Smallpox was the worst disease in history

Smallpox Disease

 Smallpox is a highly contagious disease caused by the smallpox virus, an orthopoxvirus. It causes death in up to 30% of cases. Natural infection was eradicated. The main concern about the outbreak of epidemics is linked to bioterrorism. 

It presents with severe systemic symptoms and a characteristic pustular rash. Treatment is usually supportive and potentially with antiviral drugs. Prevention involves vaccination which, due to related risks, is limited to selected patients.

No cases of smallpox have occurred in the world since 1977, due to vaccination on a worldwide scale. In 1980, the World Health Organization (WHO) recommended the suspension of the routine practice of smallpox vaccination. In the United States, this practice ceased in 1972. 

Since humans are the only natural host of the smallpox virus and because the virus cannot survive > 2 days in the environment, WHO has declared the natural infection eradicated.

Concerns regarding bioterrorism are related to smallpox virus samples stored in research centers or even artificially created viruses that could cause them to reappear (see Biological agents such as weapons and Centers for Disease Control and Prevention [CDC]: Smallpox / Bioterrorism ).

Pathophysiology of smallpox

There are at least 2 strains of the human smallpox virus:

Variola major (classic smallpox), the most virulent strain

Variola minor (alastrim), the least virulent strain

Smallpox presents human-to-human transmission by inhalation of respiratory droplets or, to a lesser extent, by direct contact. Contaminated clothing or bedding can also transmit the infection. Contagiousness is maximum for the first 7-10 days from the onset of the rash. Once the scabs have formed on the skin lesions, the infectivity decreases.

The attack rate reaches 85% in unvaccinated individuals, and infection can lead to up to 4-10 secondary cases for each index case. However, the infection tends to spread slowly and, more importantly, between people in close contact with each other.

The virus invades the oropharyngeal or respiratory mucosa and multiplies in the regional lymph nodes, then leading to viraemia. Finally, it is localized in the small blood vessels of the dermis and oropharyngeal mucosa. The other organs are rarely involved clinically, except for occasional involvement of the central nervous system, in which encephalitis can develop. Secondary bacterial infections of the skin, lungs, and skeletons can develop.

Smallpox Symptomatology

Variola major

The major variant has an incubation period of 10-12 days (ranging from 7 to 17 days), followed by a prodromal period of 2-3 days characterized by fever, headache, low back pain, and extreme malaise. Sometimes severe abdominal pain and vomiting may occur. After the prodromal phase, maculo-papular lesions appear on the oropharyngeal mucosa, face and arms, rapidly spreading to the trunk and legs. Oropharyngeal lesions ulcerate rapidly. After 1-2 days, the skin lesions become vesicular and then pustular. Papules are more numerous on the face and limbs than on the trunk and can affect the palms of the hands. The pustules are rounded and tense and appear deeply located. The skin lesions of smallpox, unlike those of chickenpox, are all at the same stage of evolution in a certain part of the body. After 8 or 9 days the pustules become scabs. Major residual scars are typical.

The mortality rate is around 30%. Mortality is due to the massive inflammatory response that causes shock and multi-organ failure and usually occurs during the 2nd week of illness.

About 5-10% of people with variola major develop a hemorrhagic or malignant variant (flatpox).

The haemorrhagic form is rarer and has a shorter and more intense prodromal period, followed by generalized erythema and cutaneous and mucous haemorrhages. It is invariably fatal within 5 to 6 days.

The malignant form has a similar severe prodromal period, followed by the development of confluent, flat, non-pustular skin lesions. In survivors, the epidermis frequently peels.

Variola minor

Variola minor causes similar but much less severe symptoms, with a less extensive rash.

The mortality rate is < 1%.

Smallpox Diagnosis

PCR (Polymerase Chain Reaction)

Electron microscopy

Unless laboratory exposure is reported or an outbreak (bioterrorism) is suspected, only patients who meet the clinical definition of smallpox should be tested for possible false-positive results. An algorithm for assessing the risk of smallpox in patients with fever and rash is available on the CDC website ( CDC Algorithm Poster for Evaluation of Suspected Smallpox ).

The diagnosis of smallpox is confirmed by documenting the presence of smallpox DNA by Polymerase Chain Reaction (PCR) in samples from vesicles or pustules. Or the presence of the virus can be identified by electron microscopy or viral culture of the material scraped from skin lesions and subsequently confirmed by PCR (Polymerase Chain Reaction). Any suspected case of smallpox must be immediately reported to the public health authorities or the Centers for Disease Control and Prevention (CDC) at 770-488-7100. ASL of reference.) These agencies, therefore, work to carry out the analyzes in a laboratory with a high level of safety (level 4 biosecurity).

Point-of-care (bedside) antigen detection tests are under development.

