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Your eyes do more than show your brain what’s happening in the world around you. They also reveal how well your brain may fare in the years ahead, including whether or not you might develop dementia.

A long‑running study of 8,623 adults has found that a subtle slowdown in detecting a faint triangle on a computer screen can hint at Alzheimer’s disease up to 12  years before diagnosis.

Lead author Eef Hogervorst of Loughborough University says the simple test “could slot into routine checkups without adding a single drop of blood.”

Vision timing signals brain trouble

Participants pressed a button when they spotted a triangle drifting amid random dots. Those who later developed dementia needed roughly two extra seconds – a gap large enough to raise their future risk by 56 percent. 

The task measures visual processing speed, the time the brain takes to register and respond to a stimulus. Sluggish scores predicted dementia even after researchers adjusted for age, education, and cardiovascular health.

“Visual sensitivity is related to memory performance,” noted Hogervorst. She adds that eyesight often declines quietly, leaving people unaware until memory falters.

A similar pattern appeared in an independent analysis showing that early amyloid plaques disrupt visual signals before memory centers suffer. Taken together, the findings suggest eye‑based tests could extend the warning window for preventive care.

Eyes offer dementia warning

The retina is an outgrowth of the brain, so toxic proteins can accumulate there first. Researchers now examine retinal layers for thinning, abnormal blood vessels, and microscopic deposits that mirror cerebral changes.

Damage often begins in the occipital cortex, the region that deciphers vision, before spreading to the hippocampus. That makes contrast sensitivity, color discrimination, and motion detection early casualties.

People with Alzheimer’s also struggle to ignore distractions. “These problems could increase the risk of driving accidents,” warned Thom Wilcockson, a psychologist at Loughborough University.

Eye-tracking research confirms the concern, showing that older drivers with dementia exhibit erratic saccades, longer fixations, and reduced scanning range – all linked to crash risk.

What slowing detection really means

Spotting a shape on a screen sounds trivial, yet it taps fast neural circuits shared with memory. When those circuits lag, forgetting names and appointments may follow.

The Norfolk data showed the triangle test remained significant after standard memory exams were considered. In clinics, combining both could improve accuracy while saving time and cost.

Slower vision also correlates with trouble recognizing faces, a social cue often missed in early dementia. Patients skim past eyes and mouths, failing to “imprint” new acquaintances and later feeling lost in familiar rooms.

Several groups are testing whether directed eye exercises can sharpen recall. Early trials of rapid left‑right movements report modest gains, though results remain mixed.

Smartphones join dementia fight

High‑grade eye trackers once cost thousands of dollars. A California team has squeezed similar optics into a smartphone app that uses the front‑facing infrared camera to measure pupil changes.

The prototype walks users through a brief pupil dilation task, then uploads data for cloud analysis. Engineers hope the approach will let families monitor brain health between clinic visits.

Consumer wearables are also inching closer. Some virtual‑reality headsets already track gaze direction at millisecond resolution, offering another route for large‑scale screening.

Still, technology alone is not enough. Experts stress the need for clear guidelines to avoid false alarms and protect privacy.

Fight dementia with eye health

Lifestyle counts, too. A 14‑year study of almost 2,000 older adults found those who read at least once a week cut cognitive decline odds by nearly half.

Reading, watching subtitles, or knitting forces the eyes to dart and refocus, a workout for neural networks. Longer education and regular exercise add extra cognitive reserve, buffering the toll of disease.

Optometrists recommend annual exams after people reach 60 years of age.

Reporting new glare, color shifts, or slowed adaptation can nudge physicians to order broader cognitive checks.

Vision‑friendly habits help, too. Good lighting, high‑contrast text, and blue‑green filters reduce strain and may delay functional loss.

Finally, keep blood vessels healthy. Controlling blood pressure, diabetes, and cholesterol supports both retinal and cerebral circulation, tying the two organs together.

The study is published in Scientific Reports.

