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Serological evidence from French Polynesia links an outbreak of Zika virus to a spike in cases of Guillain-Barré syndrome seen there in 2013-2014.
The research, published online Feb. 29 in The Lancet, is the first to use a case-control design to demonstrate that Zika, a mosquito-borne flavivirus, is associated with Guillain-Barré syndrome (Lancet. 2016 Feb 29. doi: 10.1016/S0140-6736(16)00562-6).
Guillain-Barré syndrome (GBS) is an immune-mediated flaccid paralysis that can follow viral or bacterial infections. Most patients with GBS recover with intensive care in hospitals, although the syndrome can be permanently debilitating or, in rare cases, fatal.
As a large outbreak of Zika continues in Central and South America, hospitals should be prepared for excess GBS cases, the authors of the study say, and assure adequate intensive-care capacity to treat them. Based on the 66% attack rate of Zika during the French Polynesia outbreak, investigators estimated the incidence of GBS at 0.24 per 1,000 Zika infections, but noted that it could be different in the current outbreak.
Dr. Van-Mai Cao-Lormeau of the Unit of Emerging Infectious Diseases at Institut Louis Malardé in Papeete, French Polynesia, alongside colleagues in France and French Polynesia, used a case-control design to compare serological samples from 42 patients (74% male) diagnosed at a Tahiti hospital with GBS with samples from age-and sex-matched patients who presented at the same hospital, also during the time of the outbreak, with a nonfebrile illness (n = 98) or with acute Zika disease without neurological symptoms (n = 70).
The investigators found that all but one patient with GBS had Zika virus antibodies, and all of them had neutralizing antibodies to Zika virus. By comparison, only 56% (n = 54) of the control group admitted with nonfebrile illness had neutralizing antibodies (P less than .0001).
Also, 93% of the GBS patients had Zika virus immunoglobulin M (IgM) and 88% reported symptoms consistent with Zika infection a mean of 6 days before onset of neurological symptoms. Acute Zika infection is usually characterized by rash, fever, and conjunctivitis.
Past dengue virus infection, which had been considered a possible risk factor for Zika-mediated GBS, did not differ significantly between patients in the control groups and those with GBS.
The investigators were also able to subtype the clinical characteristics of the GBS cases as consistent with acute motor axonal neuropathy, or AMAN, phenotype. However, the antibodies typically seen associated with AMAN were not seen in these patients, leading investigators to suspect that a different biological pathway was responsible.
More than a third of the GBS patients in the study required intensive care, most of these also with respiratory support, though none died.
The government of France, the European Union, and the Wellcome Trust funded the study. The researchers declared that they had no competing interests.
Zika virus can be added to our list of viruses that can cause Guillain-Barré syndrome, and investigation of these cases should include tests for Zika when there is a possibility of infection by that virus. Whether Zika will be proven to pose a greater threat in causing Guillain-Barré syndrome than its various flavivirus cousins remains to be determined. A little caution should be taken because the data are still scarce and we do not know whether the current Zika virus is identical to that in previous outbreaks, whether it will behave exactly the same in a different population with a different genetic and immunity background, or whether a cofactor or co-infection is responsible. Reassuringly, the investigators did not find any evidence that previous dengue infection enhanced the severity of the disease, which could substantially have increased the threat in areas of regular activity.
Dr. David W. Smith is a clinical professor of pathology and laboratory medicine at the University of Western Australia in Perth. John Mackenzie, Ph.D., is a professor of tropical and infectious diseases at Curtin University in Bentley, Australia. They had no competing interests to disclose.
Zika virus can be added to our list of viruses that can cause Guillain-Barré syndrome, and investigation of these cases should include tests for Zika when there is a possibility of infection by that virus. Whether Zika will be proven to pose a greater threat in causing Guillain-Barré syndrome than its various flavivirus cousins remains to be determined. A little caution should be taken because the data are still scarce and we do not know whether the current Zika virus is identical to that in previous outbreaks, whether it will behave exactly the same in a different population with a different genetic and immunity background, or whether a cofactor or co-infection is responsible. Reassuringly, the investigators did not find any evidence that previous dengue infection enhanced the severity of the disease, which could substantially have increased the threat in areas of regular activity.
Dr. David W. Smith is a clinical professor of pathology and laboratory medicine at the University of Western Australia in Perth. John Mackenzie, Ph.D., is a professor of tropical and infectious diseases at Curtin University in Bentley, Australia. They had no competing interests to disclose.
Zika virus can be added to our list of viruses that can cause Guillain-Barré syndrome, and investigation of these cases should include tests for Zika when there is a possibility of infection by that virus. Whether Zika will be proven to pose a greater threat in causing Guillain-Barré syndrome than its various flavivirus cousins remains to be determined. A little caution should be taken because the data are still scarce and we do not know whether the current Zika virus is identical to that in previous outbreaks, whether it will behave exactly the same in a different population with a different genetic and immunity background, or whether a cofactor or co-infection is responsible. Reassuringly, the investigators did not find any evidence that previous dengue infection enhanced the severity of the disease, which could substantially have increased the threat in areas of regular activity.
Dr. David W. Smith is a clinical professor of pathology and laboratory medicine at the University of Western Australia in Perth. John Mackenzie, Ph.D., is a professor of tropical and infectious diseases at Curtin University in Bentley, Australia. They had no competing interests to disclose.
Serological evidence from French Polynesia links an outbreak of Zika virus to a spike in cases of Guillain-Barré syndrome seen there in 2013-2014.
