Health
Monkeypox call seen as catch-up bid – World – Chinadaily.com.cn – China Daily
US’ health emergency declaration may come too late to halt spread, experts say
The administration of US President Joe Biden on Thursday declared the country’s monkeypox outbreak a public health emergency, but many health experts fear that it may be too late to contain the spread of infections.
Criticism of the White House’s response to the disease outbreak has been building, with experts saying the authorities have been slow off the mark in distributing treatments and vaccines.
The White House’s declaration signals that the monkeypox virus now represents a significant risk to citizens. The Secretary of Health and Human Services, Xavier Becerra, is considering a second declaration that would empower federal officials to expedite medical countermeasures, such as other potential treatments and vaccines, without going through comprehensive federal reviews.
That also would allow for greater flexibility in how the current supply of vaccines is administered, Becerra said.
Some 6,600 monkeypox infections have been reported in the United States, a number that has risen sharply over the past weeks.
Lawrence Gostin, a public health law expert at Georgetown University, said the declaration of the health emergency “signals the US government’s seriousness and purpose, and sounds a global alarm”. But he told The Associated Press that the action was overdue.
Gostin said the government has been too cautious and should have declared a nationwide emergency earlier.
On July 23, the World Health Organization declared a global health emergency over the outbreak, with cases in more than 70 countries.
California, Illinois and New York have all made declarations recently, as have New York City, San Francisco and San Diego County.
Since doctors diagnosed the first US case on May 27, the virus has been spreading rapidly in the country, with the highest rates per capita reported in Washington, New York and Georgia.
More than 99 percent of the infections are among men who have sex with men.
The virus is transmitted mostly during close physical contact. So far, no deaths from the disease have been reported in the US.
The country now has the highest case count among nonendemic countries, and the number is expected to rise as surveillance and testing improve.
Monkeypox is endemic in parts of Africa, where people have been infected through bites from rodents or small animals. Classification as endemic means a disease has a constant presence in a population but is not affecting an alarmingly large number of people, as typically seen in a pandemic.
‘Rarely fatal’
On its website, the Centers for Disease Control and Prevention says of the virus: “Monkeypox virus is part of the same family of viruses as variola virus, the virus that causes smallpox. Monkeypox symptoms are similar to smallpox symptoms, but milder, and monkeypox is rarely fatal. Monkeypox is not related to chickenpox.”
There is increasing concern that the US may have lost its chance to contain the monkeypox virus. Some public health experts have pointed fingers at the administration for its slowness in rolling out vaccines and treatments.
“The window for containing monkeypox is rapidly closing,” Gostin warned in an interview with CNN late last month. He had called for the US to declare a national public health emergency and make more vaccine doses available.
“I do think it’s still possible to contain, but it’s also equally possible that this may become endemic in the United States,” he said.
Supplies of a monkeypox vaccine called Jynneos have been limited even as demand surges. The administration has been criticized for moving too slowly to expand the number of doses.
Federal officials have identified about 1.6 million people as being at the highest risk for monkeypox, but the US has received enough Jynneos doses to fully cover only about 550,000 people.
The shortage of vaccines was caused in part because the Department of Health and Human Services failed early on to ask that bulk stocks of the vaccine it already owned be bottled for distribution, reported The New York Times, citing multiple unnamed administration officials familiar with the matter.
The government is now distributing about 1.1 million vaccine doses, less than a third of the 3.5 million that health officials now estimate are needed to fight the outbreak. It does not expect the next delivery, of 500,000 doses, until October.
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Possible cases of bird flu have been found in Caledon as potential outbreaks of the virus are popping up in Brampton and across southern Ontario.
The City of Brampton issued a warning about two possible avian flu incidents on Friday after dead birds were found in the area of Professor’s Lake and Duncan Foster Valley South.
Now the Town of Caledon says a number of dead birds have also been found in a pond near Coleraine Dr. and Harvest Moon Dr. and that the deaths may be related to bird flu.
The Town has closed a trail in the area out of precaution and says testing is being conducted by the Canadian Wildlife Health Cooperative to determine the birds’ cause of death.
Peel Public Health says that while avian influenza is a threat to birds, the risk to humans is very low.
“Most cases of human avian flu have been traced to handling infected poultry or their droppings,” said Dr. Nicholas Brandon, acting Medical Officer of Health for PPH. “Residents are asked to follow the recommended guidance to limit the spread of avian flu and protect the health and safety of residents and pets.”
Peel Public Health is recommending residents and pet owners are asked to take the following precautions:
- Keep animals away from any waterfowl or fecal matter
- Do not feed or otherwise interact with the waterfowl
- Keep cats indoors
- Keep dogs on a leash (as required under the municipal by-law)
- Do not feed pets (e.g., dogs or cats) any raw meat from game birds or poultry
- Pet birds, if not normally kept indoors, should be restricted to the indoors
- Bird feeders should be removed or washed with soap and water frequently to reduce the chance of bacterial or viral contamination
The cause of the birds’ death in all three of the cases in Peel has not been confirmed but Brampton Animal Services is actively monitoring the areas.