Smallpox Treatment

Supportive therapy

Isolation

Possibly tecovirimat, consider cidofovir or brincidofovir (CMX001)

Treatment of smallpox is usually supportive, with antibiotics for any bacterial superinfections. However, the antiviral drug tecovirimat was approved by the US Food and Drug Administration (FDA) in 2018 based on experimental studies and is the first drug to be licensed for the treatment of smallpox ( 1 ). Although its efficacy against smallpox in humans is unknown, tecorvirimat is likely the drug of choice for the treatment attempt and is available from the US Department of Health and Human Services National Strategic Reserve. Cidofovir and investigational drug brincidofovir (CMX001) can be considered ( 2 ).

Isolation of individuals with smallpox is essential. In limited outbreaks, patients can be isolated in the hospital using airborne transmission precautions in an airborne infection isolation room. In mass outbreaks, home isolation may be necessary. The contacts must be placed under surveillance, usually by measuring their body temperature daily; if they develop a temperature > 38 ° C or other signs of illness, they should be isolated in their home.

Smallpox prevention

Smallpox vaccines licensed in the United States consist of replication-competent live vaccine virus (ACAM2000) and JYNNEOS, a modified live attenuated (replication-limited) vaccinia-virus Ankara (MVA) vaccine ( 1). Vaccinia is related to smallpox and provides cross-immunity. 

The ACAM2000 vaccine is administered with a bifurcated needle dipped in the reconstituted vaccine. The needle is driven rapidly 15 times into an area approximately 5 mm in diameter with enough force to produce a slight dripping of blood. The vaccination site is covered with a bandage to prevent the vaccine virus from spreading to other areas of the body or to close contacts. Fever, malaise, and myalgia are common the week following vaccination. 

The effectiveness of vaccination is indicated by the development of a pustule around the 7th day. Revaccination can only produce a papule surrounded by erythema, of maximum intensity between the 3rd and 7th day. Individuals who do not exhibit these signs of efficacy should receive a

JYNNEOS is administered as 2 subcutaneous injections 4 weeks apart. It is licensed by the Food and Drug Administration (FDA) for people aged 18 and over and may have a particular role in vaccinating people for whom ACAM2000 may be contraindicated, such as those with immunocompromised states or atopic dermatitis.

Another experimental live vaccine, the Aventis Pasteur Smallpox Vaccine (APSV), is also available at the Strategic National Stockpile in an emergency.

After a single vaccination, the immune response begins to weaken after 5 years and is probably negligible after 20 years. In individuals successfully revaccinated one or more times, some residual immunity may persist for ≥ 30 years.

Until an outbreak in the population occurs, pre-exposure vaccination remains recommended only for those at high risk of exposure to the virus Live vaccine virus complications

Risk factors for complications include extensive skin manifestations (particularly eczema), immunosuppressive disease or therapy, eye inflammation, and pregnancy. Widespread vaccination is not recommended due to the related risks.

Serious complications occur in approximately 1 in 10 000 patients after primary vaccination and include

Post-vaccine encephalitis

Progressive vaccinia

Eczema vaccinico

Generalized vaccinia

Myocarditis and/or pericarditis

Keratinitis vaccine

Non-infectious skin rashes

Post-vaccination encephalitis occurs in approximately 1 in every 300,000 primary vaccination recipients, typically 8-15 days after inoculation.

Progressive vaccinia (vaccinia necrosum ) results in persistent vaccinia (vesicular) lesions, which spread to adjacent skin and later to other skin areas, bones, and viscera. Progressive vaccinia can occur after primary vaccination or after revaccination, but occurs almost exclusively in patients with an underlying defect in cell-mediated immunity; sometimes it is fatal.

Vaccine eczema occurs with skin lesions localized to areas of active eczema or even in remission.

Generalized vaccinia is due to hematogenous dissemination of the vaccinia virus and causes vaccine lesions in multiple parts of the body; it is usually benign.

Vaccine keratitis is a rare complication that occurs when the vaccine virus is inadvertently inoculated into the eye.

Some serious vaccination complications are treated with vaccine immunoglobulins; One case of vaccine eczema apparently successfully treated with vaccine immunoglobulins, cidofovir, and tecovirimat has been reported. In the past, high-risk patients receiving post-exposure vaccination were simultaneously given vaccine immunoglobulins in an attempt to prevent complications. The effectiveness of this procedure is unknown and is not recommended by the CDC. In the United States, vaccine immunoglobulins are only available from the CDC.

Post-exposure prophylaxis

Post-exposure vaccination with a replication-competent vaccine can significantly prevent or limit disease severity and is indicated in family members and in people in close contact with smallpox patients. Early administration is most effective, but some benefits can be seen for up to 7 days after exposure.

