Field evaluation of clinical features during chikungunya outbreak in Mayotte, 2005-2006.

BACKGROUND: To record and assess the clinical features of chikungunya fever (CHIKF), with a view to enable diagnosis based on clinical criteria rather than costly laboratory procedures in field conditions. METHODS: As part of a cross-sectional serologic survey conducted in Mayotte after a massive chikungunya outbreak in 2006, we collected data on clinical features of chikungunya infection and assessed the performance and accuracy of clinical case definition criteria combining different symptoms. RESULTS: Of 1154 participants included, 440 (38.1%) had chikungunya-specific IgM or IgG antibodies by enzyme-linked immunosorbent assay (ELISA). Of symptomatic participants, 318 (72.3%) had confirmed chikungunya, the dominant symptoms reported were incapacitating polyarthralgia (98.7%), myalgia (93.1%), backache (86%), fever of abrupt onset (85%) and headache (81.4%). There was a strong linear association between symptomatic infection and age (chi(2) for trend = 9.85, P < 0.001). Only 52% of persons with presumptive chikungunya sought medical advice, principally at public primary health care facilities. The association of fever and polyarthralgia had a sensitivity of 84% (95% CI: 79-87) and a specificity of 89% (95% CI: 86-91). This association allowed to classify correctly 87% (95% CI: 85-89) of individuals with serologically confirmed chikungunya. CONCLUSIONS: Our results suggest that the pair fever and incapacitating polyarthralgia is an accurate and reliable tool for identifying presumptive CHIKF cases in the field. These criteria provide a useful evidence base to support operational syndromic surveillance in laboratory-confirmed chikungunya epidemic settings.

Neurological complications in Chikungunya fever.

OBJECTIVE: The present prospective study was undertaken to study the clinical manifestations and mainly neurological complication of an acute febrile illness termed chikungunya which has recently attacked india after 43 years. METHOD: This prospective study has been conducted in hospitalised patients admitted in government and private hospitals of Kota city from August 2006 to October 2006. Patients showing neurological involvement with typical clinical picture of chikungunya infection were studied in detail and followed up for improvement and any permanent damage or death. RESULTS: Apart from typical clinical triad of high grade fever, arthralgia and rash of chikungunya infection we have observed a spectrum of neurological abnormalities in terms of altered mental functions, seizures, focal neurological deficit with abnormal CT scan of head and altered CSF biochemistry. Permanent neurological sequelae and even death has occurred. CONCLUSION: Typical clinical history of chikungunya infection, neurological complications with associated CSF abnormalities, supportive laboratory evidences, positive chikungunya IgM card test, exclusion of other causes and known predilection of arboviruses for CNS infection allows us to conclude the diagnosis of study cases as Chikungunya Encephalitis.

Porcine reproductive and respiratory syndrome: NEB-1 PRRSV infection did not potentiate bacterial pathogens.

A 2-phase study was conducted to evaluate the ability of the NEB-1 strain of porcine reproductive and respiratory syndrome virus (PRRSV) to potentiate common bacterial pathogens of swine. In phase I, 25 of 50 4-5-week-old specific-pathogen-free (SPF) pigs were exposed to NEB-1 PRRSV (day 0). Seven days after virus inoculation, 8 groups received 1 of 4 bacterial pathogens: Haemophilus parasuis, Streptococcus suis, Salmonella cholerasuis, and Pasteurella multocida. The ability of NEB-1 PRRSV to produce clinical disease, viremia, neutralizing antibody, gross and microscopic lesions and to potentiate bacterial pathogens was assessed. Response to NEB-1 PRRSV was similar among inoculated pigs; prolonged hyperthermia, lethargy, mild to moderate dyspnea, and cutaneous erythema were consistent clinical signs. No clinical differences were observed in groups after bacterial challenge. Virus was isolated from serum at weekly intervals through the end of the study, and all PRRSV-inoculated pigs had seroconverted by study termination. Two of 5 pigs died in non-PRRSV-inoculated groups challenged with H. parasuis and Streptococcus suis. Mortality in PRRSV-infected pigs was limited to 1 of 5 pigs from the Salmonella cholerasuis-challenged group. Gross lesions were seen in pigs dying after inoculation in H. parasuis- and Streptococcus suis-inoculated groups, in Salmonella cholerasuis- and P. multocida-challenged pigs, and in 1 non-PRRSV-inoculated control pig. Microscopic lesions consisted of mild to moderate proliferative interstitial pneumonia, nonsuppurative myocarditis, lymphoid hyperplasia, and nonsuppurative encephalitis in PRRSV-inoculated pigs. Findings in phase I indicated that NEB-1 PRRSV does not potentiate bacterial disease while inducing consistent clinical signs, viremia, seroconversion, and microscopic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Viral infection including HIV and AIDS.