If the birds test negative for Avian Influenza a full necropsy will be conducted to determine the cause of death, the City of Brampton said on Friday.
Last week the Toronto Zoo shut down some of its bird enclosures after an avian flu case was detected at a southern Ontario poultry farm.
A highly pathogenic type of H5N1 avian flu has been tearing through Canadian flocks since early 2022, killing millions of birds and infecting a record number of avian species.
The Canadian Food Inspection Agency detected a case at a commercial poultry operation southeast of Hamilton on Tuesday, the second reported Ontario site in a week after a lull in detected cases going back to the end of December.
With files from The Canadian Press
Health
Developing postoperative delirium associated with a faster rate of cognitive decline, says study
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Research published today (March 20) in the JAMA Internal Medicine finds that developing postoperative delirium is associated with a 40% faster rate of cognitive decline over those who do not develop delirium.
“Delirium is associated with faster cognitive decline,” said Zachary J. Kunicki, Ph.D., MS, MPH Assistant Professor located at the Warren Alpert Medical School of Brown University, the first author. “Whether delirium causes this faster rate of decline, or is simply a marker of those who are at risk of experiencing faster rates of decline, is still to be determined.”
“This study has the longest follow-up period of any study examining persons with delirium following surgery,” said Sharon K. Inouye, MD, MPH Director, Aging Brain Center, Hinda and Arthur Marcus Institute for Aging Research, the senior author and principal investigator on the work. “While future studies are needed, this study raises the possibility that delirium may predispose to permanent cognitive decline and potentially dementia. This highlights the importance of delirium prevention to preserve brain health in older adults who undergo surgery,” she said.
Delirium is the most common post-operative complication in older adults and is associated with poor outcomes, including long-term cognitive decline and incident dementia.
Richard N. Jones, ScD, Warren Alpert Medical School of Brown University is co-senior author of the article, “Six-year cognitive trajectory in older adults following major surgery and delirium.”
“The SAGES cohort has followed 560 older adults (age 70 and older), measuring their cognition every six months for 36 months, then annually afterwards for up to six years. Using a detailed cognitive testing battery, comprised of 11 different tests, we found that cognitive changes after surgery are complex and that delirium influences every timepoint. The average cognitive changes seen after surgery include an abrupt drop at one month after surgery, an increase at two months after surgery, a stable period from 6–30 months after surgery, and then steady decline from 3–6 years after surgery.
“Delirium is associated with a sharper drop at one month, greater recovery at two months, and faster decline in all time periods from six months to six years, respectively. The results suggest that either delirium itself may contribute to cognitive decline after surgery, or that delirium may serve to identify those at risk for future more rapid cognitive decline. Future research will be needed to examine whether either or both of these hypotheses best explain the relationship between delirium and cognitive decline,” say the authors.
More information:
Six-Year Cognitive Trajectory in Older Adults Following Major Surgery and Delirium, JAMA Internal Medicine (2023). DOI: 10.1001/jamainternalmed.2023.0144
Provided by
Hebrew SeniorLife Hinda and Arthur Marcus Institute for Aging Research
Citation:
Developing postoperative delirium associated with a faster rate of cognitive decline, says study (2023, March 20)
retrieved 20 March 2023
from https://medicalxpress.com/news/2023-03-postoperative-delirium-faster-cognitive-decline.html
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KEY POINTS
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Familial Mediterranean fever (FMF) is the most common monogenic autoinflammatory disorder; it is characterized by self-limited episodes of fever, polyserositis and elevated inflammatory markers.
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While symptoms are nonspecific, FMF should be suspected in patients with recurrent febrile episodes accompanied by peritonitis, pleuritis, pericarditis and elevated C-reactive protein, especially among people of Ashkenazi Jewish descent and other at-risk ethnic groups.
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Treatment with colchicine prevents clinical flares and the amyloidosis and renal failure that can be associated with the disease.
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Delayed diagnosis can have grave consequences for patients, including unnecessary surgeries and associated complications.
In 2015, a 28-year-old woman of Ashkenazi Jewish descent presented to the medical genetics clinic with concerns about flexible joints, easy bruising, stretchable skin, chronic back pain and mild scoliosis since childhood. Differential diagnoses included connective tissue disorders such as Ehlers–Danlos (EDS), Marfan and Loeys–Dietz syndromes. She had an elevated Beighton score (6/9), reflecting joint hypermobility, and none of the features consistent with Marfan syndrome or Loeys–Dietz syndrome. Her echocardiogram was normal and her family history was unremarkable. A 13-gene panel was negative for EDS, and she was given a clinical diagnosis of hypermobile EDS.
