Syncope

Other names:      Fainting, blacking out, passing out, swooning.

Syncope, commonly known as fainting, or passing out, is a loss of consciousness and muscle strength characterized by a fast onset, short duration, and spontaneous recovery.   It is caused by a decrease in blood flow to the brain, typically from low blood pressure.  There are sometimes symptoms before the loss of consciousness such as lightheadedness, sweating, pale skin, blurred vision, nausea, vomiting, or feeling warm.  Syncope may also be associated with a short episode of muscle twitching.  Psychiatric causes can also be determined when a patient experiences fear, anxiety, or panic; particularly before a stressful event usually medical in nature.   When consciousness and muscle strength are not completely lost, it is called presyncope.  It is recommended that presyncope be treated the same as syncope.

 

Causes range from non-serious to potentially fatal. There are three broad categories of causes: heart or blood vessel related; reflex, also known as neurally mediated; and orthostatic hypotension. Issues with the heart and blood vessels are the cause in about 10% of cases and typically the most serious while neurally mediated is the most common.  Heart related causes may include an abnormal heart rhythm, problems with the heart valves or heart muscle and blockages of blood vessels from a pulmonary embolism or aortic dissection among others.  Neurally mediated syncope occurs when blood vessels expand and heart rate decreases inappropriately.  This may occur from either a triggering event such as exposure to blood, pain, strong feelings or a specific activity such as urination, vomiting, or coughing.  Neurally mediated syncope may also occur when an area in the neck known as the carotid sinus is pressed.  The third type of syncope is due to a drop in blood pressure when changing position such as when standing up.  This is often due to medications that a person is taking but may also be related to dehydration, significant bleeding or infection. There also seems to be a genetic component to syncope. 

 

A medical history, physical examination, and electrocardiogram (ECG) are the most effective ways to determine the underlying cause.  The ECG is useful to detect an abnormal heart rhythm, poor blood flow to the heart muscle and other electrical issues, such as long QT syndrome and Brugada syndrome. Heart related causes also often have little history of a prodrome. Low blood pressure and a fast heart rate after the event may indicate blood loss or dehydration, while low blood oxygen levels may be seen following the event in those with pulmonary embolism.  More specific tests such as implantable loop recorders, tilt table testing or carotid sinus massage may be useful in uncertain cases.  Computed tomography (CT) is generally not required unless specific concerns are present.  Other causes of similar symptoms that should be considered include seizure, stroke, concussion, low blood oxygen, low blood sugar, drug intoxication and some psychiatri disorders among others.  Treatment depends on the underlying cause.  Those who are considered at high risk following investigation may be admitted to hospital for further monitoring of the heart.

 

Syncope affects about three to six out of every thousand people each year. It is more common in older people and females.  It is the reason for one to three percent of visits to emergency departments and admissions to hospital.  Up to half of women over the age of 80 and a third of medical students describe at least one event at some point in their lives. Of those presenting with syncope to an emergency department, about 4% died in the next 30 days.  The risk of a poor outcome, however, depends very much on the underlying cause.

Vasovagal (situational) syncope is one of the most common types which may occur in response to any of a variety of triggers, such as scary, embarrassing or uneasy situations, during blood drawing, or moments of sudden unusually high stress.  There are many different syncope syndromes which all fall under the umbrella of vasovagal syncope related by the same central mechanism. First, the person is usually predisposed to decreased blood pressure by various environmental factors. A lower than expected blood volume, for instance, from taking a low-salt diet in the absence of any salt-retaining tendency. Or heat causing vaso-dilation and worsening the effect of the relatively insufficient blood volume. The next stage is the adrenergic response. If there is underlying fear or anxiety (e.g., social circumstances), or acute fear (e.g., acute threat, needle phobia), the vaso-motor centre demands an increased pumping action by the heart (flight or fight response). This is set in motion via the adrenergic (sympathetic) outflow from the brain, but the heart is unable to meet requirements because of the low blood volume, or decreased return. A feedback response to the medulla is triggered via the afferent vagus nerve. The high (ineffective) sympathetic activity is thereby modulated by vagal (parasympathetic) outflow leading to excessive slowing of heart rate. The abnormality lies in this excessive vagal response causing loss of blood flow to the brain. The tilt-table test typically evokes the attack. Avoiding what brings on the syncope and possibly greater salt intake is often all that is needed.

 

Associated symptoms may be felt in the minutes leading up to a vasovagal episode and are referred to as the prodrome. These consist of light-headedness, confusion, pallor, nausea, salivation, sweating, tachycardia, blurred vision, and sudden urge to defecate among other symptoms.

Vasovagal syncope can be considered in two forms:

Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group and may be associated with fasting, exercise, abdominal straining, or circumstances promoting vaso-dilation (e.g., heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative.

Recurrent syncope with complex associated symptoms. This is neurally mediated syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance ("spots before the eyes"), sweating, lightheadedness.  The subject is usually but not always upright. The tilt-table test, if performed, is generally positive. It is relatively uncommon.

Syncope has been linked with psychological triggers.  This includes fainting in response to the sight or thought of blood, needles, pain, and other emotionally stressful situations. One theory in evolutionary psychology is that fainting at the sight of blood might have evolved as a form of playing dead which increased survival from attackers and might have slowed blood loss in a primitive environment. "Blood-injury phobia", as this is called, is experienced by about 15% of people. It is often possible to manage these symptoms with specific behavioral techniques.

Another evolutionary psychology view is that some forms of fainting are non-verbal signals that developed in response to increased inter-group aggression during the paleolithic. A non-combatant who has fainted signals that she or he is not a threat. This would explain the association between fainting and stimuli such as bloodletting and injuries seen in blood-injection-injury type phobias such as needle phobia as well as the gender differences. 

Much of this pathway was discovered in animal experiments by Bezold (Vienna) in the 1860s. In animals, it may represent a defence mechanism when confronted by danger ("playing possum").

Situational syncope

Syncope may be caused by specific behaviors including coughing, urination, defecation, vomiting, swallowing (deglutition), and following exercise.  Manisty et al. note: "Deglutition syncope is characterised by loss of consciousness on swallowing; it has been associated not only with ingestion of solid food, but also with carbonated and ice-cold beverages, and even belching."  Fainting can occur in "cough syncope" following severe fits of coughing, such as that associated with pertussis or "whooping cough".  Neurally mediated syncope may also occur when an area in the neck known as the carotid sinus is pressed.  A normal response to carotid sinus massage is reduction in blood pressure and slowing of the heart rate. Especially in people with hypersensitive carotid sinus syndrome this response can cause syncope or presyncope.

Cardiac

Heart-related causes may include an abnormal heart rhythm, problems with the heart valves or heart muscle, or blockages of blood vessels from a pulmonary embolism or aortic dissection, among others.

Cardiac arrhythmias

The most common cause of cardiac syncope is cardiac arrhythmia (abnormal heart rhythm) wherein the heart beats too slowly, too rapidly, or too irregularly to pump enough blood to the brain.  Some arrhythmias can be life-threatening.