Viruses have long been considered candidates for infectious etiologic agents or cofactors in the development of rheumatic diseases. The current epidemic of HIV infection and the recognition of "emerging viruses" has focused interest on the possible role of viruses in pathogenesis of diseases without defined etiology. Over the past year, the role of parvovirus B19 in chronic arthropathy was further defined. Additional data added to our understanding of the mechanisms by which rubella virus may cause chronic arthritis. We were reminded of the potential the togaviruses have to cause epidemics of febrile arthritis. The developing story of hepatitis C virus in essential mixed cryoglobulinemia encourages us to explore strategies for specific antiviral therapies. The members of the herpesvirus family came under scrutiny for their role in Sjögren's syndrome. The retroviruses continue to attract attention because of rheumatic disease syndromes in AIDS patients and the suggestion that still undefined retroviruses may play an etiologic role in rheumatoid arthritis. This review highlights efforts made in the past year to elucidate the role of viral infection in rheumatologic disease.

High mortality of domestic turkeys associated with Highlands J virus and eastern equine encephalitis virus infections.

High mortality occurred in two flocks of commercial turkey hens placed in southern North Carolina in fall 1991. Daily mortality peaked at 3.19% in Flock 1 and 3.79% in Flock 2. Clinical signs included restlessness, somnolence, vocalization, and acute death. Gross lesions included atrophy of the bursa of Fabricius, thymus, and spleen, and watery intestinal contents. Microscopic changes included moderate to marked lymphocyte necrosis and depletion in the bursa, thymus, and spleen, widely scattered necrosis of pancreatic acinar cells, and mild villous atrophy and fusion in the jejunum and ileum with cuboidal to low columnar epithelial cells covering the villous tips. In Flock 1, at 27 days of age, reovirus and picornavirus particles were detected in the feces. One week later, togavirus-like particles were observed in fecal contents, and two of seven serum samples showed seroconversion to Highlands J virus. Eleven days later, five of six serum samples were positive for antibodies against Highlands J virus, with a fourfold increase in the geometric mean titer. In Flock 2, seroconversion to eastern equine encephalitis virus was observed in four of 10 serum samples 11 days after the onset of clinical signs. Based on the above observations, it is suspected that these alphaviruses were the cause of the clinical syndrome.

Virological and immunological studies of Wesselsbron virus in experimentally infected red Sokoto (Maradi) goats.

Red Sokoto goats aged four to five months were experimentally infected with the Nigerian strain of Wesselsbron virus. Viraemia commenced 24-72 hours after infection and lasted for 3-4 days. A febrile reaction which was mostly biphasic coincided with viraemia. A 50% mortality rate was observed among infected animals. The virus was re-isolated in mice from almost every tissue (liver, spleen, lungs, brain, kidney, adrenal, lymph node and heart) obtained from dead goats. Complement fixing antigens were detected in the tissues of dead goats, the titre of which correlated positively with the infectivity titre. All infected animals developed complement-fixing and haemagglutination inhibiting antibodies to Wesselsbron virus. However, neutralizing antibody was detected only in goats that survived the infection.

Viruses as teratogens.

The ability of certain viruses to affect prenatal development in domestic animals is well documented. However, differentiating a viral-induced malformation from those caused by genetic or other environmental causes is a diagnostic dilemma. Understanding how viruses interact with their embryo-fetal hosts and the potential consequences on prenatal development requires refining and dispelling some old concepts and injecting new insights into this diagnostic challenge. This article discusses several viral teratogens affecting domestic animals: Akabane, bluetongue, Cache Valley, Japanese B encephalitis, bovine viral diarrhea, Border disease, Chuzan, epizootic hemorrhagic disease, hog cholera, Rift Valley fever, and Wesselsbron disease viruses.

Serological and antigenical findings indicating pestivirus in man.

An epidemiological survey for pestivirus was undertaken in Zambia and Europe, in view of the recent serological findings obtained by previous studies in Europe with humans. Collected sera were tested for anti-bovine viral diarrhea virus (BVDV) specific antibodies by IIF and Western Blotting. Of those individuals tested (n = 1272), 15.3% showed a seropositive reaction to the BVDV. Anti-BVDV antibody prevalence in immuno-depressed patients (e.g. HIV positive) was investigated. A higher prevalence was revealed in HIV patients suffering from chronic diarrhoea and in those having developed AIDS Related Complex (ARC). Our of 212 persons tested for pestivirus isolation, a non cytopathic virus strain was detected in 2 buffy coat samples using IIF with a specific anti-BVDV serum. The isolation could be repeated three times during 31 days in one person. The virus was identified as a pestivirus with radioimmuno-precipitation assays and IIF-flow cytometry. A doublet of 120 kD was identified only in cell lysates, indicating a non-structural protein. In order to rule out cross reactivity 30 sera from Hepatitis C seropositive patients were tested against the isolate by IIF-flow cytometry. No antigen-specific binding could be observed. These findings indicated the occurrence of a pestivirus in man and might suggest a relationship with a pestivirus of animal origin.

Murray Valley encephalitis acquired in Western Australia.

OBJECTIVE: To report a recent fatal case of encephalitis associated with evidence of Murray Valley encephalitis virus infection, only the second fatality from this infection in Western Australia. CLINICAL FEATURES: An 18-month-old Aboriginal boy was admitted to hospital in northwest Western Australia with proven Haemophilus influenzae type b meningitis. INTERVENTION AND OUTCOME: After an initial good response to antibiotics (amoxycillin and cefotaxime) he relapsed and died with evidence of encephalitis. Analysis of serum showed a high titre of antibody to Murray Valley encephalitis (MVE) virus with the presence of specific IgM. No evidence was found for other infective agents. CONCLUSION: It is likely that this child died from MVE which followed his bacterial meningitis. Of the strains of mosquitoes trapped in the area of suspected infection 77.8% were Culex annulirostris, the major vector species for MVE. No MVE virus was isolated from these mosquitoes, but serum from one of the sentinel chickens contained MVE virus antibodies, indicating the presence of the virus in that region.

Abnormalities of responses to autonomic stimulation in the mouse urinary bladder associated with Semliki Forest virus-induced demyelination.

The responses to autonomic stimulation of the urinary bladder were studied in mice infected with Semliki Forest Virus, which has been proposed as an animal model for multiple sclerosis. Mice infected with Semliki Forest Virus showed a decreased body weight when compared with control animals, although their bladders were proportionately heavier. The pharmacological results indicated a selective change in purinergic transmission in the bladders of mice infected with Semliki Forest Virus, while cholinergic transmission remained unchanged. This was demonstrated by a significant increase in the contractile response to beta,gamma-methylene ATP accompanied by an increase in the proportion of the nerve-mediated response blocked by alpha,beta-methylene ATP. In contrast, the contractile response to acetylcholine and the atropine-sensitive component of the neurogenic response were not significantly different between the two groups of animals. Active length-tension curves were also unchanged in the mice infected with Semliki Forest Virus when compared with controls. The results are discussed in relation to those obtained from models of urinary bladder dysfunction associated with hypertrophy; whether the alteration of atropine-resistant (purinergic) function reported here is a general secondary feature of this type of bladder dysfunction or a change specific to the Semliki Forest Virus model of multiple sclerosis is not resolved. This study provides evidence that peripheral changes as well as central nervous system demyelination occur in the Semliki Forest Virus-infected mouse.

Aetiology of Kawasaki disease.

Thirteen serum samples from nine children with Kawasaki disease and 23 control samples gave negative results on screening for antibodies to hog cholera virus, border disease of sheep, bovine diarrhoea virus, and equine arteritis virus. The sera from two children with Kawasaki disease were cytotoxic; a possible link with cytotoxin from Propionibacterium acnes is considered.

Infantile gastroenteritis associated with excretion of pestivirus antigens.

Faeces from children under 2 years old who had gastroenteritis that could not be attributed to recognised enteric pathogens were examined with a monoclonal-antibody-based immunoassay for Pestivirus antigens. Such antigens were detected in 30 of 128 episodes of gastroenteritis. Children without diarrhoeal disease and children infected with rotaviruses had little evidence of Pestivirus infection (faeces positive in 1 of 28 and 1 of 31, respectively). The diarrhoeal disease in children excreting Pestivirus antigens resembled that in other children except that it was more commonly associated with signs and symptoms of respiratory inflammation.

Differentiation of hog cholera and bovine virus diarrhoea viruses in pigs using monoclonal antibodies.

Monoclonal antibodies against hog cholera and bovine viral diarrhoea viruses were assayed on organ tissue sections of experimentally infected animals. The animals had been infected simultaneously with both viruses. The antibodies were tested using an indirect immunofluorescence test and an indirect enzyme immunoassay with a biotin/streptavidin/peroxidase detection system. A polyclonal hyperimmune serum was used as a control in direct immunofluorescence tests. Both techniques based on monoclonal antibodies were more sensitive and more specific than the conventional test, the enzyme immunoassay being more sensitive than the immunofluorescence test. Small amounts of BVD viral antigen were demonstrable with monoclonal antibodies in most organ tissues.

Enhancement of demyelination in the central nervous system of Semliki Forest virus infected mice after pretreatment with muramyl dipeptide.

Semliki Forest virus infections in mice produce an encephalitis with demyelination. If before giving the virus the mice are treated with muramyl dipeptide in Freund's incomplete adjuvant, there is a significant increase in demyelination. If ovalbumin is added to the above and then followed after an interval by a second dose of ovalbumin and finally by the virus, the demyelination is further, but only marginally increased. The addition of ovalbumin without muramyl dipeptide in the schedule appears to increase the number of infiltrating cells and to a lesser extent the perivascular cuffing, but does not increase the demyelination as compared to that obtained when Semliki Forest virus is given on its own.

Effect of viral infection on experimental allergic encephalomyelitis in mice.

BALB/c mice were irradiated with 350 R and injected with mouse spinal cord homogenate (MSCH) in complete Freund's adjuvant. Only 15-30% of these animals developed signs of experimental allergic encephalomyelitis (EAE) at 21-28 days after inoculation. Intraperitoneal infection with the non-lethal A7 strain of Semliki forest virus (SFV) 7 days after sensitization reduced the mean appearance time of the EAE symptoms to 14 days and the number of animals with clinical EAE increased up to 70%. In contrast, virus inoculation 10 days before induction of EAE decreased significantly the incidence of clinical EAE in both BALB/c and SJL mice. Demyelination with increased cellularity, presence of macrophages, stripping of myelin from the axons and sparing of oligodendrocytes was observed in spinal cords of animals at days 13-16 after induction of EAE and subsequent virus infection. No demyelination was seen in specimens taken at the same time from mice inoculated with MSCH or SFV alone. Combined MSCH and virus inoculations induced changes in the general immune response which may be one of the major reasons for the increase or decrease in demyelination in this model.