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Introduction

Over 33.3% of pregnancy-related deaths are due to cardiovascular diseases, with acute myocardial infarction (AMI) being a significant contributor to maternal mortality.¹ While the risk of AMI during pregnancy and the early postpartum period is relatively low (6 to 10 cases per 100,000 pregnancies), it is three times higher compared to non-pregnant women of reproductive age.^2,3 Pregnant women who experience AMI have a 22-fold higher in-hospital mortality risk, with a 37% mortality rate and the potential loss of both mother and child.^1,4 In the past 20 years, the incidence of AMI in pregnancy has increased, likely due to the rising average maternal age and greater prevalence of risk factors.^5,6 The etiology of AMI also differs significantly. In the general population, most cases result from atherosclerotic coronary artery disease. However, among pregnant women, approximately 40% of AMI cases are associated with spontaneous coronary artery dissection (SCAD). Atherosclerosis accounts for around 27% of cases, while myocardial infarction with non-obstructive coronary arteries (MINOCA) represents up to 29%.^2,7,8

The pathophysiology of SCAD remains unclear and likely multifactorial. It involves spontaneous coronary artery dissection due to an intramural hematoma, with or without intimal rupture.^7,8 SCAD is often linked to arteriopathies, connective tissue disorders, and autoimmune diseases.⁸ Pregnant women, especially in the third trimester and postpartum, are at higher risk, particularly those who have undergone infertility treatment, including in vitro fertilisation.^9–11

Case Report

A 28-year-old female, gravida 3, at 37 weeks of gestation, was admitted to the district central hospital via emergency medical services with complaints of a single episode of vomiting, nausea, constrictive retrosternal pain, and a sensation of rapid heartbeat. She attributed the onset of symptoms to the consumption of a low-alcohol beverage the previous evening (300 mL of light beer) along with potato chips.

Her medical history revealed a prior smoking habit, with a four-year history of tobacco use, smoking up to 15 cigarettes per day (pack-year index: 3). She discontinued smoking upon conception of the current pregnancy. Her family history was unremarkable for cardiovascular disease, connective tissue disorders, or sudden cardiac death. The patient’s obstetric history included a spontaneous miscarriage at 11 weeks of gestation in 2015. In 2018, she had an uncomplicated full-term pregnancy, resulting in a vaginal delivery of a healthy female neonate weighing 3300 g.

The emergency medical team administered antispasmodics with minimal effect. The time from the onset of symptoms to hospitalization was 7 hours. An electrocardiogram (ECG) was performed immediately upon arrival (Figure 1, ECG from 24.09.23), showing no signs of acute ischemia. Troponin I was measured at 0.10 ng/mL (normal value: up to 0.16 ng/mL). Routine laboratory tests showed elevated total cholesterol (TC) at 7.03 mmol/L, low-density lipoprotein cholesterol (LDL-C) at 4.70 mmol/L, high-density lipoprotein cholesterol (HDL-C) at 1.48 mmol/L, and triglycerides (TG) at 2.74 mmol/L. These findings were considered physiological for late pregnancy and not indicative of a primary lipid disorder.

Upon admission, the patient continued to experience recurrent episodes of constricting retrosternal pain. A repeat investigation was performed, revealing a significant rise in troponin I levels, which was 14.31 ng/mL, 4 hours after hospitalization. The repeat ECG (Figure 2, ECG from 24.09.23) showed ST-segment elevation in leads I, aVL, and V₄-V₆, with reciprocal ST depression in leads II, III, aVF, and negative T-waves in leads I and aVL. Echocardiography demonstrated septal and anterior left ventricular wall hypokinesis with left ventricular ejection fraction of 50%. Given the patient’s clinical symptoms, ECG findings, and the increase in myocardial necrosis markers, along with input from relevant specialists, the decision was made to transfer the patient to a center capable of providing specialized care.

Figure 2 Follow-up ECG displaying ST-segment elevation and reciprocal changes, indicating acute ischemic injury.

Thus, the patient was admitted to the intensive care unit of the maternity hospital for further observation and continuous cardio-respiratory monitoring. An ultrasound was immediately performed in the obstetrics department to assess the fetal condition. At the time of admission, the patient did not report any complaints, and the ECG showed no abnormalities. Considering the transient, rapidly evolving changes on the ECG, which were clearly associated with retrosternal pain, and the significant rise in myocardial necrosis markers over time, a presumed diagnosis of acute type 2 myocardial infarction was made.