 

Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks. Tachycardias include SVT (supraventricular tachycardia) and VT (ventricular tachycardia). SVT does not cause syncope except in Wolff-Parkinson-White syndrome. Ventricular tachycardia originate in the ventricles. VT causes syncope and can result in sudden death.  Ventricular tachycardia, which describes a heart rate of over 100 beats per minute with at least three irregular heartbeats as a sequence of consecutive premature beats, can degenerate into ventricular fibrillation, which is rapidly fatal without cardiopulmonary resuscitation (CPR) and defibrillation.

 

Long QT syndrome can cause syncope when it sets off ventricular tachycardia or torsades de pointes. The degree of QT prolongation determines the risk of syncope.  Brugada syndrome also commonly presents with syncope secondary to arrhythmia.

 

Typically, tachycardic-generated syncope is caused by a cessation of beats following a tachycardic episode. This condition, called tachycardia-bradycardia syndrome, is usually caused by sinoatrial node dysfunction or block or atrioventricular block.

 

Obstructive cardiac lesion

Blockages in major vessels or within the heart can also impede blood flow to the brain. Aortic stenosis and mitral stenosis are the most common examples. Major valves of the heart become stiffened and reduce the efficiency of the heart’s pumping action. This may not cause symptoms at rest but with exertion, the heart is unable to keep up with increased demands leading to syncope. Aortic stenosis presents with repeated episodes of syncope.  Rarely, cardiac tumors such as atrial myxomas can also lead to syncope.

 

Structural cardiopulmonary disease

Diseases involving the shape and strength of the heart can be a cause of reduced blood flow to the brain, which increases risk for syncope. The most common cause in this category is fainting associated with an acute myocardial infarction or ischemic event. The faint in this case is primarily caused by an abnormal nervous system reaction similar to the reflex faints. Women are significantly more likely to experience syncope as a presenting symptom of a myocardial infarction.  In general, faints caused by structural disease of the heart or blood vessels are particularly important to recognize, as they are warning of potentially life-threatening conditions.

 

Among other conditions prone to trigger syncope (by either hemodynamic compromise or by a neural reflex mechanism, or both), some of the most important are hypertrophic cardiomyopathy, acute aortic dissection, pericardial tamponade, pulmonary embolism, aortic stenosis, and pulmonary hypertension.

                                                                         

Other cardiac causes

Sick sinus syndrome, a sinus node dysfunction, causing alternating bradycardia and tachycardia. Often there is a long pause (asystole) between heartbeats.

 

Adams-Stokes syndrome is a cardiac syncope that occurs with seizures caused by complete or incomplete heart block. Symptoms include deep and fast respiration, weak and slow pulse, and respiratory pauses that may last for 60 seconds.

 

Subclavian steal syndrome arises from retrograde (reversed) flow of blood in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery.  Symptoms such as syncope, lightheadedness, and paresthesias occur while exercising the arm on the affected side (most commonly the left).

 

Aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope.

 

Various medications, such as beta blockers, may cause bradycardia induced syncope.

 

A pulmonary embolism can cause obstructed blood vessels and is the cause of syncope in less than 1% of people who present to the emergency department.

 

Blood pressure

Orthostatic (postural) hypotensive syncope is caused primarily by an excessive drop in blood pressure when standing up from a previous position of lying or sitting down. When the head is elevated above the feet the pull of gravity causes blood pressure in the head to drop. This is sensed by stretch receptors in the walls of vessels in the carotid sinus and aortic arch. These receptors then trigger a sympathetic nervous response to compensate and redistribute blood back into the brain. The sympathetic response causes peripheral vasoconstriction and increased heart rate. These together act to raise blood pressure back to baseline. Apparently healthy individuals may experience minor symptoms ("lightheadedness", "greying-out") as they stand up if blood pressure is slow to respond to the stress of upright posture. If the blood pressure is not adequately maintained during standing, faints may develop. However, the resulting "transient orthostatic hypotension" does not necessarily signal any serious underlying disease. It is as common or perhaps even more common than vasovagal syncope.

 

This may be due to medications, dehydration, significant bleeding or infection.  The most susceptible individuals are elderly frail individuals, or persons who are dehydrated from hot environments or inadequate fluid intake.   For example, medical students would be at risk for orthostatic hypotensive syncope while observing long surgeries in the operating room.   There is also evidence that exercise training can help reduce orthostatic intolerance.   More serious orthostatic hypotension is often the result of certain commonly prescribed medications such as diuretics, β-adrenergic blockers, other anti-hypertensives (including vasodilators), and nitroglycerin. In a small percentage of cases, the cause of orthostatic hypotensive faints is structural damage to the autonomic nervous system due to systemic diseases (e.g., amyloidosis or diabetes) or in neurological diseases (e.g., Parkinson's disease).

 

Hyperadrenergic orthostatic hypotension refers to an orthostatic drop in blood pressure despite high levels of sympathetic adrenergic response. This occurs when a person with normal physiology is unable to compensate for >20% loss in intravascular volume.  This may be due to blood loss, dehydration or third-spacing. On standing the person will experience reflex tachycardia (at least 20% increased over supine) and a drop in blood pressure.

 

Hypoadrenergic orthostatic hypotension occurs when the person is unable to sustain a normal sympathetic response to blood pressure changes during movement despite adequate intravascular volume. There is little to no compensatory increase in heart rate or blood pressure when standing for up to 10 minutes. This is often due to an underlying disorder or medication use and is accompanied by other hypoadrenergic signs.

 

Central nervous system ischemia

The central ischemic response is triggered by an inadequate supply of oxygenated blood in the brain.  Common examples include strokes and transient ischemic attacks. While these conditions often impair consciousness they rarely meet the medical definition of syncope. Vertebrobasilar transient ischemic attacks may produce true syncope as a symptom.

 

The respiratory system may compensate for dropping oxygen levels through hyperventilation, though a sudden ischemic episode may also proceed faster than the respiratory system can respond.  These processes cause the typical symptoms of fainting: pale skin, rapid breathing, nausea, and weakness of the limbs, particularly of the legs.  If the ischemia is intense or prolonged, limb weakness progresses to collapse. The weakness of the legs causes most people to sit or lie down if there is time to do so. This may avert a complete collapse, but whether the patient sits down or falls down, the result of an ischaemic episode is a posture in which less blood pressure is required to achieve adequate blood flow. An individual with very little skin pigmentation may appear to have all color drained from his or her face at the onset of an episode.[3] This effect combined with the following collapse can make a strong and dramatic impression on bystanders.

 

Vertebro-basilar arterial disease

Arterial disease in the upper spinal cord, or lower brain that causes syncope if there is a reduction in blood supply. This may occur with extending the neck or with use of medications to lower blood pressure.

Other causes

There are other conditions which may cause or resemble syncope.