The research, published online Feb. 29 in The Lancet, is the first to use a case-control design to demonstrate that Zika, a mosquito-borne flavivirus, is associated with Guillain-Barré syndrome (Lancet. 2016 Feb 29. doi: 10.1016/S0140-6736(16)00562-6).
Guillain-Barré syndrome (GBS) is an immune-mediated flaccid paralysis that can follow viral or bacterial infections. Most patients with GBS recover with intensive care in hospitals, although the syndrome can be permanently debilitating or, in rare cases, fatal.
As a large outbreak of Zika continues in Central and South America, hospitals should be prepared for excess GBS cases, the authors of the study say, and assure adequate intensive-care capacity to treat them. Based on the 66% attack rate of Zika during the French Polynesia outbreak, investigators estimated the incidence of GBS at 0.24 per 1,000 Zika infections, but noted that it could be different in the current outbreak.
Dr. Van-Mai Cao-Lormeau of the Unit of Emerging Infectious Diseases at Institut Louis Malardé in Papeete, French Polynesia, alongside colleagues in France and French Polynesia, used a case-control design to compare serological samples from 42 patients (74% male) diagnosed at a Tahiti hospital with GBS with samples from age-and sex-matched patients who presented at the same hospital, also during the time of the outbreak, with a nonfebrile illness (n = 98) or with acute Zika disease without neurological symptoms (n = 70).
The investigators found that all but one patient with GBS had Zika virus antibodies, and all of them had neutralizing antibodies to Zika virus. By comparison, only 56% (n = 54) of the control group admitted with nonfebrile illness had neutralizing antibodies (P less than .0001).
Also, 93% of the GBS patients had Zika virus immunoglobulin M (IgM) and 88% reported symptoms consistent with Zika infection a mean of 6 days before onset of neurological symptoms. Acute Zika infection is usually characterized by rash, fever, and conjunctivitis.
Past dengue virus infection, which had been considered a possible risk factor for Zika-mediated GBS, did not differ significantly between patients in the control groups and those with GBS.
The investigators were also able to subtype the clinical characteristics of the GBS cases as consistent with acute motor axonal neuropathy, or AMAN, phenotype. However, the antibodies typically seen associated with AMAN were not seen in these patients, leading investigators to suspect that a different biological pathway was responsible.
More than a third of the GBS patients in the study required intensive care, most of these also with respiratory support, though none died.
The government of France, the European Union, and the Wellcome Trust funded the study. The researchers declared that they had no competing interests.
Serological evidence from French Polynesia links an outbreak of Zika virus to a spike in cases of Guillain-Barré syndrome seen there in 2013-2014.
The research, published online Feb. 29 in The Lancet, is the first to use a case-control design to demonstrate that Zika, a mosquito-borne flavivirus, is associated with Guillain-Barré syndrome (Lancet. 2016 Feb 29. doi: 10.1016/S0140-6736(16)00562-6).
Guillain-Barré syndrome (GBS) is an immune-mediated flaccid paralysis that can follow viral or bacterial infections. Most patients with GBS recover with intensive care in hospitals, although the syndrome can be permanently debilitating or, in rare cases, fatal.
As a large outbreak of Zika continues in Central and South America, hospitals should be prepared for excess GBS cases, the authors of the study say, and assure adequate intensive-care capacity to treat them. Based on the 66% attack rate of Zika during the French Polynesia outbreak, investigators estimated the incidence of GBS at 0.24 per 1,000 Zika infections, but noted that it could be different in the current outbreak.
Dr. Van-Mai Cao-Lormeau of the Unit of Emerging Infectious Diseases at Institut Louis Malardé in Papeete, French Polynesia, alongside colleagues in France and French Polynesia, used a case-control design to compare serological samples from 42 patients (74% male) diagnosed at a Tahiti hospital with GBS with samples from age-and sex-matched patients who presented at the same hospital, also during the time of the outbreak, with a nonfebrile illness (n = 98) or with acute Zika disease without neurological symptoms (n = 70).
The investigators found that all but one patient with GBS had Zika virus antibodies, and all of them had neutralizing antibodies to Zika virus. By comparison, only 56% (n = 54) of the control group admitted with nonfebrile illness had neutralizing antibodies (P less than .0001).
Also, 93% of the GBS patients had Zika virus immunoglobulin M (IgM) and 88% reported symptoms consistent with Zika infection a mean of 6 days before onset of neurological symptoms. Acute Zika infection is usually characterized by rash, fever, and conjunctivitis.
Past dengue virus infection, which had been considered a possible risk factor for Zika-mediated GBS, did not differ significantly between patients in the control groups and those with GBS.
The investigators were also able to subtype the clinical characteristics of the GBS cases as consistent with acute motor axonal neuropathy, or AMAN, phenotype. However, the antibodies typically seen associated with AMAN were not seen in these patients, leading investigators to suspect that a different biological pathway was responsible.
More than a third of the GBS patients in the study required intensive care, most of these also with respiratory support, though none died.
The government of France, the European Union, and the Wellcome Trust funded the study. The researchers declared that they had no competing interests.
FROM THE LANCET
Key clinical point: Acute infection with Zika virus in French Polynesia was associated with Guillain-Barré syndrome.
Major finding: Among GBS patients admitted to hospitals during an 2013-2014 outbreak of Zika virus, nearly all had antibodies or neutralizing antibodies to Zika, vs. 56% of age and sex-matched controls (P less than .0001).
Data source: A case-cohort study comparing blood results from 42 GBS cases and two cohorts of controls, one with acute Zika infection without GBS (n = 70) and another admitted during the outbreak for other illnesses (n = 98).
Disclosures: The French government, the European Union, and the Wellcome Trust sponsored the study. Investigators disclosed no conflicts of interest.