A decision was reached to proceed with conservative management, and the patient was started on enoxaparin 0.4 mL twice daily subcutaneously and acetylsalicylic acid (ASA) 100 mg once daily. The following day, the patient again complained of severe retrosternal pain, which did not alleviate despite the administration of nitrates and required opioid analgesics. In response, an echocardiogram was immediately performed, revealing hypokinesis of the anterior segment of the left ventricular wall. The repeat ECG (Figure 3, ECG from 26.09.23) was registered. The aforementioned changes were interpreted as an expansion of AMI, prompting the decision to proceed with urgent coronary angiography to determine the subsequent treatment strategy. During the coronary angiography, a femoral access was used. A long dissection in the mid-distal segment of the left anterior descending artery (LAD) was noted (Figure 4A). Two Resolute Integrity (DES) stent systems were then implanted using the “stent-in-stent” technique. Follow-up angiography showed complete stent deployment in the LAD, with adequate positioning and restoration of the main blood flow through the LAD (TIMI – 3; TIMI myocardial perfusion grade – 3) (Figure 4B). No significant narrowings were identified in the left circumflex artery or the right coronary artery.

Figure 3 ECG taken during symptom recurrence, revealing expansion of ischemic changes.

Figure 4 (A) Coronary angiography identifying a long dissection in the left anterior descending artery (arrow). (B) Post-stenting angiography confirming restored blood flow in the affected artery (ellipse).

Following PCI, clopidogrel (75 mg once daily) and bisoprolol (1.25 mg once daily) were added to the patient’s treatment regimen. Regarding pregnancy management, multiple consultations were held with a multidisciplinary team comprising specialists in obstetrics and cardiology. The patient remained under continuous surveillance in the high-risk obstetric intensive care unit. Given the gestational age of 37–38 weeks and the elevated risk associated with surgical delivery, adjustments were made to the antiplatelet and anticoagulant therapy. Specifically, clopidogrel was discontinued, and enoxaparin was replaced with heparin. Heparin was administered at a dose of 7,000 IU every six hours, with activated partial thromboplastin time monitoring. It was recommended that the final dose be administered no later than four hours before the planned delivery.

At 39 weeks of gestation, due to the onset of spontaneous labor and rupture of membranes in the presence of a pure breech presentation, a decision was made to proceed with delivery via cesarean section. A female neonate was delivered, weighing 3,300 g and measuring 54 cm in length, with Apgar scores of 8/8. On postoperative day 4, the patient and her newborn were discharged home. Recommendations were provided regarding ongoing pharmacological therapy, specifically the continuation of DAPT (ASA and clopidogrel) for the next 12 months.

The subsequent follow-up period was uneventful. At 4 months postpartum, her lipid profile had normalized: total cholesterol 4.71 mmol/L, LDL-C 2.9 mmol/L, HDL-C 1.54 mmol/L, and triglycerides 0.93 mmol/L, supporting the interpretation that the earlier elevation was related to physiological gestational changes. One year after myocardial infarction, ECG revealed persistent scarring at the apex extending to the interventricular septum, mild ST-segment elevation, and biphasic T waves in leads V₃–V₄ (Figure 5, ECG from 11.11.2024). Echocardiography showed a preserved left ventricular ejection fraction. No clinical evidence of a vascular or systemic connective tissue disorder has been observed during the one-year follow-up to date.

Figure 5 Follow-up ECG one year later, showing residual non-specific ST-T abnormalities.

