Demographics, travel characteristics and source of exposure for 60 travel-associated human rabies cases (1990–2012).

1<p>France: 7, Russia and other former USSR countries: 7, United Kingdom and Ireland: 5, Germany: 4, The Netherlands: 2, Italy; 2, Austria: 1, Portugal: 1, Sweden: 1.</p>2<p>US: 12, Canada: 1.</p>3<p>China: 3, Japan: 2, Philippines: 1, Myanmar: 1.</p>4<p>Mexico: 3, Haiti: 1.</p>5<p>Israel: 1, United Arabian Emirates: 1, Iraq: 1.</p>6<p>Algeria: 1, Nigeria: 1.</p>7<p>non-recent migrants or their descendants visiting friends and relatives in their origin countries.</p

Imported Human Rabies Cases Worldwide, 1990–2012

<div><p>Sixty cases of human rabies in international travelers were reviewed from 1990–2012. A significant proportion of the cases were observed in migrants or their descendants when emigrating from their country of origin or after a trip to visit friends and relatives or for other reasons (43.3%). The cases were not necessarily associated with long-term travel or expatriation to endemic countries; moreover, cases were observed in travelers after short trips of two weeks or less. A predominance of male patients was observed (75.0%). The proportion of children was low (11.7%). Cases from India and Philippines were frequent (16 cases/60). In a significant proportion of cases (51.1%), diagnosis was challenging, with multiple missed diagnoses and transfers from ward to ward before the final diagnosis of rabies. Among the 28 patients whose confirmed diagnosis was obtained ante-mortem, the mean time between hospitalization and diagnosis was 7.7 days (median time: 6.0 days, range 2–30) including four cases with a diagnosis delayed by 15 or more days. In five cases, a patient traveled through one or more countries before ultimately being hospitalized. Three factors played a role in delaying the diagnosis of rabies in a number of cases: (i) a low index of suspicion for rabies in countries where the disease has been eradicated for a long time or is now rare, (ii) a negative history of animal bites or exposure to rabies, and (iii) atypical clinical presentation of the disease. Clinical symptomatology of rabies is complex and commonly confuses physicians. Furthermore, failure in diagnosing imported cases in more developed countries is most likely related to the lack of medical familiarity with even the typical clinical features of the disease.</p> </div

Treatment in 60 travel-associated human rabies cases (1990–2012).

1<p>Incomplete course in 2 cases.</p>2<p>Treatment was initiated after the onset of symptoms in all cases.</p>3<p>induction of coma with pentobarbital, midazolam and ketamine and use of antivirals amantadine and ribavirin.</p

Clinical and microbiological features of 60 travel-associated human rabies cases (1990–2012).

1<p>Furious form : classic febrile encephalitic form where signs of irritation of the central nervous system predominate, including agitation, confusion, hydrophobia and aerophobia; paralytic form : paralysis involving the peripheral nerves, usually accompanied by fever.</p>2<p>The sum of percentages is over 100% because rabies was confirmed by more than one method in a number of patients.; RTPCR = reverse transcriptase polymerase chain reaction; FAT = fluorescent antibody test.</p

Number of human rabies cases in travelers per year (60 cases, 1990–2012).

<p>Number of human rabies cases in travelers per year (60 cases, 1990–2012).</p

Country of exposure and place where the case was imported for 60 human rabies cases in travelers (1990–2012).

<p>Country of exposure: circle placed in, place where the cases was imported: according to color of circle.</p

Incubation time (47 human rabies cases in travelers (1990–2012).

<p>Logarithmic scale. Each circle represents one patient.</p

Confirmed rabies in imported nonhuman primates.

1<p>confirmed by histological observation of Negri bodies in the brain.</p>2<p>confirmed by mouse inoculation with brain material.</p>3<p>confirmed by fluorescent antibody testing of brain samples.</p>4<p>This monkey had been vaccinated with a modified live-virus rabies vaccine of avian origin, 13 days before the onset of symptoms. The viral isolate from the rabid monkey had characteristics consistent with an egg-adapted vaccine strain suggesting that the monkey's infection was vaccine-induced. These included a short incubation period in mice (4–5 days), absence of fluorescent rabies antibodies detectable virus in salivary glands and corneas of the mice, only rare inclusions typical of Negri bodies produced on mouse passage, and high titered growth in eggs on first passage.</p>5<p>These monkeys had been vaccinated with a modified live-virus rabies vaccine (strain ERA) 43 and 28 days before the onset of the symptoms, suggesting that the monkey's infection was vaccine induced, although sequencing or typing were not done.</p>6<p>species not stated.</p

Proportion of injuries caused by nonhuman primates among international travelers injured by potentially rabid animals.

<p>Proportion of injuries caused by nonhuman primates among international travelers injured by potentially rabid animals.</p

Human rabies¹ cases following nonhuman primate-related injuries.

1<p>confirmed by molecular analysis.</p>2<p>confirmed by histological observation of Negri bodies in the brain.</p>3<p>rabies diagnosis was assessed on clinical criteria only.</p>4<p>confirmed by fluorescent antibody testing of brain samples, molecular analysis and mouse inoculation with brain material.</p>5<p>species not stated.</p