Over the next 5 years, the patient developed recurrent episodes of fever, elevated C-reactive protein (CRP), abdominal pain and other symptoms (Table 1). Although most episodes lasted 1–3 days, the patient often noted recurrence or worsening of symptoms after interventions, such as fever or abdominal pain after various surgeries.
Table 1:
Chronology of events for a 28-year-old woman with familial Mediterranean fever
In 2016, the patient had an ovarian cystectomy for suspected ovarian torsion (no torsion found), an appendectomy for suspected appendicitis (no appendicitis found) and an endoscopic retrograde cholangiopancreatography with stent placement for presumed chronic pancreatitis. In 2017, she received diagnoses of cholecystitis, chronic pancreatitis and malnutrition, which led to a cholecystectomy and central line placement for total parenteral nutrition. She also had chest pain and shortness of breath with pleural effusions; presumed volvulus, which led to emergency laparotomy, with no evidence of volvulus intraoperatively; and thrombophlebitis of the internal jugular vein. Intermittent abdominal pain, distension and nausea were attributed to colonic dysmotility related to hypermobile EDS. She had serious malnutrition, and her body mass index dropped from 20.3 to 15.8, which led to placement of a gastrojejunostomy tube to support enteral feeds and avoid complications associated with prolonged total parenteral nutrition.
The patient’s clinical status deteriorated through 2018, with flares of abdominal pain, constipation and feeding intolerance, which continued to be attributed to colonic dysmotility secondary to hypermobile EDS. Gram-negative enteric bacteria were identified on blood cultures twice, and were attributed to the impact of her EDS on the integrity of the bowel wall leading to bacterial translocation. Total colectomy and ileostomy were performed, followed by prolonged recovery, with recurrent fevers, elevated CRP and abdominal pain. After a period of stability, reversal of her ileostomy with J-pouch formation was complicated by postoperative abdominal pain, fever and elevated CRP. In 2019, she had episodes of left lower quadrant pain and tenesmus, diagnosed as pouchitis and managed with antibiotics. In 2020, the patient had episodes of pelvic pain and fever lasting 2–3 days, elevated inflammatory markers, pericardial effusion, hepatosplenomegaly and blood cultures positive for Escherichia coli. She was given a diagnosis of urosepsis and prescribed antibiotics.
In 2020 the patient sought a genetics reassessment. No clinical diagnosis was made; however, it was thought that her history could not be explained by hypermobile EDS. A geneticist ordered whole exome sequencing, which found compound heterozygous pathogenic DNA variants in the MEFV gene, namely c.2084A>G (p.Lys695Arg) and c.2177T>C (p.Val726Ala), consistent with familial Mediterranean fever (FMF).
The patient was referred to a rheumatologist and started on colchicine 0.6 mg once a day. During the 2 years since she started taking colchicine, she has had 2 mild, self-resolving flares of FMF that did not require hospital admission or intervention. She has returned to her baseline strength and nutritional status, and has stopped all other medications. She has no evidence of renal amyloidosis; her serum creatinine (71 mmol/L) and urea (4.4 mmol/L) are within normal ranges, and she has no protein in her urine.
Discussion
Familial Mediterranean fever is the most common monogenic autoinflammatory disorder; it is characterized by self-limited episodes of fever, polyserositis and elevated inflammatory markers.1–4 The condition is associated with gain-of-function sequence variations in the MEFV gene that encodes for the pyrin protein, and results in uncontrolled production of interleukin-1β and an exaggerated inflammatory response.1,2,4 The disease manifests as recurrent bouts of fever, abdominal pain and chest pain that start abruptly and peak soon after onset, last for 1–4 days and then resolve spontaneously. Patients typically have no symptoms between attacks.2 Familial Mediterranean fever should be considered for patients who have undergone laparotomy or laparoscopy with no pathology identified. Stress, cold exposure, fat-rich meals, infections, vigorous exercise, surgery and the menstrual cycle may all provoke an attack. Familial Mediterranean fever may present uncommonly as erysipelas-like erythema, aseptic meningitis, recurrent urticaria or vasculitis.3
Laboratory abnormalities during attacks are nonspecific and include elevated systemic markers of inflammation, leukocytosis with neutrophilia, and elevated erythrocyte sedimentation rate, CRP and fibrinogen. Serum amyloid A protein is also elevated during attacks, but is not routinely measured unless a diagnosis of FMF is suspected.3 One of the long-term complications of untreated disease is amyloidosis of the kidneys, which has been reported to be present in about 12% of patients with FMF; it can have severe complications, including renal failure. 1,2 Amyloidosis may also develop in the spleen, liver, gastrointestinal tract, thyroid and testes. Small bowel obstruction may develop because of recurrent peritonitis and adhesion formation. Before colchicine was used in the treatment of FMF, infertility was common and was thought to be caused by obstruction of fallopian tubes in females and testicular amyloidosis in males.2,3
Familial Mediterranean fever is common in people of Ashkenazi Jewish descent, with a substantial gene carrier rate (about 1:7.8).5 The prevalence is about 1 in 500 to 1 in 1000 among people of other at-risk ethnic descents, including those of Turkish, Armenian, Arabic, non-Ashkenazi Jewish, North African, Italian, Greek, Chinese and Japanese ancestry. Known risk factors include family history of FMF, present in 30%–50% of people with the condition, and belonging to an at-risk ethnic group.6 More than 95% of genetic carriers are asymptomatic; however, some individuals with a single mutation may manifest symptoms and may benefit from treatment with colchicine.1
Our patient’s many episodes of fever and abdominal pain led to different diagnoses, invasive procedures and complications. Intraoperative findings and postoperative pathology reports were often inconsistent with the initial diagnosis of hypermobile EDS, and hospital admissions were prolonged owing to postoperative flares of pain, fever and elevated CRP. Over the course of her illness, treating clinicians appeared not to have considered FMF.