Discussion

Cardiovascular risk factors in pregnancy are consistent with those in the general population, including a family history of cardiovascular disease, dyslipidemia, diabetes, and smoking.¹² Pregnancy-specific factors include polycystic ovary syndrome, early menarche, maternal age over 35, gestational diabetes, pre-eclampsia, and hormonal therapy use.¹³

Although the patient had ceased smoking during pregnancy, her prior tobacco use may have contributed to vascular vulnerability. Several studies have identified smoking as a potential risk factor for SCAD, both in pregnancy-associated and non-pregnancy cases, likely due to its role in vascular inflammation and endothelial dysfunction. In particular, a meta-analysis of women with SCAD, smoking was among the most frequently reported cardiovascular risk factors, present in nearly a quarter of cases.¹⁴ Another study found a significant association between smoking and increased mortality in SCAD patients.¹⁵

Similarly, while gestational hyperlipidemia has been proposed to influence vascular function through mechanisms such as endothelial dysfunction or oxidative stress, its direct role in SCAD remains unproven. SCAD is typically not associated with lipid deposition or coronary atherosclerotic plaque.¹⁶ During pregnancy, physiological hyperlipidemia is well recognized: total cholesterol and LDL-C typically rise by 30–50%, triglycerides by 50–100%, and HDL-C by 20–40% as gestation progresses.¹⁷ The patient’s third-trimester lipid profile was consistent with these expected changes, and normalization at follow-up supported the interpretation of a transient physiological response. These findings underscore the importance of interpreting lipid values in pregnancy within trimester-specific reference ranges, rather than assuming pathological significance in isolation.

Pregnancy-related SCAD likely results from increased shear stress, elevated progesterone reducing arterial elasticity, and estrogen-induced hypercoagulation and collagen inhibition. Increased cardiac output and blood volume further contribute. It often affects major coronary arteries, leading to reduced ejection fraction and severe maternal-fetal complications.^18–23

Managing patients with pregnancy-related SCAD is challenging, particularly in diagnosing the condition. In 70% of cases, SCAD presents with typical ST-segment elevation on ECG.²⁴ However, nearly one-third of patients show no ECG signs of coronary circulation impairment.^10,25 In the presented clinical case, early ECG showed a transient ST elevation in the anterior-lateral wall, which resolved after pain relief, initially suggesting vasospastic angina. The key indicator of myocardial injury was the sustained rise in troponin I levels. Notably, troponin is preferred over CK-MB in pregnant women, as CK-MB can rise due to uterine contractions or cell breakdown during delivery, with lower specificity in pregnancy and postpartum.²⁶

Given the absence of pronounced clinical symptoms at the time of our patient’s transfer, a conservative treatment approach was initially chosen. However, this was later reassessed due to the recurrence of symptoms (angina, vomiting), accompanied by deteriorating ECG changes and severe arrhythmias. There is no consensus on the preferred management strategy for pregnant women with AMI, and each case requires an individual approach. Conservative management of SCAD not related to pregnancy has shown better outcomes than in pregnant women and the early postpartum period.^9,23,24 In pregnant women with SCAD, coronary interventions were associated with a higher risk of dissection progression and the occurrence of new iatrogenic dissections during the procedure.^23–25 Additionally, concern arises over the potential impact of X-ray exposure on the fetus during coronary angiography (CAG). During CAG, the patient’s radiation dose is less than 20 mGy, while the fetal radiation dose is estimated at 0.074 mGy.²⁷ The teratogenic risk to the fetus is minimal for doses below 50 mGy and potentially fatal for doses above 150 mGy, depending on gestational age.²⁸ Therefore, it can be concluded that the radiation dose during coronary angiography is generally safe for most pregnant patients.²⁹ An alternative option is the use of computed tomography coronary angiography, particularly in non-ST elevation myocardial infarction patients, but it may cause delays and is not always effective in detecting small areas of dissection.³⁰ The access route for percutaneous intervention is also crucial. Radial access, as opposed to femoral access, reduces radiation exposure to the fetus, as it avoids direct X-ray exposure, making it more often recommended for pregnant women. Moreover, radial access is associated with a lower risk of complications, such as bleeding.³¹ However, some studies suggest that femoral access may be more effective for pregnant women with SCAD, as it has been linked to nearly three times fewer iatrogenic dissections compared to radial access.^32,33 In our patient, femoral access was used, and no expansion of the dissection zone was observed during the procedure.

