinical disease or no clinical disease; group 4 animals (n=5) were negative for clinical disease and were housed as a negative control group. A variable antibody response was detected following resolution of the initial outbreak. Excretion of virus antigen was assessed at different time points following vaccination. Importantly, animals that were vaccinated (group 2a) excreted antigen in fecal matter for 1 month following vaccination whilst unvaccinated animals (group 2b) continued to shed virus antigen for 2 months. The potential for virus excretion in fecal matter and effects of vaccination upon virus infection are discussed. We postulate that excretion in fecal material may represent a mechanism of virus transmission following natural infection and that this mechanism may demonstrate a potential method by which PPRV outbreaks occur spontaneously in areas not previously known to have circulating virus.