 

Seizures and syncope can be difficult to differentiate. Both often present as sudden loss of consciousness and convulsive movements may be present or absent in either. Movements in syncope are typically brief and more irregular than seizures. Akinetic seizures can present with sudden loss of postural tone without associated tonic-clonic movements. Absence of a long post-ictal state is indicative of syncope rather than an akinetic seizure.

 

Subarachnoid hemorrhage may result in syncope. Often this is in combination with sudden, severe headache. It may occur as a result of a ruptured aneurysm or head trauma.

 

Heat syncope occurs when heat exposure causes decreased blood volume and peripheral vasodilatation.  Position changes, especially during vigorous exercise in the heat, may lead to decreased blood flow to the brain.  Closely related to other causes of syncope related to hypotension (low blood pressure), such as orthostatic syncope. 

 

Lactose intolerance can cause "a release of histamine, resulting in an extreme dilatation of the bloodvessels, resulting in a drop of blood pressure so that not enough blood reaches the brains, leading to dizziness, fainting, syncope, itching, hives, tingling or swelling of the lips, tongue, or throat; chest tightness, shortness of breath, or difficulty breathing, wheezing." (More in the article on Lactose intolerance).

 

Some psychological conditions (anxiety disorder, somatic symptom disorder, conversion disorder) may cause symptoms resembling syncope. A number of psychological interventions are available.

 

Low blood sugar can be a rare cause of syncope.

 

Narcolepsy may present with sudden loss of consciousness similar to syncope.

 

Diagnostic approach

A medical history, physical examination, and electrocardiogram (ECG) are the most effective ways to determine the underlying cause of syncope.  Guidelines from the American College of Emergency Physicians and American Heart Association recommend a syncope workup include a thorough medical history, physical exam with orthostatic vitals, and a 12-lead ECG.  The ECG is useful to detect an abnormal heart rhythm, poor blood flow to the heart muscle and other electrical issues, such as long QT syndrome and Brugada syndrome. Heart related causes also often have little history of a prodrome.   Low blood pressure and a fast heart rate after the event may indicate blood loss or dehydration, while low blood oxygen levels may be seen following the event in those with pulmonary embolism.  Routine broad panel laboratory testing detects abnormalities in 2–3% of results and is therefore not recommended.

 

Based on this initial workup many physicians will tailor testing and determine whether a person qualifies as 'high-risk', 'intermediate risk' or 'low-risk' based on risk stratification tools.  More specific tests such as implantable loop recorders, tilt table testing or carotid sinus massage may be useful in uncertain cases.   Computed tomography (CT) is generally not required unless specific concerns are present.  Other causes of similar symptoms that should be considered include seizure, stroke, concussion, low blood oxygen, low blood sugar, drug intoxication and some psychiatric disorders among others. Treatment depends on the underlying cause. Those who are considered at high risk following investigation may be admitted to hospital for further monitoring of the heart.

A hemoglobin count may indicate anemia or blood loss. However, this has been useful in only about 5% of people evaluated for fainting. The tilt table test is performed to elicit orthostatic syncope secondary to autonomic dysfunction (neurogenic). A number of factors make a heart related cause more likely including age over 35, prior atrial fibrillation, and turning blue during the event.

 

Electrocardiogram

Electrocardiogram (ECG) finds that should be looked for include signs of heart ischemia, arrhythmias, atrioventricular blocks, a long QT, a short PR, Brugada syndrome, signs of hypertrophic obstructive cardiomyopathy (HOCM), and signs of arrhythmogenic right ventricular dysplasia (ARVD/C).   Signs of HOCM include large voltages in the precordial leads, repolarization abnormalities, and a wide QRS with a slurred upstroke.  Signs of ARVD/C include T wave inversion and epsilon waves in lead V1 to V3.

 

It is estimated that from 20 to 50% of people have an abnormal ECG. However, while an ECG may identify conditions such as atrial fibrillation, heart block, or a new or old heart attack, it typically does not provide a definite diagnosis for the underlying cause for fainting.  Sometimes, a Holter monitor may be used. This is a portable ECG device that can record the wearer's heart rhythms during daily activities over an extended period of time. Since fainting usually does not occur upon command, a Holter monitor can provide a better understanding of the heart's activity during fainting episodes. For people with more than two episodes of syncope and no diagnosis on "routine testing", an insertable cardiac monitor might be used.  It lasts 28–36 months and is inserted just beneath the skin in the upper chest area.

 

ECG showing HOCM

         

        

Imaging

Echocardiography and ischemia testing may be recommended for cases where initial evaluation and ECG testing is nondiagnostic. For people with uncomplicated syncope (without seizures and a normal neurological exam) computed tomography or MRI is not generally needed. Likewise, using carotid ultrasonography on the premise of identifying carotid artery disease as a cause of syncope also is not indicated. Although sometimes investigated as a cause of syncope, carotid artery problems are unlikely to cause that condition. Additionally an electroencephalogram (EEG) is generally not recommended.  A bedside ultrasound may be performed to rule out abdominal aortic aneurysm in people with concerning history or presentation.

 

Differential diagnosis

Other diseases which mimic syncope include seizure, low blood sugar, and certain types of stroke.  While these may appear as "fainting", they do not fit the strict definition of syncope being a sudden reversible loss of consciousness due to decreased blood flow to the brain. 

 

Management

Management of syncope focuses on treating the underlying cause.  This can be challenging as the underlying cause is unclear in half of all cases.  Several risk stratification tools (explained below) have been developed to combat the vague nature of this diagnosis. People with an abnormal ECG reading, history of congestive heart failure, family history of sudden cardiac death, shortness of breath, HCT<30, hypotension or evidence of bleeding should be admitted to the hospital for further evaluation and monitoring. Low-risk cases of vasovagal or orthostatic syncope in younger people with no significant cardiac history, no family history of sudden unexplained death, and a normal EKG and initial evaluation may be candidates for discharge to follow-up with their primary care provider.

 

Recommended acute treatment of vasovagal and orthostatic (hypotension) syncope involves returning blood to the brain by positioning the person on the ground, with legs slightly elevated or sitting leaning forward and the head between the knees for at least 10–15 minutes, preferably in a cool and quiet place. For individuals who have problems with chronic fainting spells, therapy should focus on recognizing the triggers and learning techniques to keep from fainting. At the appearance of warning signs such as lightheadedness, nausea, or cold and clammy skin, counter-pressure maneuvers that involve gripping fingers into a fist, tensing the arms, and crossing the legs or squeezing the thighs together can be used to ward off a fainting spell. After the symptoms have passed, sleep is recommended. Lifestyle modifications are important for treating people experiencing repeated syncopal episodes. Avoiding triggers and situations where loss of consciousness would be seriously hazardous (operating heavy machinery, commercial pilot, etc.) has been shown to be effective.