Pharmacological management, particularly dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI), has specific considerations. According to the latest European Society of Cardiology guidelines, clopidogrel is recommended as part of DAPT in pregnant women post-PCI, as it is considered safer than glycoprotein IIb/IIIa inhibitors, due to a lack of data on their use in pregnancy.¹⁰ However, there are no clear guidelines on the duration of DAPT during labour for patients at high risk of thrombosis or those with recent intervention. Some studies show positive outcomes, while others report serious side effects from prolonged DAPT use.²⁵ A decision was made to continue long-term DAPT, with a short-term discontinuation of clopidogrel before the planned cesarean section. After discharge, the patient continued DAPT for 12 months with no complications.

While the case highlights key aspects of diagnosis and management, it also has certain limitations. These are inherent to a single-patient observation. Intravascular ultrasound or optical coherence tomography was not performed, which might have provided more precise characterization of the arterial dissection. Additionally, no further investigations were undertaken to evaluate possible underlying vascular or connective tissue disorders. However, the case reflects real-world clinical complexity, where decisions must often be made based on evolving symptoms and limited diagnostic data.

Conclusion

The issue of myocardial infarction during pregnancy involves several aspects, including challenges in emergency diagnosis due to a low index of suspicion among young women without traditional risk factors, as well as the absence of clear, definitive algorithms for selecting a management strategy (conservative/invasive). Additionally, there is uncertainty regarding the volume and duration of anticoagulant and antiplatelet therapy. Since the likelihood of conducting randomized clinical trials among pregnant women is quite limited and problematic, the accumulation of sufficient clinical case reports from real-world practice will, in the future, allow for the formulation of a well-founded expert opinion and evidence-based recommendations for managing this patient cohort.

Date and Materials Statement

This is a case report without statistical analysis of the raw medical record data. All medical data involving the patient were documented in the patient’s medical records. If necessary, more detailed imaging data or laboratory data can be provided by the corresponding author upon reasonable request.

Ethics Statement

Ethical review and approval were not required for the study involving human participants in accordance with the local legislation and institutional requirements. Written informed consent was obtained from the patient for the publication of any potentially identifiable images or data included in this report.

Informed Consent for Publication

The patient agreed to publish her medical data including imaging data and laboratory data, and signed the informed consent.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Funding

This study was not supported by any external funds.

Disclosure

All the authors declare that they have no conflicts of interest in this medical case report and have not received any financial support.

References

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9. Saw J, Humphries K, Aymong E, et al. Spontaneous coronary artery dissection: clinical outcomes and risk of recurrence. J Am Coll Cardiol. 2017;70(9):1148–1158. doi:10.1016/j.jacc.2017.06.053

10. Lebrun S, Bond RM. Spontaneous coronary artery dissection (SCAD): the underdiagnosed cardiac condition that plagues women. Trends Cardiovasc Med. 2018;28(5):340–345. doi:10.1016/j.tcm.2017.12.004

11. Zeven K. Pregnancy-associated spontaneous coronary artery dissection in women: a literature review. Curr Ther Res. 2023;98:100697. doi:10.1016/j.curtheres.2023.100697

12. Kealey A. Coronary artery disease and myocardial infarction in pregnancy: a review of epidemiology, diagnosis, and medical and surgical management. Can J Cardiol. 2010;26(6):185–189. doi:10.1016/s0828-282x(10)70397-4

13. Nguyen AH, Murrin E, Moyo A, et al. Ischemic heart disease in pregnancy: a practical approach to management. Am J Obstet Gynecol MFM. 2024;6(3):101295. doi:10.1016/j.ajogmf.2024.101295

14. Apostolović S, Ignjatović A, Stanojević D, et al. Spontaneous coronary artery dissection in women in the generative period: clinical characteristics, treatment, and outcome-a systematic review and meta-analysis. Front Cardiovasc Med. 2024;11:1277604. doi:10.3389/fcvm.2024.1277604

15. Adams C, He M, Hughes I, Singh K. Mortality in spontaneous coronary artery dissection: a systematic review and meta-analysis. Catheter Cardiovasc Interv. 2021;98(7):1211–1220. doi:10.1002/ccd.29488

