This is a topic of recent interest, which could mean that it crops up in a paper somewhere, but thus far the College has not asked about it in the SAQs. Given the very tenuous association of intensive care medicine with this largely mild illness, its appearance in the SAQs would be fairly unlikely, or sadistic and unexpected. However, some Zika-related stuff could appear at some stage. In view of this, a brief overview of this disease is offered here.
Virology and pathology of Zika virus
- Known since 1947
- Named after the East African rain forest where it was discovered
- Transmitted by the Aedes mosquito which also transmit Dengue and yellow fever. This is a daytime vector, in contrast to the mainly nocturnal Anopheles sp.
- ccording to Baombe (2016), interiors of planes are fumigated upon return form at-risk areas, which prevents the mosquito-borne spread of the disease in developed countries
- Apart from monsquitos, Zika is spread by body fluids and is present in them long after the clinical course of the disease is completed
- Developmental defects in the foetus (microencephaly) and the possibility of sexual transmission have been the major sources of media attention.
History and clinical features
- As the physician looking at a case of non-specific viral-sounding illness in a returnign traveller, the follwoing historical data will be of interest:
- Travel history (compared with the epidemiological map)
- Features sugestive of malaria (eg. jaundice, dark urine, history of malarial prophylaxis)
- Features suggestive of Dengue (eg. severe arthralgias)
- Features which may raise suspicion of Ebola
- Essentially, all the mentioned diseases can look like Zika but have a much higher case fatality rate.
- Symptoms are similar to Dengue and malaria:
- skin rash (maculopapular)
- eye pains
- 80% of infections may be asymptomatic
Characteristic findings on investigation
- Laboratory diagnosis is based on detection of ZIKV RNA by polymerase chain reaction (PCR) in blood.
- Viraemia only persist for ~ 5 days
- Viral load is usually low
- Serological diagnosis is difficult: antibodies to flaviviridae all tend to cross-react and are non-virus-specific
Zika-associated Guillain–Barré Syndrome
- Virtually all of the data on this entity comes from a case-control study from a Zika-associated GBS outbreak in French Polynesia (Cao-Lormeau et al, 2016). 42 patient cases were reviewed.
- The risk of GBS was estimated at 0.24/1000 ZIKV infections.
- By comparison, the risk with other illnesses is much greater. It is around 0.25-0.65/1000 for Campylobacter infections and 0.6-2.2 for CMV, i.e. GBS is over ten times as likely with CMV as with Zika.
- Median time to onset of neurological symptomswas 6 days since the beginning of the clinically apparent Zika illness
- The progression of symptoms is very rapid, also about 6 days.
- Cranial nerve involvement is to be expected
- The electrophysiology findings are consistent with acute motor axonal neuropathy (AMAN).
- ICU stay was very long, median was 51 days.
- Treatment is the same as for any GBS: 2g/kg of IV immunoglobulin over 5 days
Issues of concern:
- When Zika outbreaks occur, they tend to be in resource poor areas
- The case load is sually high
- In spite of low GBS case inciudence rate, in outbreaks there may be numerous simultaneous GBS presentations
- In resource-poor areas, such outbreaks of GBS may strain local (small-scale) critical care resources, particularly as the patients tend to stay ventilated for many weeks. This needs to be planned for: according to Thiery et al, "the French West Indies preparedness plan has expected 160 GBS cases including 40 requiring ICU admission for a global population of 800,000 inhabitants"
Apart from GBS, Zika has also been associated with an encephalitis (in two cases, a 81 year old Parisian man and a 15-year-old girl from the French West Indies.