 

If fainting spells occur often without a triggering event, syncope may be a sign of an underlying heart disease. In the case where syncope is caused by cardiac disease, the treatment is much more sophisticated than that of vasovagal syncope and may involve pacemakers and implantable cardioverter-defibrillators depending on the precise cardiac cause.

 

Risk tools

The San Francisco syncope rule was developed to isolate people who have higher risk for a serious cause of syncope. High risk is anyone who has: congestive heart failure, hematocrit less than 30%, electrocardiograph abnormality, shortness of breath, or systolic blood pressure less than 90 mmHg.  The San Francisco syncope rule however was not validated by subsequent studies.

 

The Canadian syncope risk score was developed to help select low-risk people that may be viable for discharge home.  A score of <0 on the Canadian syncope risk score is associated with <2% risk of serious adverse event within 30 days. It has been shown to be more effective than older syncope risk scores, even combined with cardiac biomarkers at predicting adverse events.

 

Epidemiology

There are 18.1–39.7 syncope episodes per 1000 people in the general population.  This is likely because of the high rates of vasovagal syncope in the young adult population. Older adults are more likely to have orthostatic or cardiac syncope.

 

 

Syncope affects about three to six out of every thousand people each year.  It is more common in older people and females. It is the reason for 2–5% of visits to emergency departments and admissions to hospital.  Up to half of women over the age of 80 and a third of medical students describe at least one event at some point in their lives.

 

Prognosis

Of those presenting with syncope to an emergency department, about 4% died in the next 30 days. The risk of a poor outcome, however, depends very much on the underlying cause. Situational syncope does not lead to increased risk of death or adverse outcomes. Cardiac syncope is associated with worse prognosis compared to noncardiac syncope. Factors associated with poor outcomes include history of heart failure, history of myocardial infarction, ECG abnormalities, palpitations, signs of hemorrhage, syncope during exertion, and advanced age.

 

Society and culture

Fainting in women was a commonplace trope or stereotype in Victorian England and in contemporary and modern depictions of the period.

 

Syncope and presyncope are common in young athletes. In 1990 the American college basketball player Hank Gathers suddenly collapsed and died during a televised intercollegiate basketball game.  He had previously collapsed during a game a few months prior. He was diagnosed with exercise-induced ventricular tachycardia at the time. There was speculation that he had since stopped taking the prescribed medications on game days.

 

Falling-out is a culture-bound syndrome primarily reported in the southern United States and the Caribbean.

 

Etymology

The term is derived from the Late Latin syncope, from Ancient Greek συγκοπή (sunkopē) 'cutting up', 'sudden loss of strength', from σύν (sun, "together, thoroughly") and κόπτειν (koptein, "strike, cut off").

Jan Ricks Jennings, MHA, LFACHE

Senior Consultant

Senior Management Resources, LLC

 

412.913.0636 Cell

724.730509 Office

 

Jan.Jennings@EagleTalons.net

JanJennings.BlogSpot.com

 

12.31.2022

                                                           Falling (accident)

Overview

Falling is a normal experience for young children but falling from a significant height or onto a solid surface can be dangerous.

Complications:  Head injury, concussion, bone fracture, abrasion, bruise

Risk factors:        Convulsion, vision impairment, difficulty walking, home hazards. 

Frequency:          226 million

Deaths:                527,000

Falling is the action of a person or animal losing stability and ending up in a lower position, often on the ground. It is the second-leading cause of accidental death worldwide and a major cause of personal injury, especially for the elderly.  Falls in older adults are a major class of preventable injuries. Construction workers, electricians, miners, and painters are occupations with high rates of fall injuries.

 

Long-term exercise decreases the rate of falls in older people.  About 226 million cases of significant accidental falls occurred in 2015. These resulted in 527,000 deaths.

Causes

Accidents

The most common cause of falls in healthy adults is accidents. It may be by slipping or tripping from stable surfaces or stairs, improper footwear, dark surroundings, uneven ground, or lack of exercise.  Studies suggest that women are more prone to falling than men in all age groups.

 

Age

Older people and particularly those with dementia are at greater risk than young people to injuries due to falling.  Older people are at risk due to accidents, gait disturbances, balance disorders, changed reflexes due to visual, sensory, motor, and cognitive impairment, medications and alcohol consumption, infections, and dehydration.

Illness

People who have experienced stroke are at risk for falls due to gait disturbances, reduced muscle tone and weakness, side effects of drugs to treat MS, low blood sugar, low blood pressure, and loss of vision.

 

People with Parkinson's disease are at risk of falling due to gait disturbances, loss of motion control including freezing and jerking, autonomic system disorders such as orthostatic hypotension, fainting, and postural orthostatic tachycardia syndrome.  Parkinson’s patients are also at risk due to neurological and sensory disturbances including muscle weakness of lower limbs, deep sensibility impairment, epileptic seizure, cognitive impairment, visual impairment, balance impairment, and side effects of drugs to treat PD.

 

People with multiple sclerosis are at risk of falling due to gait disturbances, drop foot, ataxia, reduced proprioception, improper or reduced use of assistive devices, reduced vision, cognitive changes, and medications to treat MS.

 

Workplace

At-risk workers without appropriate safety equipment

In the occupational setting, falling incidents are commonly referred to as slips, trips, and falls. Falls are an important topic for occupational safety and health services. Any walking/working surface could be a potential fall hazard. An unprotected side or edge which is six feet (1.8 m) or more above a lower level should be protected from falling using a guard rail system, safety net system, or personal fall arrest system.

 

The National Institute for Occupational Safety and Health has compiled certain known risk factors that have been found responsible for STFs in the workplace setting.  While falling can occur at any time and by any means in the workplace, these factors have been known to cause same-level falls, which are less likely to occur than falls to a lower level.

 

Workplace factors: spills on walking surfaces, ice, precipitation (snow/sleet/rain), loose mats or rugs, boxes/containers, poor lighting, uneven walking surfaces

 

Work organization factors: fast work pace, work tasks involving liquids or greases

 

Individual factors: age; employee fatigue; failing eyesight / use of bifocals; inappropriate, loose, or poor-fitting footwear

 

Preventive measures: warning signs

 

For certain professions such as stunt performers and skateboarders, falling and learning to fall is part of the job.

Intentionally caused falls

Main articles: Jumper (suicide) and Defenestration

Injurious falls can be caused intentionally, as in cases of defenestration or deliberate jumping.

 

Height and severity

The severity of injury increases with the height of the fall but also depends on body and surface features and the manner of the body's impacts against the surface.   The chance of surviving increases if landing on a highly deformable surface (a surface that is easily bent, compressed, or displaced) such as snow or water.

 

Injuries caused by falls from buildings vary depending on the building's height and the age of the person. Falls from a building's second floor/story (US English) or first floor/storey (British English and equivalent idioms in continental European languages) usually cause injuries but are not fatal. Overall, the height at which 50% of children die from a fall is between four and five storey heights (around 12 to 15 meters or 40 to 50 feet) above the ground.