16. Stanojevic D, Apostolovic S, Kostic T, et al. A review of the risk and precipitating factors for spontaneous coronary artery dissection. Front Cardiovasc Med. 2023;10:1273301. doi:10.3389/fcvm.2023.1273301

17. Mulder JWCM, Kusters DM, Roeters van Lennep JE, Hutten BA. Lipid metabolism during pregnancy: consequences for mother and child. Curr Opin Lipidol. 2024;35(3):133–140. doi:10.1097/MOL.0000000000000927

18. Maas AHEM, Bouatia-Naji N, Persu A, Adlam D. Spontaneous coronary artery dissections and fibromuscular dysplasia: current insights on pathophysiology, sex and gender. Int J Cardiol. 2019;286:220–225. doi:10.1016/j.ijcard.2018.11.023

19. Yip A, Saw J. Spontaneous coronary artery dissection – a review. Cardiovasc Diagn Ther. 2015;5(1):37–48. doi:10.3978/j.issn.2223-3652.2015.01.08

20. Giacoppo D, Capodanno D, Dangas G, Tamburino C. Spontaneous coronary artery dissection. Int J Cardiol. 2014;175(1):8–20. doi:10.1016/j.ijcard.2014.04.178

21. Vijayaraghavan R, Verma S, Gupta N, Saw J. Pregnancy-related spontaneous coronary artery dissection. Circulation. 2014;130(21):1915–1920. doi:10.1161/CIRCULATIONAHA.114.011422

22. Abbott JD, Curtis JP, Murad K, et al. Spontaneous coronary artery dissection in a woman receiving 5-fluorouracil: a case report. Angiology. 2003;54(6):721–724. doi:10.1177/000331970305400613

23. Havakuk O, Goland S, Mehra A, Elkayam U. Pregnancy and the risk of spontaneous coronary artery dissection: an analysis of 120 contemporary cases. Circ Cardiovasc Interv. 2017;10(3):e004941. doi:10.1161/CIRCINTERVENTIONS.117.004941

24. Tweet MS, Hayes SN, Codsi E, Gulati R, Rose CH, Best PJM. Spontaneous coronary artery dissection associated with pregnancy. J Am Coll Cardiol. 2017;70(4):426–435. doi:10.1016/j.jacc.2017.05.055

25. Lindor RA, Tweet MS, Goyal KA, et al. Emergency department presentation of patients with spontaneous coronary artery dissection. J Emerg Med. 2017;52(3):286–291. doi:10.1016/j.jemermed.2016.09.005

26. Siromakha SO, Arvanytakvy SS, Rudenko SA, Lazorishenetc VV. Coronary insufficiency during pregnancy. Epidemiology, methods of diagnosis and treatment. Ukr J Perinatol Pediatr. 2019;3:32–39. doi:10.15574/PP.2019.79.32

27. Colletti PM, Lee KH, Elkayam U. Cardiovascular imaging of the pregnant patient. Am J Roentgenol. 2013;200(3):515–521. doi:10.2214/AJR.12.9864

28. Kuba K, Wolfe D, Schoenfeld AH, Bortnick AE. Percutaneous coronary intervention in pregnancy: modeling of the fetal absorbed dose. Case Rep Obstet Gynecol. 2019;2019:8410203. doi:10.1155/2019/8410203

29. Alameh A, Jabri A, Aleyadeh W, et al. Pregnancy-associated myocardial infarction: a review of current practices and guidelines. Curr Cardiol Rep. 2021;23:142. doi:10.1007/s11886-021-01579-z

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Salmonella cases in England are the highest they’ve been in a decade, according to recent UK Health Security Agency (UKHSA) data. There was a 17% increase in cases observed from 2023 to 2024 – culminating in 10,388 detected infections last year. Children and older adults accounted for around a fifth of cases.

Although the number of infections caused by foodborne diseases such as Salmonella had broadly decreased over the last 25 years, this recent spike suggests a broader issue is at play. A concurrent increase in Campylobacter cases points to a possible common cause that would affect risk of both foodborne pathogens – such as changes in consumer behaviour or food supply chains.

While the UK maintains a high standard of food safety, any increase in the incidence of pathogens such as Salmonella warrants serious attention.

