Ross River Virus Antibody Prevalence, Fiji Islands, 2013–2015

A unique outbreak of Ross River virus (RRV) infection was reported in Fiji in 1979. In 2013, RRV seroprevalence among residents was 46.5% (362/778). Of the residents who were seronegative in 2013 and retested in 2015, 10.9% (21/192) had seroconverted to RRV, suggesting ongoing endemic circulation of RRV in Fiji.


R oss River virus (RRV) is an Alphavirus of the family
Togaviridae and is transmitted to humans by Aedes and Culex mosquitoes (1). Marsupials are considered important reservoirs of RRV (1). Clinical manifestations of RRV infections include fever, rash, and arthralgia. RRV is endemic to Australia, where it causes ≈5,000 cases of epidemic polyarthritis annually (1) (4).
The Republic of the Fiji Islands comprises 322 islands distributed among 4 administrative divisions (Central, Western, Eastern, and Northern) and has a population of ≈830,000. Apart from RRV, the 4 serotypes of dengue virus were the only mosquitoborne viruses known to circulate in Fiji until the recent emergence of Zika and chikungunya viruses (5). We report evidence of endemic RRV circulation in Fiji on the basis of serologic analysis of blood samples collected in 2013 and 2015.
Our study included 778 participants recruited during September-November 2013 from the Central, Western, and Northern divisions for a community-based serosurvey for leptospirosis and typhoid (6). Among the residents from the Central division who had participated in the 2013 survey, 333 had blood drawn again during October-November 2015, including 311 whose serum sample collected in 2013 was available for testing. We tested all blood samples for RRV IgG by using a recombinant antigen-based microsphere immunoassay (7). We analyzed the data with Graph-Pad Prism 6.03 using the Fisher or χ 2 test. We considered p values <0.05 to be significant.
The prevalence of RRV antibodies among participants in 2013 was 46.5% and was lower in the Central (38.1%) than the Western (58.6%; p<0.0001) and Northern (55.9%; p = 0.0108) divisions (Table). The prevalence of RRV antibodies among the participants sampled in the Central division in 2015 (37.2%) was similar to results from this division in 2013 (38.1%). In 2013, a total of 37.4% of the participants born after 1982 (postoutbreak) had RRV antibodies, and this rate in 2015 (26.9%) was not significantly different (p = 0.0685). The prevalence of RRV antibodies increased with age (p<0.0001 in 2013, p = 0.0020 in 2015) and was higher in rural than in urban (p<0.0001 in 2013, p = 0.0197 in 2015) and periurban areas (p = 0.0060 in 2013). No difference by sex was observed. Among the 311 participants with available serum   (2). In our study, which was conducted in 2013, RRV antibody prevalence in the Western, Central, and Northern divisions ranged from 38.1% to 58.6%, and 37.4% of persons born after 1982 had RRV antibodies, suggesting that RRV circulated in all 3 divisions after the 1979 outbreak. The report of RRV infection in travelers or inhabitants from Fiji during 1997-2009 (3,4), the observations that 10.9% of the seronegative participants in our study seroconverted to RRV during 2013-2015, and the increase in the prevalence of RRV antibodies with age, strongly suggest endemic RRV transmission in Fiji.
The finding that RRV seroprevalence was higher in rural than in urban and periurban environments suggests increased transmission risks in the rural areas, potentially because of higher-risk occupations of rural residents (including farming and outdoor work), greater exposure related to rural housing or other environmental factors, greater animal reservoir density, the possibility that nondomestic mosquito species in Fiji such as Aedes vigilax, Ae. polynesiensis, Ae. pseudoscutellaris, Ae. albopictus, and Culex annulirostris might be more competent vectors of RRV than peridomestic mosquito species such as Ae. aegypti (8).
Serosurveys conducted in American Samoa in 2010 (1), in French Polynesia during 2011-2013 (9) and 2014-2015 (7), and our study in Fiji during 2013-2015 suggest that endemic circulation of RRV in the Pacific region continued, or recommenced, after 1979-1980. These data provide further evidence for endemic transmission of RRV in areas where marsupials are absent (10). Because of extensive travel between Australia and the Pacific Islands, it is plausible that RRV is repeatedly seeded into the Pacific region. Whether this plays an important role in perpetuating local transmission in the Pacific Islands is unknown. As previously illustrated with Zika and chikungunya viruses, a risk exists for emerging arboviruses to be imported from the Pacific to other parts of the world, and RRV could be the next unexpected threat.
We report a case of malignant otitis externa with jugular vein thrombosis caused by Aspergillus flavus. Magnetic resonance imaging revealed an unusual ink smudge pattern deep in a cervical abscess. The pattern was consistent with mycetoma and may be important for diagnosing these life-threatening infections.
A 73-year-old male patient sought care from the otorhinolaryngology department at University Hospital, Marseille, France. He had a 5-month history of malignant otitis externa (MOE), which was worsening despite 4 months of treatment with intravenous ceftazidime, oral ciprofloxacin, and topical neomycin, polymyxin B, dexamethasone, and thiomersal combination. The patient had a history of high blood pressure, treated with perindopril and nicardipine, and diabetes mellitus, inadequately controlled (hemoglobin A1c 7.7%) with metformin and sitagliptin.
The patient was admitted, and otoscopic examination found otorrhea, inflammation, and stenosis of the right external auditory canal; we could not see the tympanic membrane. Examination of the cranial nerve was normal. Pure-tone audiogram showed a right mixed hearing loss with air-bone gap at 15 dB and symmetric bone curve by presbycusis. Laboratory testing showed elevated erythrocyte sedimentation level (42 mm at 1 h, 82 mm at 2 h) and leukocytosis (11 g/L); C-reactive protein results were within reference range. A computed tomography (CT) scan of the head showed thickening of the ear skin; focal tympanal bone osteolysis; partial right mastoid air cells and middleear cavity opacification; and osteolysis of the occipital, styloid, and mastoid bones consistent with MOE (Appendix Figure, https://wwwnc.cdc.gov/EID/article/25/4/18-0710-App1.pdf). Magnetic resonance imaging (MRI) with contrast media confirmed skull base osteomyelitis, evidenced by bone lysis and marrow enhancement of the clivus (Figure, panels A-C). Both MRI and CT showed a right jugular vein thrombosis and cellulitis and abscess in the carotid and perivertebral spaces. Abscess content had an unusual aspect: T2-weighted imaging signal void foci surrounded by a hypersignal rim.
We treated the right jugular vein thrombosis with enoxaparin. The patient underwent surgical debridement with facial nerve monitoring; we collected transmastoid biopsy samples and pus for microbiological analysis and inserted a transtympanic aerator. Direct microscopic examination of the samples showed hyaline septate hyphae consistent with hyalohyphomycosis. Biopsy samples grew 2 bacteria, Corynebacterium striatum and Enterococcus faecalis, and 1 filamentous fungus, Aspergillus flavus, that we identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (Microflex LT, https:// www.bruker.com) against an in-house database described by Normand et al. (1). Etest antifungal susceptibility testing (bioMérieux, https://www.biomerieux.com) showed that the A. flavus strain was sensitive to voriconazole (MIC 0.380 mg/L) and resistant to amphotericin B (MIC 12 mg/L). We stopped administration of auricular drops, continued intravenous ceftazidime (1.5 g/d) and oral ciprofloxacin (1.5 g/d), and started voriconazole therapy (6 mg/kg/12 h intravenously, followed by 400 mg/d orally). Otalgia, otorrhea, and inflammatory external auditory canal symptoms were relieved, and the patient recovered after 6 weeks. No further follow-up was available.
Jugular vein thrombosis (JVT) was previously reported in MOE (5) and other conditions such as Lemierre syndrome, invasive fungal infection, or any inflammatory process including otitis media. Various pathogens can cause JVT, especially Fusobacterium necrophorum and zygomycetes.