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Diagnosis of Alzheimer's Disease

 

Diagnosis of Alzheimer's

The diagnosis of Alzheimer's disease is based on several investigations, as there is still no specific test for detecting the disease.

 

To diagnose Alzheimer's disease, the skills of various specialists are essential, including the psychiatrist, the neurologist, and the geriatrician; furthermore, the testimonies of the relatives of the patient are important, as they compensate for the patient's difficulties in exhibiting the symptoms and ailments that concern him.

 

The diagnosis of Alzheimer's also includes an approach by exclusion: it is the so-called differential diagnosis, which involves examinations and tests aimed at ruling out the possibility that the present manifestations are due to other pathologies with similar symptoms.

 

It should be noted that some scientific literature sites are keen to clarify, about the Alzheimer's topic, that only the post-mortem autopsy examination on the brain of the presumed patient and the detection of amyloid plaques and tau protein clusters confirm the presence of the pathology.

Tests to Diagnosis Alzheimer's Disease

Generally, the diagnosis of Alzheimer's is based on information from:

 

Anamnesis;

Physical examination;

Neurological examination;

Cognitive and neuropsychological test;

Laboratory tests ;

Brain imaging tests.

Anamnesis

Also known as clinical history, anamnesis is the acquisition, from the direct voice of the patient and/or his family, of all the information useful to explain certain symptomatology.

 

The medical history typically includes questions regarding the patient's general health, habits, lifestyle, drug therapies followed, any past pathologies, the medical history of his family, etc.

 

In the diagnosis of Alzheimer's, the anamnesis is important because it allows us to understand if the present symptomatology is attributable to the dementia in question.

 

Physical examination for Alzheimer's Disease

 

Physical examination (or physical examination ) consists of a medical assessment of the patient's general health.

 

It provides for diagnostic maneuvers that are used by the doctor to ascertain the presence or absence of signs indicative of some pathological condition.

 

Physical examination is a necessary step in the diagnosis of any disease, including Alzheimer's disease, although in itself it is not sufficient to draw firm conclusions.

 

Neurological examination for Alzheimer's Disease

 

The neurological exam evaluates tendon reflexes, motor skills (eg balance, coordination, etc.), and sensory functions.

 

In the diagnosis of Alzheimer's, the neurological examination can be considered as a more specific physical examination, which serves to deepen the information relating to the patient's state of health.

Cognitive and Neuropsychological Test

The cognitive and neuropsychological examination tests the patient on various fronts and skills, such as:

 

Memory;

Caution;

Problem-solving skills ;

Language and communication skills;

Reasoning and calculation skills;

Behavioral and psychiatric function.

The cognitive and neuropsychological examination can provide very useful diagnostic information, sometimes decisive for the confirmation of the pathology; however, it is good to specify the importance of performing it always taking into account some aspects of the patient, such as the level of education and general physical health (hearing level, sight capacity, etc.), which could distort the outcome of the assessment (a low level of education could be mistaken for a memory problem or impaired calculation ability).

 

The cognitive test is used for diagnostic purposes and to evaluate the progression and severity of Alzheimer's.

 

Alzheimer's Diagnosis: the Mini-Mental Test

A cognitive test particularly suitable for diagnosing Alzheimer's is the Mini-Mental Test, also known as the Mini-Mental State Examination or Folstein Test.

The Mini-Mental Test is a questionnaire consisting of 30 questions, which allow you to analyze the skills of calculation, memory, reasoning, language, attention, etc. of the person.

 

The Mini-Mental State Examination is useful in diagnosing all dementias, not just Alzheimer's disease.

 

Laboratory exams of Alzheimer's Disease

The diagnostician wants to analyze a series of parameters through specific laboratory tests, blood but not limited to, whose alteration is typically associated with symptoms that can resemble those of Alzheimer's disease.

 

Laboratory tests, therefore, are used in a differential diagnosis perspective: they exclude pathologies and conditions characterized by manifestations superimposed on Alzheimer's and could be mistaken for the latter.

 

Laboratory tests useful for the diagnosis of Alzheimer's include:

 

Blood sugar ;

Blood measurement of vitamin B12 ;

Urinalysis ;

Toxicological test (allows you to understand whether or not the symptoms are attributable to the intake of some drug or other toxic substance);

Blood measurement of thyroid hormones.

Diagnostic Imaging: CT and MRI of the Brain

Brain CT and MRI of the brain provide detailed, three-dimensional images of the brain organ.

 

Like laboratory tests, CT and magnetic resonance imaging are used for a differential diagnosis: they are no specific tests for Alzheimer's, but they can identify brain pathologies, such as strokes, tumors, vascular anomalies, etc., which produce symptoms similar to aforementioned dementia.