Hypermobile EDS is the mildest subtype of EDS, with no life-threatening complications, although patients with hypermobile EDS can have various types of gastroesophageal dysmotility such as esophageal dysmotility, gastroparesis, small bowel or colon altered transit time or global dysmotility.7 However, unlike the vascular EDS subtype, hypermobile EDS does not cause bowel wall fragility or rupture. Genes for hypermobile EDS have not yet been identified. Vascular EDS and other EDS subtypes were highly unlikely in this patient, given her negative results from genetic testing. Hypermobile EDS would not explain this patient’s symptoms, except perhaps colonic dysmotility.7
After the patient developed new symptoms in 2015, genetics specialists were not consulted again until the patient requested a follow-up in 2020. She qualified for whole genome sequencing based on the Ministry of Health of Ontario’s testing criteria of severe functional impairment, multisystem involvement and progressive clinical course. When FMF or another periodic fever syndrome is suspected, a gene panel for periodic fever syndromes can identify pathogenic DNA variants. When variants of unknown clinical importance or single pathogenic DNA variants are found, a diagnosis can still be made based on clinical findings, with the help of diagnostic criteria such as the Eurofever-PRINTO classification criteria.1,8 Whole genome sequencing can be useful in patients with severe multisystem involvement, even in the absence of a clear diagnosis. A patient may also have more than 1 genetic disorder, as in our patient with FMF and hypermobile EDS.
Most patients with FMF are symptomatic by age 20 years.4 In hindsight, the patient had fevers with severe abdominal pain a few times a year, starting in early childhood. Familial Mediterranean fever should be considered in a differential for recurrent fevers, peritonitis and elevated CRP (Table 2).
Table 2:
Differential diagnosis for patients with periodic fevers and elevated inflammatory markers
Treatment with colchicine is effective, preventing FMF flares in more than 60% of patients and reducing the number of attacks in a further 20%–30% of patients. Colchicine can also prevent deposition of amyloid fibrils and subsequent renal failure.2–4,7,9 Anti–interleukin-1 biological therapy can be used in patients unresponsive to colchicine.2–4
The symptoms of FMF can mimic other conditions and, unfortunately, patients with FMF often experience years of misdiagnosis, unnecessary surgeries and prolonged hospital admissions. 4,6,10 Delays in diagnosis likely occur because of the lack of specificity in symptoms, and the relapsing and remitting pattern of disease. Furthermore, clinicians may not consider the disease in at-risk ethnic populations.4
The section Cases presents brief case reports that convey clear, practical lessons. Preference is given to common presentations of important rare conditions, and important unusual presentations of common problems. Articles start with a case presentation (500 words maximum), and a discussion of the underlying condition follows (1000 words maximum). Visual elements (e.g., tables of the differential diagnosis, clinical features or diagnostic approach) are encouraged. Consent from patients for publication of their story is a necessity. See information for authors at www.cmaj.ca.
Footnotes
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Competing interests: None declared.
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This article has been peer reviewed.
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The authors have obtained patient consent.
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Contributors: All of the authors contributed to the conception and design of the article. Kayla Richard and Sara Glazer drafted the first version of the manuscript and have contributed equally. All of the authors revised the manuscript critically for important intellectual content, gave final approval of the version to be published and agreed to be accountable for all aspects of the work.
This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY-NC-ND 4.0) licence, which permits use, distribution and reproduction in any medium, provided that the original publication is properly cited, the use is noncommercial (i.e., research or educational use), and no modifications or adaptations are made. See: https://creativecommons.org/licenses/by-nc-nd/4.0/
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