 

Prevention

 

Workplace safety campaigns attempt to reduce injuries from falling.

Long-term exercise decreases the rate of falls in older people.  Rates of falls in hospital can be reduced with several interventions together by 0.72 from baseline in the elderly.   Nursing homes develop fall prevention programs that involve several interventions prevent recurrent falls.

Surviving falls

A falling person at low altitude typically reaches terminal velocity of 190 km/h (120 mph) after about 12 seconds, falling some 450 m (1,500 ft) in that time. Without alterations to their aerodynamic profile, the person maintains this speed without falling any faster. Terminal velocity at higher altitudes is greater due to the thinner atmosphere and consequent lower air resistance.

 

JAT flight attendant Vesna Vulović survived a fall of 10,000 meters (33,000 ft. on January 26, 1972, pinned within the broken fuselage of the DC-9 of JAT Flight 367. The plane was brought down by explosives over Srbská Kamenice in the former Czechoslovakia (now the Czech Republic). The Serbian flight attendant suffered a broken skull, three broken vertebrae (one crushed completely), and was in a coma for 27 days. In an interview, she commented that, according to the man who found her, "…I was in the middle part of the plane. I was found with my head down and my colleague on top of me. One part of my body with my leg was in the plane and my head was out of the plane. A catering trolley was pinned against my spine and kept me in the plane. The man who found me, says I was incredibly lucky. He was in the German Army as a medic during World War Two. He knew how to treat me at the site of the accident."

 

In World War II there were several reports of military aircrew surviving long falls from severely damaged aircraft: Flight Sergeant Nicholas Alkemade jumped at 5,500 meters (18,000 ft) without a parachute and survived as he hit pine trees and soft snow. He suffered a sprained leg. Staff Sergeant Alan Magee exited his aircraft at 6,700 meters (22,000 ft) without a parachute and survived as he landed on the glass roof of a train station. Lieutenant Ivan Chisov bailed out at 7,000 meters (23,000 ft). While he had a parachute, his plan was to delay opening it as he had been during an air-battle and was concerned about getting shot while hanging below the parachute. He lost consciousness due to lack of oxygen and hit a snow-covered slope while still unconscious. While he suffered severe injuries, he was able to fly again in three months.

 

It was reported that two of the victims of the Lockerbie bombing survived for a brief period after hitting the ground (with the forward nose section fuselage in freefall mode) but died from their injuries before help arrived.

 

Juliane Koepcke survived a long free fall resulting from the December 24, 1971, crash of LANSA Flight 508 (a LANSA Lockheed Electra OB-R-941 commercial airliner) in the Peruvian rainforest. The airplane was struck by lightning during a severe thunderstorm and exploded in midair, disintegrating 3.2 km (2 mi) up. Kipke, who was 17 years old at the time, fell to earth still strapped into her seat. The German Peruvian teenager survived the fall with only a broken collarbone, a gash to her right arm, and her right eye swollen shut.

 

As an example of "freefall survival" that was not as extreme as sometimes reported in the press, a skydiver from Staffordshire was said to have plunged 1,800 m (6,000 ft) without a parachute in Russia and survived. James Boole said that he was supposed to have been given a signal by another skydiver to open his parachute, but it came two seconds too late. Boole, who was filming the other skydiver for a television documentary, landed on snow-covered rocks and suffered a broken back and rib.  While he was lucky to survive, this was not a case of true freefall survival, because he was flying a wingsuit, decreasing his vertical speed. This was over descending terrain with deep snow cover, and he impacted while his parachute was beginning to deploy. Over the years, other skydivers have survived accidents where the press has reported that no parachute was open, yet they were being slowed by a small area of tangled parachute. They might still be lucky to survive, but an impact at 130 km/h (80 mph) is much less severe than the 190 km/h (120 mph) that might occur in normal freefall.

 

Parachute jumper and stuntman Luke Aikins successfully jumped without a parachute from about 7,600 meters (25,000 into a 930-square-metre (10,000 sq ft) net in California, US, on 30 July 2016.

 

Epidemiology

In 2013, unintentional falls resulted in an estimated 556,000 deaths globally, up from 341,000 deaths in 1990. They are the second most common cause of death from unintentional injuries after motor vehicle collisions.

 

Deaths due to falls per million persons in 2012

 

Disability-adjusted life year for falls per 100,000 inhabitants in 2004.  no data   less than 40   40–110   110–180   180–250   250–320   320–390   390–460   460–530   530–600   600–670   670–one thousand   more than one thousand

Disability-adjusted life year for falls per 100,000 inhabitants in 2004.

 United States They were the most common cause of injury seen in emergency departments in the United States. One study found that there were 7.9 million emergency department visits involving falls, 35.7% of all encounters.  Among children nineteen and below, about 8,000 visits to the emergency rooms are registered every day.

In 2000, in the USA 717 workers died of injuries caused by falls from ladders, scaffolds, buildings, or other elevations.  More recent data in 2011, found that STFs contributed to 14% of all workplace fatalities in the United States that year.

Jan Ricks Jennings, MHA, LFACHE

Senior Consultant

Senior Management Resources, LLC

 

Jan.Jennings@EagleTalons.net

Jan.JenningsBlog.Blogspot.com

 

412.913.0636 Cell

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December 18, 2022

Joseph Stalin became the General Secretary of the Communist Party of the Soviet Union.  He was born on December 18, 1878.  Stalin was ruthless, temperamentally cruel, and had a propensity for violence high even among the Bolsheviks.  With a high number of excess deaths occurring under his rule, Stalin has been labelled "one of the most notorious figures in history."  These deaths occurred because of collectivization, famine, terror campaigns, disease, war, and mortality rates in the Gulag.   The historian Robert Conquest stated that Stalin perhaps "determined the course of the twentieth century" more than any other individual. 

                                                                               

Factors in the Emergence of Infectious Diseases

 

Abstract

"Emerging" infectious diseases can be defined as infections that have newly appeared in a population or have existed but are rapidly increasing in incidence or geographic range. Among recent examples are HIV/AIDS, hantavirus pulmonary syndrome, Lyme disease, and hemolytic uremic syndrome (a foodborne infection caused by certain strains of Escherichia coli). Specific factors precipitating disease emergence can be identified in virtually all cases. These include ecological, environmental, or demographic factors that place people at increased contact with a previously unfamiliar microbe or its natural host or promote dissemination. These factors are increasing in prevalence; this increase, together with the ongoing evolution of viral and microbial variants and selection for drug resistance, suggests that infections will continue to emerge and probably increase and emphasizes the urgent need for effective surveillance and control.  

 

 

Infectious diseases emerging throughout history have included some of the most feared plagues of the past. New infections continue to emerge today, while many of the old plagues are with us still. These are global problems (William Foege, former CDC director now at the Carter Center, terms them global infectious disease threats). As demonstrated by influenza epidemics, under suitable circumstances, a new infection first appearing anywhere in the world could traverse entire continents within days or weeks.