 

Therefore, the diagnostic imaging based on CT and magnetic resonance includes procedures useful for the exclusion of pathologies characterized by manifestations similar to Alzheimer's.

 

PET (Positron Emission Tomography) in Alzheimer's Diagnosis

Some variants of PET (positron emission tomography) allow the identification of amyloid plaques, neurofibrillary tangles of tau protein, and other signs of brain degeneration typical of Alzheimer's. However, it should be noted that these procedures are used in the field of research and clinical study of the disease, and not in the normal diagnosis.

 

Differential diagnosis

Diseases and Conditions that Cause Alzheimer's-like Symptoms

As part of the detection of Alzheimer's disease, the differential diagnosis aims mainly to exclude:

 

Stroke;

Parkinson's disease ;

Sleep disturbances ;

Adverse effects of drugs or toxic substances;

Cognitive decline related to old age ;

Dementias are other than Alzheimer's (e.g. vascular dementia, Lewy body dementia, etc.).

Early diagnosis
Importance of Early Diagnosis in Alzheimer's

An early diagnosis of Alzheimer's allows you to implement all the appropriate therapies in the early stages of the disease.

 

Although Alzheimer's disease is a progressive neurodegenerative disease, its early symptomatic treatment helps to maintain cognitive functions longer, somewhat slowing the course of the disease.

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Alzheimer's disease

 

Alzheimer's disease definition

Alzheimer's disease is the most common form of dementia.

Typical of old age, this condition is a neurodegenerative syndrome, which involves a gradual and irreversible loss of cognitive functions.

The most characteristic symptoms of Alzheimer's consist of memory deficits, language problems, personality changes, lack of initiative, confusion, disorientation, and loss of reasoning and judgment.

Experts believe that genetic and environmental factors, plus a certain style and sometimes familiarity with the disease, contribute to causing Alzheimer's disease.

The evidence is clear on the pathophysiology of this form of dementia: the patient's brain undergoes a process of atrophy and at an extra- and intracellular level it accumulates protein aggregates, which seem to affect the survival and function of neurons.

The diagnosis of Alzheimer's disease is complex; In fact, numerous investigations are needed, including physical examination, anamnesis, neurological examination, cognitive and neuropsychological tests, laboratory tests of various kinds, and imaging diagnostics ( brain CT and magnetic resonance imaging of the brain).

Currently, Alzheimer's is not curable. However, patients can count on various symptomatic treatments, which can alleviate the symptoms and slow down the inexorable cognitive deterioration typical of the disease.

Alzheimer's disease: what is it?

Alzheimer's disease is a neurodegenerative disease that involves a gradual and irreversible loss of cognitive functions.

Also known as Alzheimer's disease or simply Alzheimer's, Alzheimer's disease is a form of dementia that usually occurs in old age, but can also affect young individuals between the ages of 30 and 60 ( early-onset Alzheimer's or juvenile Alzheimer's ).

Without going into too much detail, Alzheimer's is known to cause memory deficits, language problems, personality changes, lack of initiative, confusion, disorientation, loss of reasoning and judgment, etc.

Alzheimer's disease compromises the patient's life expectancy: complications of the disease in its most advanced stages can be fatal.

 

Alzheimer's: why is it called that?

Alzheimer's disease owes its name to the German neuropathologist and psychiatrist Alois Alzheimer, who is credited with having first described the disease in 1906.

 

Alzheimer's observations were the result of studies conducted on an elderly woman, who died of a then-unknown mental illness, who had abnormal brain tissue.

 

Did you know that ...

Although Dr. Alzheimer's made his observations in 1906, Alzheimer's disease only became known by this name in 1910.

 

Epidemiology

How common is Alzheimer's disease?

In 2020, the World Health Organization (WHO) reported that there were approximately 50 million people with dementia worldwide.

Now, taking into account that Alzheimer's disease accounts for 60-70% of all forms of dementia, this disease, in the year reported above, had between 30 and 35 million patients.

 

As a result of the lengthening of the average life span of the human being, experts believe that the number of people with Alzheimer's and, more generally, those with dementia is destined to increase progressively.

This forecast is also confirmed in past data: in 2010, there were 36 million people with dementia in the world, therefore 14 million fewer than in 2020.

 

Alzheimer's disease and the number of new cases per year

Also according to what is reported by the WHO, every year, in the world, there are 6 to 7 million new cases of Alzheimer's (10 million new cases of dementia in total).

 

Alzheimer's disease and age

Alzheimer's disease is a typical disease of old age: most patients are over 65 years old.

 

It should be noted that from the age of 65 the risk of Alzheimer's progressively increases, confirming that aging plays a pivotal role in the onset of the disease.

 

As anticipated, there is also a form of juvenile Alzheimer's (early-onset Alzheimer's); uncommon, this condition affects people between the ages of 30 and 60 and constitutes 5-10% of all Alzheimer's cases.

 

Alzheimer's disease and life expectancy

Alzheimer's disease shortens the life expectancy of the people who suffer from it.

Statistics suggest that, generally, from the time of diagnosis, the disease takes between 3 and 10 years to cause death (a longer life expectancy is typical of "younger" patients).

Causes

Alzheimer's Disease: What Are the Causes?

The precise causes of Alzheimer's are still unclear; undoubtedly, the complexity of the human brain makes it difficult to study and understand.

 

At the moment, experts believe that a combination of various factors, including genetics, environmental factors, familiarity, and lifestyle, are at the root of the disease.

 

Based on the research conducted to date, this set of factors would seem capable of altering the patrimony of some brain proteins, to the point of having toxic effects on the brain itself.

 

Alzheimer's disease: pathogenesis

On magnetic resonance and PET investigations, and post-mortem examination, the brain of an Alzheimer's patient shows various abnormalities.

 

From the macroscopic point of view, a phenomenon of cerebral atrophy is evident; this means that there has been a reduction in brain tissue, following cell necrosis or a shrinking of nerve cells.

In this regard, it is particularly interesting to note that atrophy is particularly accentuated in the hippocampus and amygdala, the main brain areas involved in the ability to memorize.

 

From the microscopic point of view, however, the presence of protein aggregates is commonly found, both outside (extracellular) and inside (intracellular) of neurons.

Outside the neurons, the aggregates (or plaques ) of beta-amyloid peptide (or simply Aβ ) are reported, while inside the neurofibrillary clusters of hyperphosphorylated tau protein are characteristic.

 

The precise role of protein aggregates has not yet been fully clarified; however, they believe that beta-amyloid plaques and clusters of tau protein interfere with normal interneuronal (ie between neurons) nerve transmission and are capable of causing nerve cell death.

Early Onset Alzheimer's: the Causes

In early-onset Alzheimer's, genetic factors and family history appear to play a greater role than in the more common form of Alzheimer's.

 

Indeed, for some patients, the disease is the result of inherited genetic mutations.

 

According to some studies, 60% of people with juvenile Alzheimer's would have a positive family history of Alzheimer's disease, and 13% of these would result from an inherited genetic mutation.

 

This evidence, however, does not exclude the possibility that juvenile Alzheimer's can also arise in people without a particular familiarity with the disease.

 

Alzheimer's and Genetics: the genes involved in the disease

The research has identified some genes whose mutation is associated with Alzheimer's disease; among these genes, we note:

 

APOE-e4, located on chromosome 19 and involved in the formation of apolipoprotein E.

Alterations of APOE-e4 are common in people with the traditional form of Alzheimer's;

APP, located on chromosome 21 and coding for the amyloid precursor protein, PSEN1, located on chromosome 14 and coding for presenilin 1, and PSEN2, located on chromosome 1 and coding for presenilin 2.

Unlike the previous case, alterations of APP, PSEN1, and PSEN2 are commonly found in people with family-related juvenile Alzheimer's.

Risk factors

Alzheimer's: Who Is Most at Risk?

Research has shown that some specific factors increase the likelihood of getting Alzheimer's; among these risk conditions, the most significant are:

 

Advanced age. It is undoubtedly the most important contributing factor. Proof of this is the fact that most of the patients are over the age of 65.

The age of 65 is a very significant time limit for Alzheimer's: some interesting studies have shown that, after this age, the probability of developing the disease doubles every 5 years.

Aging involves changes in the structure of DNA and cells in general (including nerve cells); moreover, it weakens the natural cellular repair systems and promotes hypertension. All these significant changes appear to underlie the risk associated with old age.

Familiarity and genetic predisposition. This issue has already been discussed above.

It is a fact that the risk of developing Alzheimer's is higher for people with a first-degree relative (parent or sibling) who has the same disease.

The sex . Epidemiological studies have shown that women are more likely to develop Alzheimer's disease; from these same studies, however, it also emerged that sick women would live longer than sick men.

The risk associated with sex is probably justified by hormonal factors.

The lifestyle. Important research has shown that the same risk factors for heart disease are also associated with an increased likelihood of developing Alzheimer's.

Among these factors are above all: aforementioned hypertension, sedentary lifestyle, obesity, cigarette smoking, hypercholesterolemia, and type 2 diabetes.

Down syndrome. Carriers of Down syndrome are particularly prone to developing Alzheimer's. This trend seems to be linked to the presence of the third chromosome 21 and, consequently, to a third APP gene encoding the amyloid precursor protein (remember that APP gene mutations are associated with the onset of juvenile Alzheimer's).

Cognitive decline (or decline ) related to old age. This is a normal evolutionary process that the brain undergoes during aging.

Trauma to the head. Some studies suggest that a medical history of severe head trauma increases the risk of developing a form of dementia, which in many cases is Alzheimer's disease.

Symptoms and Complications of Alzheimer's disease

Alzheimer's disease is a condition characterized by the progressive death of brain nerve cells; this phenomenon implies that the resulting symptoms - which consist of neurological manifestations - are destined to undergo, over time, a gradual and inexorable worsening.

 

It is customary to divide the evolution of symptoms associated with Alzheimer's disease into three phases (or stages):

 Diagnosis of Alzheimer's disease

The early symptom stage (or early stage of Alzheimer's);

The phase of the intermediate symptoms (or the intermediate phase of Alzheimer's);

The stage of final symptoms (or late or late stage of Alzheimer's).

The early stage of Alzheimer's: the first symptoms

The early stage of Alzheimer's is the time of the disease when the first symptoms appear.

 

The onset manifestations of Alzheimer's typically consist of:

 

Small short-term memory problems ( anterograde amnesia )

Apraxia, i.e. inability to perform common actions such as whistling;

Sporadic personality changes

Occasional lack of judgment

Repeat the same question several times;

Slight  difficulties in the language (principle of aphasia ), the calculation (principle of acalculia), reasoning, and understanding of new concepts;

Tendency to passivity and lack of initiative,

The patient forgets recent events or conversations in which he participated; loses items; does not remember the names of places and things (anomia); struggles to recognize objects and things that were previously known ( agnosia ); begins to lose the faculties of writing and reading.

 

Intermediate Stage of Alzheimer's: Intermediate Symptoms

The intermediate stage of Alzheimer's is characterized by a worsening of the initial symptoms, in particular, short-term memory problems and language and calculation difficulties; moreover, it leads to the appearance of new ailments.

 

New manifestations of this second stage of the disease include:

 

Obvious loss of part of the cognitive abilities, from reasoning and learning to judgment skills;

Long-term memory problems

Emotional instability, mood swings, depression, anxiety, and/or agitation;

Obsessive, repetitive, and/or impulsive behaviors;

Episodes of delirium and paranoid behavior (without any reason, the patient is suspicious of the people around him, to the point of sometimes proving to be aggressive);

Space-time confusion (or disorientation), with the patient struggling to realize where he is, to say with certainty the day of the week, etc;

Difficulty in quantifying distances approximately;

Auditory hallucinations;

Disturbed sleep.

At this stage of Alzheimer's, it is very common for the patient to begin to need the support of other people to help him in daily life; for example, they may need support in washing, dressing, or using the bathroom.

 

Final Phase of Alzheimer's: The Final Symptoms

The final stage of Alzheimer's is the moment of the disease in which the now complete symptomatological picture worsens further and becomes incompatible with a normal life.

 

Cognitive abilities are now completely compromised: this is demonstrated by the degree of extreme severity reached by memory deficits and language difficulties.

Episodes of delirium and paranoia are increasingly common, as are mood swings.

In addition, new issues appear, including:

 

Difficulty swallowing

Loss of control of bowel and bladder function ( incontinence )

Loss of motor control, with the patient walking and moving less and less;

Weight Loss.

At this stage of the disease, the person with Alzheimer's becomes completely unable to take care of himself, therefore he needs someone daily to help him eat, wash, move, etc.

 

Alzheimer's Disease: Complications

The severe impairment of memory and language skills induced by advanced Alzheimer's means that the patient is unable to:

 

Communicate any pain ;

Communicating the symptoms of another disease presumably caused by old age;

Independently follow a therapeutic plan;

Communicate the side effects produced by a drug taken to control some disease.

All these problems complicate the possibility of early diagnosis and treatment of other pathologies, sometimes even very serious ones, which could arise especially considering the advanced age of the patient.

 

Furthermore, with the onset of swallowing, walking, incontinence, and intestinal control problems, the patient tends to develop:

 

Inhaled pneumonia and bronchopneumonia, and other respiratory tract infections. Due to the difficulty in swallowing, they have important repercussions on the patient's state of health.

Malnutrition and/or dehydration. These are also due to swallowing difficulties.

Constipation or diarrhea. They depend on the loss of control of intestinal functions.

Fractures and bedsores. They are due to walking problems.

Alzheimer's disease: when do you die?

Alzheimer's leads to death when it reaches its most advanced stage, therefore when it has seriously compromised the cognitive faculties and more.

 

The main cause of death is respiratory complications induced by inhalation pneumonia and bronchopneumonia that the patient tends to develop as a result of swallowing problems.

 

As stated in an earlier passage of the article, Alzheimer's disease takes 3 to 10 years to reach its final stage and causes the individual to die.

Being mostly elderly, many times people with Alzheimer's suffer from other typical pathologies of aging, such as hypertension, heart disease, etc.

Consequently, it happens quite frequently that the Alzheimer's patient dies earlier from a complication of the aforementioned conditions than from the more advanced form of dementia.

Senile Dementia: When to Worry?

For the elderly individual, manifesting some too many amnesias, experiencing unusual calculation difficulties and having language problems, and understanding new concepts must represent an alarm bell, such as to lead to consulting a doctor (to understand it deals with early Alzheimer's or another condition) and to ask for support from family members.

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Syphilis in male

 

Syphilis || Symptoms, Prevention, and Cure

Syphilis (or lue) is a disease caused by a bacterium ( Treponema pallidum ), which causes a chronic progressive infection with potential permanent damage to all organs.

Syphilis in Man

Man contracts this pathology mainly through sexual intercourse not protected by condoms, both genital and oral, with a previously infected person.

The onset of the first symptoms of syphilis in males occurs three to four weeks after infection, with the development of ulcersor rounded wounds at the injection site of the pathogen (i.e. in areas that have come into contact with the infected areas of the other person). Such lesions are typically associated with swelling of the regional lymph nodes.

Often, primary syphilitic lesions are localized in the genital area, in particular at the level of the penis, the foreskin (the portion of skin that covers the glans penis ), or the anus and, if left untreated, tend to evolve towards the secondary stage of the disease.

Secondary syphilis occurs approximately six weeks after the primary lesion (called syphiloma ) disappears with a macular rash on the limbs and trunk, sometimes accompanied by fever, joint pain, fatigue, and hair loss.

In the latent period, the man does not show any symptoms, but he can still transmit the disease. If healing does not occur, syphilis can evolve into the third stage (tertiary syphilis), which can occur even after thirty years from the first infection.

The diagnosis of syphilis in humans is based on clinical and anamnestic data, on the microscopic identification of T. pallidum, and the results of serological investigations. Treatment involves antibiotic therapy, while prevention must be implemented by practicing safe and protected sex to reduce the risk of infection.

Note. Syphilis is one of the most important sexually transmitted diseases. The infection can affect both sexes, but men are more frequently affected by the problem.

Causes and risk factors of Syphilis

Syphilis is caused by Treponema pallidum, a spirochete (a spiral-shaped bacterium) that can spread easily in the body.

This infectious agent can penetrate through intact mucous membranes (genital, rectal, and oropharyngeal) or damaged skin, so it can be easily transmitted through oral contact and unprotected vaginal and anal sexual intercourse.

Without adequate treatment, syphilis evolves within weeks or months: this microorganism migrates through the skin capillaries, then spreads to the lymph nodes, where it multiplies until it reaches levels sufficient to cause clinical disease. Typically, syphilis incubation times extend from 2 to 12 weeks.

In people with the disease, Treponema Pallidum is found in all body fluids, such as semen and vaginal secretions. In addition, the bacterium is found in skin, genital and mucosal lesions, including that of the mouth, which occur in the course of syphilis.

Without a timely diagnosis and therapy, progressive evolution of the disease is possible, which can induce serious permanent damage to multiple organs and systems, such as the skin, heart, brain, and skeleton.

Infection

How can humans get syphilis?

A man usually contracts the disease through unprotected sexual intercourse, both genital (vaginal or anal), and oral with a person suffering from syphilis.

Other possible modes of transmission are petting (ie simple contact between genitals) without protection and the exchange of contaminated sexual tools (eg sex toys).

However, the infection can also be contracted non-sexually, through direct contact with wounds or ulcers of the skin and mucous membranes, which form in the areas where the disease mainly occurs (genital, anus, mouth, throat, or skin surface damaged). In some cases, some of these manifestations are painless or go unnoticed, so the man may not be aware that he is suffering from syphilis, thus risking infecting his partner.

Occasionally, the disease can be transmitted through blood transfusions (now a very rare mode of contagion).

In the case of the congenital form, it is also possible to pass the bacterium transplacental from the infected mother to the child (maternal-fetal transmission).

Syphilis does not confer immunity against subsequent reinfections; this means that the patient recovered from the disease can contract the infection over and over again in the course of life.

Symptoms of Syphilis

The natural course of untreated syphilis follows four developmental stages:

Primary syphilis;

Secondary syphilis;

Latent syphilis;

Tertiary syphilis.

In any case, the disease is complex and, if not properly treated, can lead to various complications, such as heart disease and neurological disorders, up to death.

Primary syphilis in humans

The initial stage of infection occurs approximately 3-4 weeks after contagion, with the appearance of a localized, rosacea, circular and sharp-margin papular lesion ( syphiloma ) at the injection site of Treponema pallidum.

In men, the most frequent localization of syphiloma is the scrotal skin, the balance-preputial sulcus, the outlet of the urethra on the penis and the region around the anus; less often, this lesion can occur on the skin of the hands or inside the oral cavity, then on the lips, gums, pharynx or tongue. Syphiloma does not generally cause pain but is typically associated with an increase in the volume of the regional lymph nodes, which are not, however, painful on palpation.

Within a short time, the surface of the syphiloma tends to ulcerate, exposing a bright red background, from which a serous exudate, containing the treponemes, comes out.

Symptoms of the first stage of syphilis in humans generally persist for between 2 and 6 weeks. Without treatment, syphilis progresses to the secondary stage.

Secondary syphilis in humans

Secondary syphilis begins 3-6 weeks after the onset of syphiloma. This phase is characterized by a diffuse macular rash in one or more areas of the body surface, associated with the swelling of the lymph glands. This manifestation is transient or recurrent and can have a very variable appearance: for example, roundish cracks may appear on the palms of the hands and the soles of the feet or groups of pink spots spread on the trunk and limbs, reminiscent of the measles rash. 

Furthermore, in this stage, the man with syphilis manifests flu-like systemic disorders, due to the proliferation and diffusion of Treponema pallidum through the blood and lymphatics. In particular, the following may appear fever, asthenia, headache, muscle aches, and general malaise. Syphilis in humans can also lead to sore throat, lack of appetite, weight loss, visual disturbances, hearing, and balance changes, bone pain, hair loss

in clumps and the appearance of thickened, gray, or pink skin rashes ( warts ).

In humans, a rarer form of syphilitic manifestation is intense balanoposthitis (inflammation of the glans penis and foreskin), apparently caused by other infectious agents.

Latency period

At the end of the secondary stage, a long latency period begins, which can last for months or even years. This phase is due to the immune control of the disease: the man with syphilis does not present any symptoms, however, the infection persists.  

Tertiary syphilis in humans

After many years (usually after about 10-25 years from the moment of infection), syphilis progresses to the tertiary phase.

At this stage, the disease is characterized by the formation of painless lumps ( gums ) in the skin or brain, bones, and joints, and by severe impairment of the body's internal organs (including the liver, kidneys, lungs, and heart).

Once syphilis enters the third stage, the individual may present with personality changes, gradual blindness, dementia, inability to control muscle movements, and progressive paralysis. In severe cases, syphilis leads to the patient's death.

The evolution of syphilis can be accelerated by one coexisting HIV infection; in these cases, ocular involvement, meningitis, and other nerve complications are more frequent and severe.

Diagnosis of Syphilis

The diagnosis of syphilis in humans can be formulated with the evaluation of the signs and the set of symptoms reported by the patient during a careful medical examination, and through the observation under the microscope of the material taken from the lesions (which allows recognizing the treponemes ).

In support of these investigations, the execution of blood tests is also indicated to detect the possible presence of antibodies against the bacterium already in the early stages of the infection, taking into account that these appear in a period ranging from 2 to 5 weeks.

These analyzes are essentially divided into:

Non-specific tests for Treponema - including the Venereal Disease Research Laboratory ( VDRL ) - aimed at identifying a lipoid antigen deriving from the bacterium or its interaction with the host; these investigations can offer an advantage in disease control.

Treponemal tests, such as the passive agglutination test of treponemal particles (TP-PA) or fluorescence for the search for the absorption of anti-treponemal antibodies (FTA-ABS); these tests make it possible to establish the degree of activity of the infection, then define the most appropriate therapeutic protocol for the case.

If the man is infected, all sexual partners of the previous 3 months (in case of confirmed primary syphilis) or of the previous year (in case of confirmed secondary syphilis) will be evaluated and treated.

Treatment of Syphilis in Humans

Treatment of syphilis in humans involves the parenteral administration of penicillin.

In patients allergic to this active ingredient, other drugs such as doxycycline and tetracycline can be used.

To determine the correct dosage and duration of antibiotic therapy, the doctor will rely on the stage of the disease defined during the diagnostic process. Prompt treatment allows for regression of lesions and prevention of secondary or tertiary syphilis, but any permanent organ damage tends to persist.

During drug treatment, to avoid infecting one's partner, abstinence from any type of sexual intercourse is mandatory, until the lesions caused by syphilis are completely healed. It should always be remembered that wounds and skin ulcers can transmit the infection even during oral sex or any other skin contact with infected areas.

Prevention of Syphilis

Regarding the prevention of syphilis, a good measure is the correct use of condoms, which must be used from the beginning to the end of sexual intercourse (whether vaginal, anal, or oral) and to also protect any objects used. during intimate contact. 

Furthermore, it is possible to avoid exposing oneself to the risk of contagion by refraining from sexual practices with potentially infected people, and by reducing the number of partners.

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