Salmonella is a species of bacteria that is one of the most common causes of foodborne illnesses globally. The bacteria causes salmonellosis – an infection that typically causes vomiting and diarrhoea.

Most cases of salmonellosis don’t require medical intervention. But approximately one in 50 cases results in more serious blood infections. Fortunately, fatalities from Salmonella infections in the UK are extremely rare – occurring in approximately 0.2% of all reported infections.

Salmonella infections are typically contracted from contaminated foods. But a key challenge in controlling Salmonella in the food supply chain lies in the diverse range of foods it can contaminate.

Salmonella is zoonotic, meaning it’s present in animals, including livestock. This allows it to enter the food chain and subsequently cause human disease. This occurs despite substantial efforts within the livestock industry to prevent it from happening – including through regular testing and high welfare practices.

Salmonella can be present on many retail food products – including raw meat, eggs, unpasteurised milk, vegetables and dried foods (such as nuts and spices). When present, it’s typically at very low contamination levels. This means it doesn’t pose a threat to you if the product is stored and cooked properly.

Vegetables and leafy greens can also become contaminated with Salmonella through cross-contamination, which may occur from contaminated irrigation water on farms, during processing or during storage at home. As vegetables are often consumed raw, preventing cross-contamination is particularly critical.

Spike in cases

It’s premature to draw definitive conclusions regarding the causes of this recent increase in Salmonella cases. But the recent UKHSA report suggests the increase is probably due to many factors.

One contributing factor is that diagnostic testing has increased. This means we’re better at detecting cases. This can be viewed as a positive, as robust surveillance is integral to maintaining a safe food supply.

The UKHSA also suggests that changes in the food supply chain and the way people are cooking and storing their food due to the cost of living crisis could also be influential factors.

To better understand why Salmonella cases have spiked, it will be important for researchers to conduct more detailed examinations of the specific Salmonella strains responsible for the infections. While Salmonella is commonly perceived as a singular bacterial pathogen, there are actually numerous strains (serotypes).

DNA sequencing can tell us which of the hundreds of Salmonella serotypes are responsible for human infections. Two serotypes, Salmonella enteritidis and Salmonella Typhimurium, account for most infections in England.

Although the UKHSA reported an increase in both serotypes in 2024, the data suggests that Salmonella enteritidis has played a more significant role in the observed increase. This particular serotype is predominantly associated with egg contamination.

Salmonella enteritidis is now relatively rare in UK poultry flocks thanks to vaccination and surveillance programmes that were introduced in the 1980s and 1990s. So the important question here is where these additional S enteritidis infections are originating.

Although the numbers may seem alarming, what the UKHSA has reported is actually a relatively moderate increase in Salmonella cases. There’s no reason for UK consumers to be alarmed. Still, this data underscores the importance of thoroughly investigating the underlying causes to prevent this short-term increase from evolving into a longer-term trend.

Staying safe

The most effective way of lowering your risk of Salmonella involves adherence to the “4 Cs” of food hygiene:

1. Cleaning

Thoroughly wash hands before and after handling any foods – especially raw meat. It’s also essential to keep workspaces, knives and utensils clean before, during and after preparing your meal.

2. Cooking

The bacteria that causes Salmonella infections can be inactivated when cooked at the right temperature. In general, foods should be cooked to an internal temperature above 65°C – which should be maintained for at least ten minutes. When re-heating food, it should reach 70°C or above for two minutes to kill any bacteria that have grown since it was first cooked.

3. Chilling

Raw foods – especially meat and dairy – should always be stored below 5°C as this inhibits Salmonella growth. Leftovers should be cooled quickly and also stored at 5°C or lower.

4. Cross-contamination

To prevent Salmonella passing from raw foods to those that are already prepared or can be eaten raw (such as vegetables and fruit), it’s important to wash hands and clean surfaces after handling raw meat, and to use different chopping boards for ready-to-eat foods and raw meat.

Most Salmonella infections are mild and will go away in a few days on their own. But taking the right steps when storing and preparing your meals can significantly lower your risk of contracting it.