We can define as emerging infections that have newly appeared in the population or have existed but are rapidly increasing in incidence or geographic range. Recent examples of emerging diseases in various parts of the world include HIV/AIDS, classic cholera in South America and Africa, cholera due to Vibrio cholerae O139, Rift Valley fever, hantavirus pulmonary syndrome, Lyme disease; and hemolytic uremic syndrome, a foodborne infection caused by certain strains of Escherichia coli (in the United States, surety.

Although these occurrences may appear inexplicable, rarely if ever do emerging infections appear without reason. Specific factors responsible for disease emergence can be identified in virtually all cases studied.  known causes for a number of infections that have emerged recently. It has been suggested that infectious disease emergence can be viewed operationally as a two-step process: Introduction of the agent into a new host population (whether the pathogen originated in the environment, possibly in another species, or as a variant of an existing human infection), followed by establishment and further dissemination within the new host population. Whatever its origin, the infection emerges when it reaches a new population. Factors that promote one or both of these steps will, therefore, tend to precipitate disease emergence. Most emerging infections, and even antibiotic-resistant strains of common bacterial pathogens, usually originate in one geographic location and then disseminate to new places.

Regarding the introduction step, the numerous examples of infections originating as zoonoses suggest that the zoonotic pool introductions of infections from other species is an important and potentially rich source of emerging diseases; periodic discoveries of new zoonoses suggest that the zoonotic pool appears by no means exhausted. Once introduced, an infection might then be disseminated through other factors, although rapid course and high mortality combined with low transmissibility are often limiting. However, even if a zoonotic agent is not able to spread readily from person to person and establish itself, other factors (e.g., nosocomial infection) might transmit the infection. Additionally, if the reservoir host or vector becomes more widely disseminated, the microbe can appear in new places. Bubonic plague transmitted by rodent fleas and rat borne hantavirus infections are examples.

Most emerging infections appear to be caused by pathogens already present in the environment, brought out of obscurity or given a selective advantage by changing conditions and afforded an opportunity to infect new host populations (on rare occasions, a new variant may also evolve and cause a new disease. The process by which infectious agents may transfer from animals to humans or disseminate from isolated groups into new populations can be called microbial traffic.  A number of activities increase microbial traffic and as a result promote emergence and epidemics. In some cases, including many of the most novel infections, the agents are zoonotic, crossing from their natural hosts into the human population; because of the many similarities, I include here vector-borne diseases. In other cases, pathogens already present in geographically isolated populations are given an opportunity to disseminate further. Surprisingly often, disease emergence is caused by human actions, however inadvertently; natural causes, such as changes in climate, can also at times be responsible. Although this discussion is confined largely to human disease, similar considerations apply to emerging pathogens in other species.

Any categorization of the underlying factors responsible for emergence is, of course, somewhat arbitrary but should be representative of the underlying processes that cause emergence. I have essentially adopted the categories developed in the Institute of Medicine report on emerging infections, with additional definitions from the CDC emerging infections plan. Responsible factors include ecological changes, such as those due to agricultural or economic development or to anomalies in climate, human demographic changes and behavior, travel and commerce; technology and industry, microbial adaptation and change, and breakdown of public health measures. Each of these will be considered in turn.  Examples of infections originating as zoonoses suggest that the zoonotic pool introductions of infections from other species is an important and potentially rich source of emerging diseases; periodic discoveries of new zoonoses suggest that the zoonotic pool appears by no means exhausted. Once introduced, an infection might then be disseminated through other factors, although rapid course and high mortality combined with low transmissibility are often limiting. However, even if a zoonotic agent is not able to spread readily from person to person and establish itself, other factors (e.g., nosocomial infection) might transmit the infection. Additionally, if the reservoir host or vector becomes more widely disseminated, the microbe can appear in new places. Bubonic plague transmitted by rodent fleas and rat borne hantavirus infections are examples.

Ecological interactions can be complex, with several factors often working together or in sequence. For example, population movement from rural areas to cities can spread a once-localized infection. The strain on infrastructure in the overcrowded and rapidly growing cities may disrupt or slow public health measures, perhaps allowing establishment of the newly introduced infection. Finally, the city may also provide a gateway for further dissemination of the infection. Most successful emerging infections, including HIV, cholera, and dengue, have followed this route.

Consider HIV as an example. Although the precise ancestry of HIV-1 is still uncertain, it appears to have had a zoonotic origin. Ecological factors that would have allowed human exposure to a natural host carrying the virus that was the precursor to HIV-1 were, therefore, instrumental in the introduction of the virus into humans. This probably occurred in a rural area. A plausible scenario is suggested by the identification of an HIV-2-infected man in a rural area of Liberia whose virus strain resembled viruses isolated from the sooty mangabey monkey (an animal widely hunted for food in rural areas and the putative source of HIV-2) more closely than it did strains circulating in the city. Such findings suggest that zoonotic introductions of this sort may occur on occasion in isolated populations but may well go unnoticed so long as the recipients remain isolated. But with increasing movement from rural areas to cities, such isolation is increasingly rare. After its likely first move from a rural area into a city, HIV-1 spread regionally along highways, then by long distance routes, including air travel, to more distant places. This last step was critical for HIV and facilitated today's global pandemic. Social changes that allowed the virus to reach a larger population and to be transmitted despite its relatively low natural transmissibility were instrumental in the success of the virus in its newfound human host. For HIV, the long duration of infectivity allowed this normally poorly transmissible virus many opportunities to be transmitted and to take advantage of such factors as human behavior (sexual transmission, intravenous drug use) and changing technology (early spread through blood transfusions and blood products.

Ecological Changes and Agricultural Development

Ecological changes, including those due to agricultural or economic development, are among the most frequently identified factors in emergence. They are especially frequent as factors in outbreaks of previously unrecognized diseases with high case-fatality rates, which often turn out to be zoonotic introductions. Ecological factors usually precipitate emergence by placing people in contact with a natural reservoir or host for an infection hitherto unfamiliar but usually already present (often a zoonotic or arthropod-borne infection), either by increasing proximity or, often, also by changing conditions so as to favor an increased population of the microbe or its natural host. The emergence of Lyme disease in the United States and Europe was probably due largely to reforestation, which increased the population of deer and the deer tick, the vector of Lyme disease. The movement of people into these areas placed a larger population in close proximity to the vector.

Agricultural development, one of the most common ways in which people alter and interpose themselves into the environment, is often a factor.  Hantan virus, the cause of Korean hemorrhagic fever, causes over 100,000 cases a year in China and has been known in Asia for centuries. The virus is a natural infection of the field mouse Apodemus agrarius. The rodent flourishes in rice fields; people usually contract the disease during the rice harvest from contact with infected rodents. Junin virus, the cause of Argentine hemorrhagic fever, is an unrelated virus with a history remarkably similar to that of Hantan virus. Conversion of grassland to maize cultivation favored a rodent that was the natural host for this virus, and human cases increased in proportion with expansion of maize agriculture. Other examples, in addition to those already known, are likely to appear as new areas are placed under cultivation.

