To this day, all new influenza epidemics are usually compared with the Spanish flu pandemic, which began in 1918. It was probably the deadliest pandemic in human history: the Spanish Flu claimed more lives than the deadliest military conflict at that time - First World War and every pandemic known to mankind.

It is now believed that from 20 to 100 million people around the world died from the Spanish flu. For comparison, the First World War claimed the lives of approximately 15 million people, the AIDS epidemic - about 14 million. In one year, the "Spanish flu" killed more people than the plague ("Black Death") killed in a century in Medieval Europe.

The epidemic destroyed 17 million Indians (5% of the country's population), 550 thousand Americans, 400 thousand French, 260 thousand Japanese, 200 thousand British. However, there are historians of epidemics who also name large numbers, including 100 million. Pete Davies, author of the book “The Devil's Flu: The World's Deadliest Influenza Epidemic and the Scientific Hunt for the Virus” That Caused, believes that population censuses were rare in the early 20th century, and many regions of the planet affected by influenza were not surveyed. It is known, for example, that the flu destroyed 60% of the Eskimos of North America. As a result of this epidemic, some tribes in Africa completely disappeared, the population of some cities decreased by 90%. The population of the Fiji archipelago decreased by 14%, Western Samoa - by 22%. Probably the only large settlement where not a single person fell ill with the flu was the city of Belem, located on an island in the Amazon delta. In any case, every fifth person suffered from the flu; the pandemic destroyed from 2.5% to 5% of the world's population. The flu seriously hit the armies of the warring states: for example, in the United States, 40% of sailors and 35% of soldiers were ill.

It is now believed that the first outbreak of the "Spanish flu" arose in the United States - it was there that, most likely, a mutation of the virus occurred, which previously only affected waterfowl (this version is particularly advocated by John Barry, author of the book "The Great Influenza" ). However, no one still knows exactly why the influenza virus became so deadly (in the 1950s, attempts to detect the Spanish flu virus began, and in 2005, were successfully completed - for this purpose, victims of this epidemic were exhumed, buried in permafrost conditions) .

The pandemic began first in a small town in the Midwest, and from there, apparently, was transferred to a military camp located near the city of Kansas City. The cook was the first to fall ill (in the morning), and in the evening more than a hundred soldiers and officers were sick. A week later, Spanish flu patients appeared in absolutely all US states. A little later, foci of infection were discovered in Spain, France and Italy. The pandemic spread in three waves: March–July 1918 (relatively few deaths), September–December 1918 (the deadliest wave), and February–April 1919 (deaths declined slightly).

The influenza epidemics known at that time claimed the lives of approximately 0.1% of those sick; the Spanish flu was 25 times more deadly. The flu knew no racial, national or class differences - its victims were representatives of all nations, rich and poor alike. It is striking that the victims of influenza were primarily young and healthy people, while children and old people, usually included in the “risk group,” got sick much less frequently and more easily (primarily children under the age of 5, people aged 20- 40 years old, and old people in the age group of 70-74 years). It is not yet possible to explain this phenomenon. One theory is that older people were somehow able to “accumulate” immunity by surviving previous epidemics, while children and teenagers were more likely to healthy image lives than the adults who suffered most seriously from the stress caused by the World War.

The war and its attendant factors - poor nutrition and hygiene, overcrowding, etc. - contributed to the spread of the disease. In principle, wars and epidemics have always gone hand in hand. Traditionally, more troops died from disease than from enemy bullets and shells. For example, during the Boer War of 1899-1902, the British Army lost 10 soldiers to disease for every soldier killed by the Boers. Fighting the partisans, the British drove a quarter of the civilian population into concentration camps, where diseases also began to rage, killing every eighth.

The flu received the name "Spanish flu" thanks to military censorship, which prohibited newspapers from publishing information about epidemics. In a similar way the authorities sought, firstly, not to give trump cards to military opponents, and, secondly, to prevent panic. Spain did not participate in the war, so the Spanish newspapers were the first to report the disaster. It is significant that in newspapers in the USA, Canada, Great Britain and other English-speaking countries, the “Spanish flu” was not even called by its “official” name - influenza. They preferred to use the word "flu", which can be translated as "illness". Influenza patients choked and coughed up blood (which is why the “Spanish flu” was sometimes called the “purple death”) and experienced serious suffering, which did not fit well with the meaning of the word “illness.”

The outbreaks of influenza followed the maps of communications - they arose along railways, in ports, etc. In the United States, there were situations where the flu did not reach remote villages and farms for a long time. However, as soon as a postman or policeman appeared in the “bear corner”, the epidemic broke out there too. There are many known cases when the “Spanish flu” primarily destroyed local doctors, who, on duty, were the first to contact the sick. As a result, entire cities found themselves without medical care. It was difficult to bury the dead - mass graves appeared, the corpses of the dead lay in houses and on the streets for days and even weeks, which made the emergence of other deadly infections possible. On some islands of the Pacific Ocean, the main cause of death was not influenza and its complications, as such, but hunger: the sick and those recovering were so weak that they were unable to take care of themselves and their neighbors. Due to the death of adults, many young children were left orphans and providing them with a means of subsistence during the epidemic has become another serious problem. In many countries around the world, railway traffic was almost completely paralyzed (situations were described when trains simply stopped in an open field because the driver fell ill). Serious problems tested postal services.

The fight against influenza was carried out by both states and individual cities and villages. The generally accepted means of protection against the Spanish flu was the introduction of quarantines. Alfred W. Crosby, author of America's Forgotten Pandemic: The Influenza of 1918, describes a grim picture: individual communities created armed patrols that ordered all outside travelers who wanted to enter the forbidden territory to return back - at gunpoint. In many places, theaters, dance halls and other public buildings, sometimes even churches, were closed, and in some cases they remained closed for an entire year. In one American town, local legislators sought to slow down spread of epidemic, passed a law prohibiting handshakes (curiously, they forgot to repeal this law, and it is still in effect to this day, having passed into the category of absurd legislative acts). Even in cities where there were relatively few patients, new hostel rules were introduced. For example, stores traded in a new way: the buyer remained on the street - he slipped money and a list of goods he needed into the mailbox or window, the seller put out packages with the order through the door, without coming into direct contact with the buyer.

Lynette Lezzoni, author of Influenza 1918, has compiled an extensive collection of methods that doctors tried to combat the epidemic. As a main precaution, people were asked to gargle with sea water and wear a gauze bandage covering their mouth and nose. Patients were ordered to be kept warm. Warm compresses on the chest, as well as onions, garlic, turnips, spinach, asparagus and even kerosene were offered as treatments. However, medicines that could seriously help those who were ill simply did not exist at that moment, despite the fact that pharmacists had by that time created medicines and vaccines that could fight diphtheria, anthrax, meningitis... In an effort to cope with the epidemic, doctors and pharmacists quickly developed dozens of flu vaccines - but none of them worked.

The “Spanish flu” proceeded according to a pattern atypical for influenza: unlike previous epidemics, in almost all patients the disease progressed to pneumonia. They did not yet know how to treat pneumonia, since antibiotics appeared in the arsenal of doctors only decades later. Doctors didn’t even know that large doses of vitamin C could help cope with the disease. There was aspirin, probably the only drug that somehow alleviated the suffering of patients. However, it was a rare and quite expensive medicine. In addition, aspirin was developed and produced only by the German company Bayer, which in the conditions of World War II made the supply of this drug to Germany’s enemy countries almost impossible. There was another problem - public opinion. Gina Kolata, author of the study “Flu: The Story of the Great Influenza Pandemic,” notes that since the causes of the epidemic were unknown, it became popular in American society that Bayer was adding pathogenic bacteria to tablets aspirin.

In general, the “Spanish flu” gave rise to many rumors. Newspapers wrote about German spies and warships that delivered ampoules of poison to the territories of other countries and poisoned wells. The Bolsheviks and anarchists were blamed for the spread of the epidemic. To avoid infection, it was recommended to wear diamond necklaces, since the causative agent of the disease cannot tolerate the presence of diamonds. Smoking was also considered a way to avoid the flu. More exotic methods of combating the epidemic were also proposed, for example, special voodoo rituals and dried chicken stomachs.

It is now believed that many of the viruses that caused major influenza epidemics in the 20th century are direct descendants of the Spanish flu virus. In 1976, a serviceman died in the United States - a virus was found in his blood that was extremely reminiscent of the Spanish flu pathogen. This case became the reason for the launch of large-scale programs to protect the population from influenza.

After the Spanish Flu, the world faced a number of serious influenza pandemics. In 1957-1958, the “Asian flu” raged. It first appeared in China in February, and six months later the epidemic spread throughout the world. The exact number of victims of the “Asian flu” is unknown; according to various estimates, 2-4 million people died as a result of the epidemic. The Asian flu virus mutated and caused the Hong Kong flu epidemic in 1968-1969. Its victims ranged from 750 thousand to 2 million people. In 2005, an epidemic of “bird flu” began, which, fortunately, was localized relatively quickly, and in 2009, the “swine” or “Mexican” flu began. The latest virus is also quite atypical: it is most dangerous for people under 50 years of age - usually the elderly and children are at risk.

History is being written in the 2003-2004 season

In the wake of postal biological terror, humanity began to forget about the flu. But this cannot be done, especially in the fall. The influenza virus, unlike the causative agent of anthrax, has already caused mass casualties of people amounting to tens of millions.

Americans are facing the worst flu epidemic in 30 years

The alarm comes as the medical world prepares for a flu season that some doctors expect will be the worst in decades. The virus struck hard early in Britain and America, hospitals said. When did SARS appear this year? SARS), scientists initially thought they were dealing with a new strain of influenza. SARS has been defined as a particularly aggressive form of the virus that is activated by the common cold. This year, 774 people have died from SARS.

According to statistics, about 20% of Americans get sick with the flu every year, and 114 thousand are hospitalized. In a study published in early 2003. V Journal of the American Medical Association an increase in influenza-related mortality was reported to 36 thousand. cases compared to 20 thousand. according to previous assessment. Most of those who died were aged 65 years or older (underscoring the need for improved prevention efforts among older people). And by the end of the year, specialists from the vaccine development center of the American clinic Mayo Clinic Vaccine Research Group It is predicted that twice as many US citizens will die from the flu this coming winter. The number of deaths will be 50–70 thousand. Human. The basis for such forecasts is the low immunity of Americans to the influenza virus. The reason for this is that the vaccine was compiled on the basis of virological data from the beginning of the year, but by now one of the pathogens has mutated. At the same time, you still shouldn’t refuse the vaccine - it reduces the chances of death by about half.

Researchers from the clinic St Jude Children's Research Hospital in Memphis published an article in the journal Science. The authors recommend increasing supplies of antiviral drugs and believe that governments should fund technology for making drugs using the so-called “reverse genetics” method.

Mednovosti.ru
Financial Times

Flu epidemic in France - hospitals overcrowded

A sharp and unexpected surge in the flu epidemic has occurred in recent days in France. According to medical authorities, in the central regions of the country in recent days there has been a significant increase in the number of cases of influenza, bronchitis and gastroenteritis. Hospitals in Paris and its suburbs are now overcrowded, people have to wait in queues for up to 7 hours waiting for a doctor.

The situation is further aggravated by the fact that mostly primary schoolchildren get sick. The authorities went on radio and television calling on the population to call an ambulance only in extreme cases and treat children at home. The epidemic is expected to peak in mid-December.

The French healthcare system has once again demonstrated that in moments of crisis it is not able to quickly and flexibly respond to the current epidemiological situation.

NewSru.com

Flu hits Spain and UK

The number of flu cases in Spain is already 20 times higher than the same period last year. Spanish doctors declare a flu epidemic when there are 100,000 people. There are more than 100 patients in the population. According to November data, per 100 thousand. Spaniards already account for 189 patients with influenza. Such a high incidence of influenza in Spain, according to the Minister of Health, has not been recorded in recent decades.

Meanwhile, an unprecedentedly early rise in the incidence of influenza is also observed in the UK. The World Health Organization has sent out a warning to countries that the flu epidemic may begin earlier than usual.

The epidemic that has struck Spain and the UK is caused by a variety of influenza A (H 3 N 2), but along with the well-known “Panama” strain, on the basis of which vaccines are made in recent years, a new “Fujian” strain is also circulating, which is particularly aggressive. Since Europe is just a stone's throw away from us, doctors advise getting vaccinated without delay.

IZV.info

In Russia, up to 3 million people will get the flu in winter

In Russia, this coming winter, according to doctors’ forecasts, up to 3 million people will get the flu. Human. This was announced by the chief sanitary doctor of Russia Gennady Onishchenko at a meeting of heads of the centers of the State Sanitary and Epidemiological Supervision of Siberia in Barnaul (Altai Territory). Another 20 million. people, according to the forecast, will suffer from acute respiratory infections in the winter, Onishchenko added. He also noted that new dangerous influenza viruses are expected to emerge this coming winter.

Eliminating the epidemic, according to preliminary data alone, will require about 50 billion. rubles Great hopes are placed on vaccinations. However, out of 10 million. Only a third of people subject to mandatory vaccination have been vaccinated to date. Also, there is still a high probability of a new wave of SARS. In addition, widespread diphtheria is predicted.

According to the chief epidemiologist of the Ministry of Health of the Russian Federation, deputy director of the Moscow Research Institute of Epidemiology and Microbiology, Evgenia Selkova, this year the influenza epidemic lasted in Russia for an average of 14 weeks from February to April. Overall, just over 2% of the population was ill. The flu was of moderate intensity. However, she noted, the economic damage from the epidemic amounted to 51 billion. rubles Just one case of influenza, including the provision of medicines and payment for sick leave, cost the state an average of 2,130 rubles, said the chief epidemiologist of the Ministry of Health.

Director of the Research Institute of Viral Drugs, academician Russian Academy Medical Sciences Vitaly Zverev noted that today there are no reliable drugs against influenza and vaccines are the most reliable means of protection against this disease. Moreover, Zverev noted, one should be vaccinated annually. Zverev recommended that those who were vaccinated last year should also do it this year.

The UNUSUALLY disastrous “Spanish” flu pandemic of 1918-1919 penetrated almost every corner of the globe. The uniqueness of the clinical picture of the disease, the presence of various complications, the appearance of cases of the disease with a picture of general severe intoxication and, finally, the high mortality rate among patients with pulmonary forms - all this made doctors think that they were not dealing with ordinary influenza, but with a completely new form of it. This point of view was held until the genome of the Spanish flu virus was deciphered at the end of the 20th century.

But the knowledge obtained with such difficulty baffled the researchers - it turned out that the killer of 22 million people did not have any serious differences from the less dangerous pandemic strains of the influenza virus known today in any gene.

A COMPLETELY HEALTHY VIRUS

When the staff of the US Army Institute of Pathology in Washington (Armed Forces Institute of Pathology, Washington) began these studies in the mid-1990s, they had at their disposal: 1) formaldehyde-fixed tissue sections of American military personnel who died during the 1918 pandemic; 2) the corpses of members of the so-called Teller mission, who tragically died almost entirely from the Spanish flu in November 1918 and were buried in the permafrost of Alaska. In addition, the researchers had modern methods at their disposal molecular diagnostics and the strong belief that characterization of the virus's genes can help explain the mechanisms by which new pandemic influenza viruses replicate in humans.

First of all, they genetically confirmed the retrospective serological data known since the late 1930s that the causative agent of the Spanish flu was an influenza virus of the H1N1 serotype. But the antigenic properties of the virus, while explaining much of its epidemic significance, provided little insight into the causes of the mass death of the world's population during the 1918 influenza pandemic.

A study of the genes of the Spanish influenza virus suggested the presence of a common ancestor - an avian virus, both for generations of the human H1N1 virus and for a similar virus in pigs. The 1918 strain has been proposed to be the ancestor of modern epidemic influenza viruses of swine and human origin. But the results of further research began to raise more questions than provide answers.

It turned out that the Spanish flu virus was not an "epidemic novelty" of 1918 - its "ancestral" variant "entered" the human population around 1900 and circulated in limited human populations for almost 18 years. Therefore, its hemagglutinin (HA), a cellular recognition receptor that ensures the fusion of the virion membrane with the cell membrane, came under “pressure” from the human immune system even before the virus caused the 1918-1921 pandemic. For example, the HA1 sequence of the Spanish flu virus differed from the closest “ancestral” avian virus by 26 amino acids, while the 1957 H2 and 1968 H3 differed by 16 and 10, respectively.

Moreover, analysis of HA genes showed that the Spanish flu virus entered the pig population in 1918 and circulated there, practically unchanged, for at least 12 more years, without leading to pandemic outbreaks of influenza. The “Spanish flu” viruses that circulated during the 1918-1919 pandemic among people in different areas of the United States practically did not differ from each other in the structure of the HA and NA genes.

Another mechanism by which the influenza virus evades the immune system is by acquiring regions that mask the regions of antigens recognized by antibodies (epitopes). However, the modern H1N1 virus has 5 such regions in addition to the 4 found in all avian viruses. The Spanish flu virus has only 4 conserved avian regions. That is, it could not “go unnoticed” by the normally functioning immune system of people and, thanks to this, multiply to such quantities that the fight against it became useless for the human body.

American researchers have attempted to detect two known mutations of the HA gene in the Spanish flu virus, which can expand the “damaging” ability of the virus to other tissues.

Theoretically, this approach to elucidating the reasons for the lethality of the Spanish flu viruses was completely justified. Certain strains of avian influenza virus subtypes H5 and H7 are highly pathogenic for some bird species, including domestic chickens. This mutation has not previously been described in mammalian influenza virus samples. To confirm the hypothesis that the 1918 strain had a similar mutation, special tests were developed, but no mutations were found in the Spanish flu virus.

Clinical and pathological findings of that time also do not give reason to believe that the virus had an increased tropism for other tissues outside the respiratory tract. That is, the virus that killed 22 million people did not have structures that would allow scientists to understand the mechanism of this mass murder, and perhaps, with their help, to obtain such a “killer” themselves, just in case, of course, for example, for study " reasons for the appearance of dangerous viruses among people,” etc.

Thus, the mass death of people took place in the absence of their killer. