40 research outputs found

    Yellow Fever Outbreak, Southern Sudan, 2003

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    In May 2003, an outbreak of fatal hemorrhagic fever, caused by yellow fever virus, occurred in southern Sudan. Phylogenetic analysis showed that the virus belonged to the East African genotype, which supports the contention that yellow fever is endemic in East Africa with the potential to cause large outbreaks in humans

    Human rabies associated with domestic cat exposures in South Africa, 1983–2018

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    Rabies is a fatal encephalitic disease caused by lyssaviruses belonging to the family Rhabdoviridae. At the time of this report, a total of 16 species of lyssaviruses, which included the prototype rabies virus (RABV), and 2 related but unclassified bat lyssaviruses, Taiwan and Kothalati, had been recognised by the International Committee on Taxonomy of Viruses (ICTV 2019). Globally RABV, also referred to as ‘classic rabies’, circulates in natural transmission cycles involving domestic dogs and various wildlife species. In the Americas, RABV is found in certain insectivorous and haematophagous bat species (Banyard et al. 2013). The public health burden of rabies is, however, very closely related to the occurrence of the disease in domestic dogs; thus, human cases of rabies are mostly reported from areas where dog rabies is uncontrolled (Hampson et al. 2015). An annual estimation of 59 000 human deaths occur worldwide with 95% of rabies cases occurring in Africa and Asia (Hampson et al. 2015). In South Africa, RABV circulates both in domestic animals and wildlife cycles, involving the canid and mongoose variants of the virus (Nel, Thomson & Von Teichman 1993). The urban cycle involves domestic dogs reported from various locations in the country, but particularly from the KwaZulu-Natal, Eastern Cape, Limpopo and Mpumalanga provinces (Cohen et al. 2007; Zulu, Sabeta & Nel 2009). Sylvatic cycles of the canid variant RABV in bat-eared foxes and black-backed jackal (Zulu et al. 2009) and the mongoose variant RABV in certain species of mongoose occur in South Africa (Van Zyl, Markotter & Nel 2010). Apart from the reservoir species, canid and mongoose RABV infections are reported in an array of domestic and wildlife species in the country, with these animals primarily serving as dead-end hosts (Sabeta et al. 2018). Laboratory-confirmed human rabies cases in South Africa are predominantly dogmediated, and seven cases of rabies linked to other domestic species and wildlife have been reported (Weyer et al. 2011).http://www.jsava.co.zaam2020Medical VirologyVeterinary Tropical Disease

    Serum levels of inflammatory cytokines in Rift Valley fever patients are indicative of severe disease

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    BACKGROUND : Rift Valley fever (RVF) is a mosquito-borne viral zoonosis affecting domestic and wild ruminants, camels and humans. Outbreaks of RVF are characterized by a sudden onset of abortions and high mortality amongst domestic ruminants. Humans develop disease ranging from a mild flu-like illness to more severe complications including hemorrhagic syndrome, ocular and neurological lesions and death. During the RVF outbreak in South Africa in 2010/11, a total of 278 human cases were laboratory confirmed, including 25 deaths. The role of the host inflammatory response to RVF pathogenesis is not completely understood. METHODS : Virus load in serum from human fatal and non-fatal cases was determined by standard tissue culture infective dose 50 (TCID50) titration on Vero cells. Patient serum concentration of chemokines and cytokines involved in inflammatory responses (IL-8, RANTES, CXCL9, MCP-1, IP-10, IL-1β, IL-6, IL-10, TNF and IL-12p70) was determined using cytometric bead assays and flow cytometry. RESULTS : Fatal cases had a 1-log10 higher TCID50/ml serum concentration of RVF virus (RVFV) than survivors (p < 0.05). There were no significant sequence differences between isolates recovered from fatal and non-fatal cases. Chemokines and pro- and anti-inflammatory cytokines were detected at significantly increased (IL-8, CXCL9, MCP-1, IP-10, IL-10) or decreased (RANTES) levels when comparing fatal cases to infected survivors and uninfected controls, or when comparing combined infected patients to uninfected controls. CONCLUSIONS : The results suggest that regulation of the host inflammatory responses plays an important role in the outcome of RVFV infection in humans. Dysregulation of the inflammatory response contributes to a fatal outcome. The cytokines and chemokines identified in this study that correlate with fatal outcomes warrant further investigation as markers for disease severity.The Poliomyelitis Research Foundation (PRF), grant number 12/10. PJvV is further supported by a grant from the Incentive Funding for Rated Researchers program of the National Research Foundation (NRF), South Africa. This work is based on the research supported in part by the National Research Foundation of South Africa (Grant specific unique reference number UID 85544).http://www.virologyj.comam201

    Virus Detection and Monitoring of Viral Load in Crimean-Congo Hemorrhagic Fever Virus Patients

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    We developed a real-time reverse transcription–-PCR that detected 1,164 copies/mL of Crimean-Congo hemorrhagic fever virus per milliliter of serum at 95% probability (probit analysis) and was 100% concordant with nested PCR on 63 samples from 31 patients with confirmed infection. Infected patients who died appeared to have higher viral loads; low viral loads correlated with IgG detection

    Fatal Human Infection with Rabies-related Duvenhage Virus, South Africa

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    Duvenhage virus was isolated from a patient who died of a rabieslike disease after being scratched by a bat early in 2006. This occurred ≈80 km from the site where the only other known human infection with the virus had occurred 36 years earlier

    Mammarenaviruses of rodents, South Africa and Zimbabwe

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    We conducted a survey for group-specific indirect immunofluorescence antibody to mammarenaviruses by using Lassa fever and Mopeia virus antigens on serum specimens of 5,363 rodents of 33 species collected in South Africa and Zimbabwe during 1964–1994. Rodents were collected for unrelated purposes or for this study and stored at −70°C. We found antibody to be widely distributed in the 2 countries; antibody was detected in serum specimens of 1.2%–31.8% of 14 species of myomorph rodents, whereas 19 mammarenavirus isolates were obtained from serum specimens and viscera of 4 seropositive species. Phylogenetic analysis on the basis of partial nucleoprotein sequences indicates that 14 isolates from Mastomys natalensis, the Natal multimammate mouse, were Mopeia virus, whereas Merino Walk virus was characterized as a novel virus in a separate study. The remaining 4 isolates from 3 rodent species potentially constitute novel viruses pending full characterization.http://www.cdc.gov/eidam2022Medical VirologyMicrobiology and Plant PathologyUP Centre for Sustainable Malaria Control (UP CSMC)Veterinary Tropical Disease

    Phylogenetic Relationships of Southern African West Nile Virus Isolates

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    Phylogenetic relationships were examined for 29 southern African West Nile virus (formal name West Nile virus [WNV]) isolates from various sources in four countries from 1958 to 2001. In addition sequence data were retrieved from GenBank for another 23 WNV isolates and Kunjin and Japanese encephalitis viruses. All isolates belonged to two lineages. Lineage 1 isolates were from central and North Africa, Europe, Israel, and North America; lineage 2 isolates were from central and southern Africa and Madagascar. No strict correlation existed between grouping and source of virus isolate, pathogenicity, geographic distribution, or year of isolation. Some southern African isolates have been associated with encephalitis in a human, a horse, and a dog and with fatal hepatitis in a human and death of an ostrich chick

    Lack of Marburg virus transmission from experimentally infected to susceptible in-contact Egyptian fruit bats

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    Egyptian fruit bats (Rousettus aegyptiacus) were inoculated subcutaneously (n = 22) with Marburg virus (MARV). No deaths, overt signs of morbidity, or gross lesions was identified, but microscopic pathological changes were seen in the liver of infected bats. The virus was detected in 15 different tissues and plasma but only sporadically in mucosal swab samples, urine, and fecal samples. Neither seroconversion nor viremia could be demonstrated in any of the in-contact susceptible bats (n = 14) up to 42 days after exposure to infected bats. In bats rechallenged (n = 4) on day 48 after infection, there was no viremia, and the virus could not be isolated from any of the tissues tested. This study confirmed that infection profiles are consistent with MARV replication in a reservoir host but failed to demonstrate MARV transmission through direct physical contact or indirectly via air. Bats develop strong protective immunity after infection with MARV.This work was supported by the National Institute for Communicable Diseases.http://jid.oxfordjournals.orgam2016Paraclinical Science
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