Perhaps most surprisingly, pandemic influenza appears to have an agricultural origin, which is integrated pig-duck farming in China. Strains causing the frequent annual or biennial epidemics generally result from mutation , but pandemic influenza viruses do not generally arise by this process. Instead, gene segments from two influenza strains reassort to produce a new virus that can infect humans. Evidence amassed by Webster, Scholtissek, and others, indicates that waterfowl, such as ducks, are major reservoirs of influenza and that pigs can serve as mixing vessels for new mammalian influenza strains. Pandemic influenza viruses have generally come from China. Scholtissek and Naylor suggested that integrated pig-duck agriculture, an extremely efficient food production system traditionally practiced in certain parts of China for several centuries, puts these two species in contact and provides a natural laboratory for making new influenza recombinants. Webster has suggested that, with high-intensity agriculture and movement of livestock across borders, suitable conditions may now also be found in Europe.

Water is also frequently associated with disease emergence. Infections transmitted by mosquitoes or other arthropods, which include some of the most serious and widespread diseases, are often stimulated by expansion of standing water, simply because many of the mosquito vectors breed in water. There are many cases of diseases transmitted by water-breeding vectors, most involving dams, water for irrigation, or stored drinking water in cities. (See Changes in Human Demographics and Behavior for a discussion of dengue.) The incidence of Japanese encephalitis, another mosquito-borne disease that accounts for almost 30,000 human cases and approximately 7,000 deaths annually in Asia, is closely associated with flooding of fields for rice growing. Outbreaks of Rift Valley fever in some parts of Africa have been associated with dam building as well as with periods of heavy rainfall. In the outbreaks of Rift Valley fever in Mauritania in 1987, the human cases occurred in villages near dams on the Senegal River. The same effect has been documented with other infections that have aquatic hosts, such as schistosomiasis.

Because humans are important agents of ecological and environmental change, many of these factors are anthropogenic. Of course, this is not always the case, and natural environmental changes, such as climate or weather anomalies, can have the same effect. The outbreak of hantavirus pulmonary syndrome in the southwestern United States in 1993 is an example. It is likely that the virus has long been present in mouse populations but an unusually mild and wet winter and spring in that area led to an increased rodent population in the spring and summer and thus to greater opportunities for people to come in contact with infected rodents (and, hence, with the virus); it has been suggested that the weather anomaly was due to large-scale climatic effects. The same causes may have been responsible for outbreaks of hantaviral disease in Europe at approximately the same time. With cholera, it has been suggested that certain organisms in marine environments are natural reservoirs for cholera vibrios, and that large scale effects on ocean currents may cause local increases in the reservoir organism with consequent flare-ups of cholera.

Changes in Human Demographics and Behavior

Human population movements or upheavals, caused by migration or war, are often crucial factors in disease emergence. In many parts of the world, economic conditions are encouraging the mass movement of workers from rural areas to cities. The United Nations has estimated that, largely as a result of continuing migration, by the year 2025, 65% of the world population (also expected to be larger in absolute numbers), including 61% of the population in developing regions, will live in cities. As discussed above for HIV, rural urbanization allows infections arising in isolated rural areas, which may once have remained obscure and localized, to reach larger populations. Once in a city, the newly introduced infection would have the opportunity to spread locally among the population and could also spread further along highways and interurban transport routes and by airplane. HIV has been, and in Asia is becoming, the best known beneficiary of this dynamic, but many other diseases, such as dengue, stand to benefit. The frequency of the most severe form, dengue hemorrhagic fever, which is thought to occur when a person is sequentially infected by two types of dengue virus, is increasing as different dengue viruses have extended their range and now overlap. Dengue hemorrhagic fever is now common in some cities in Asia, where the high prevalence of infection is attributed to the proliferation of open containers needed for water storage (which also provide breeding grounds for the mosquito vector) as the population size exceeds the infrastructure. In urban environments, rain-filled tires or plastic bottles are often breeding grounds of choice for mosquito vectors. The resulting mosquito population boom is complemented by the high human population density in such situations, increasing the chances of stable transmission cycles between infected and susceptible persons. Even in industrialized countries, e.g., the United States, infections such as tuberculosis can spread through high-population density settings e.g., day care centers or prisons.

Human behavior can have important effects on disease dissemination. The best known examples are sexually transmitted diseases, and the ways in which such human behavior as sex or intravenous drug use have contributed to the emergence of HIV are now well known. Other factors responsible for disease emergence are influenced by a variety of human actions, so human behavior in the broader sense is also very important. Motivating appropriate individual behavior and constructive action, both locally and in a larger scale, will be essential for controlling emerging infections. Ironically, as AIDS prevention efforts have demonstrated, human behavior remains one of the weakest links in our scientific knowledge.

 

International Travel and Commerce

The dissemination of HIV through travel has already been mentioned. In the past, an infection introduced into people in a geographically isolated area might, on occasion, be brought to a new place through travel, commerce, or war. Trade between Asia and Europe, perhaps beginning with the silk route and continuing with the Crusades, brought the rat and one of its infections, the bubonic plague, to Europe. Beginning in the 16th and 17th centuries, ships bringing slaves from West Africa to the New World also brought yellow fever and its mosquito vector, Aedes aegypti, to the new territories. Similarly, smallpox escaped its Old World origins to wreak new havoc in the New World. In the 19th century, cholera had similar opportunities to spread from its probable origin in the Ganges plain to the Middle East and, from there, to Europe and much of the remaining world. Each of these infections had once been localized and took advantage of opportunities to be carried to previously unfamiliar parts of the world.

Similar histories are being repeated today, but opportunities in recent years have become far richer and more numerous, reflecting the increasing volume, scope, and speed of traffic in an increasingly mobile world. Rats have carried hantaviruses virtually worldwide. Aedes albopictus (the Asian tiger mosquito) was introduced into the United States, Brazil, and parts of Africa in shipments of used tires from Asia. Since its introduction in 1982, this mosquito has established itself in at least 18 states of the United States and has acquired local viruses including Eastern equine encephalomyelitis, a cause of serious disease. Another mosquito-borne disease, malaria, is one of the most frequently imported diseases in non-endemic-disease areas, and cases of airport malaria are occasionally identified.

A classic bacterial disease, cholera, recently entered both South America (for the first time this century) and Africa. Molecular typing shows the South American isolates to be of the current pandemic strain, supporting the suggestion that the organism was introduced in contaminated bilge water from an Asian freighter. Other evidence indicates that cholera was only one of many organisms to travel in ballast water; dozens, perhaps hundreds, of species have been exchanged between distant places through this means of transport alone. New bacterial strains, such as the recently identified Vibrio cholerae O139, or an epidemic strain of Neisseria meningitidis (also examples of microbial adaptation and change) have disseminated rapidly along routes of trade and travel, as have antibiotic-resistant bacteria.

 

Technology and Industry

High-volume rapid movement characterizes not only travel, but also other industries in modern society. In operations, including food production, that process or use products of biological origin, modern production methods yield increased efficiency and reduced costs but can increase the chances of accidental contamination and amplify the effects of such contamination. The problem is further compounded by globalization, allowing the opportunity to introduce agents from far away. A pathogen present in some of the raw material may find its way into a large batch of final product, as happened with the contamination of hamburger meat by E. coli strains causing hemolytic uremic syndrome. In the United States the implicated E. coli strains are serotype O157:H7; additional serotypes have been identified in other countries. Bovine spongiform encephalopathy (BSE), which emerged in Britain within the last few years, was likely an interspecies transfer of scrapie from sheep to cattle that occurred when changes in rendering processes led to incomplete inactivation of scrapie agent in sheep byproducts fed to cattle.

The concentrating effects that occur with blood and tissue products have inadvertently disseminated infections unrecognized at the time, such as HIV and hepatitis B and C. Medical settings are also at the front line of exposure to new diseases, and a number of infections, including many emerging infections, have spread nosocomial in health care settings.  Among the numerous examples, in the outbreaks of Ebola fever in Africa many of the secondary cases were hospital acquired, most transmitted to other patients through contaminated hypodermic apparatus, and some to the health care staff by contact. Transmission of Lassa fever to health care workers has also been documented.

On the positive side, advances in diagnostic technology can also lead to new recognition of agents that are already widespread. When such agents are newly recognized, they may at first often be labeled, in some cases incorrectly, as emerging infections. Human herpesvirus 6 (HHV-6) was identified only a few years ago, but the virus appears to be extremely widespread and has recently been implicated as the cause of roseola (exanthem subitum), a very common childhood disease.  Because roseola has been known since at least 1910, HHV-6 is likely to have been common for decades and probably much longer. Another recent example is the bacterium Helicobacter pylori, a probable cause of gastric ulcers and some cancers. We have lived with these diseases for a long time without knowing their cause. Recognition of the agent is often advantageous, offering new promise of controlling a previously intractable disease, such as treating gastric ulcers with specific antimicrobial therapy.

 

 

Microbial Adaptation and Change

Microbes, like all other living things, are constantly evolving. The emergence of antibiotic-resistant bacteria as a result of the ubiquity of antimicrobials in the environment is an evolutionary lesson on microbial adaptation, as well as a demonstration of the power of natural selection. Selection for antibiotic-resistant bacteria and drug-resistant parasites has become frequent, driven by the wide and sometimes inappropriate use of antimicrobial drugs in a variety of applications. Pathogens can also acquire new antibiotic resistance genes from other, often nonpathogenic, species in the environment, selected or perhaps even driven by the selection pressure of antibiotics.

Many viruses show a high mutation rate and can rapidly evolve to yield new variants.  A classic example is influenza. Regular annual epidemics are caused by antigenic drift in a previously circulating influenza strain. A change in an antigenic site of a surface protein, usually the hemagglutinin (H) protein, allows the new variant to reinfect previously infected persons because the altered antigen is not immediately recognized by the immune system.

On rare occasions, perhaps more often with nonviral pathogens than with viruses, the evolution of a new variant may result in a new expression of disease. The epidemic of Brazilian purpuric fever in 1990, associated with a newly emerged clonal variant of Hemophilus influenzae, bio group aegyptius, may fall into this category. It is possible, but not yet clear, that some recently described manifestations of disease by group A Streptococcus, such as rapidly invasive infection or necrotizing fasciitis, may also fall into this category.

Breakdown of Public Health Measures and Deficiencies in Public Health Infrastructure

Classical public health and sanitation measures have long served to minimize dissemination and human exposure to many pathogens spread by traditional routes such as water or preventable by immunization or vector control. The pathogens themselves often still remain, albeit in reduced numbers, in reservoir hosts or in the environment, or in small pockets of infection and, therefore, are often able to take advantage of the opportunity to reemerge if there are breakdowns in preventive measures.

Reemerging diseases are those, like cholera, that were once decreasing but are now rapidly increasing again. These are often conventionally understood and well recognized public health threats for which (in most cases) previously active public health measures had been allowed to lapse, a situation that unfortunately now applies all too often in both developing countries and the inner cities of the industrialized world. The appearance of reemerging diseases may, therefore, often be a sign of the breakdown of public health measures and should be a warning against complacency in the war against infectious diseases.

Cholera, for example, has recently been raging in South America (for the first time in this century) and Africa. The rapid spread of cholera in South America may have been abetted by recent reductions in chlorine levels used to treat water supplies. The success of cholera and other enteric diseases is often due to the lack of a reliable water supply. These problems are more severe in developing countries, but are not confined to these areas. The U.S. outbreak of waterborne Cryptosporidium infection in Milwaukee, Wisconsin, in the spring of 1993, with over 400,000 estimated cases, was in part due to a nonfunctioning water filtration plant; similar deficiencies in water purification have been found in other cities in the United States.

 

For our Future

Dr. David Satcher has discussed the history of infectious diseases and the many infections that, from the dawn of history to the present, have traveled with the caravans and followed the invading armies. The history of infectious diseases has been a history of microbes on the march, often in our wake, and of microbes that have taken advantage of the rich opportunities offered them to thrive, prosper, and spread. And yet the historical processes that have given rise to the emergence of new infections throughout history continue today with unabated force; in fact, they are accelerating, because the conditions of modern life ensure that the factors responsible for disease emergence are more prevalent than ever before. Speed of travel and global reach are further borne out by studies modeling the spread of influenza epidemics and HIV.

Humans are not powerless, however, against this relentless march of microbes. Knowledge of the factors underlying disease emergence can help focus resources on the key situations and areas worldwide and develop more effective prevention strategies. If we are to protect ourselves against emerging diseases, the essential first step is effective global disease surveillance to give early warning of emerging infections. This must be tied to incentives, such as national development, and eventually be backed by a system for an appropriate rapid response. World surveillance capabilities are critically deficient. Efforts, such as the CDC plan, now under way in the United States and internationally to remedy this situation are the essential first steps and deserve strong support. Research, both basic and applied, will also be vital.

 Jan Ricks Jennings, MHA, LFACHE

Senior Consultant

Senior Management Resources, LLC

 

Jan.Jennings@EagleTalons.net

JanJenningsBlog.Blogspot.com

 

412.913.0636 Cell

724.733.0509 Office

 

December 11, 2022

P.S.  Pope Leo the X was born on December 11, 1475.  As popes go, he did not go down in history as the most successful leader of the Roman Catholic church.  He borrowed and spent money without circumspection.  He was incredibly opposed to the protestant reformation.  He was a notable patron of the arts and had considerable success in the rebuilding of the Bassilica at the Vatican.  He died at age 45.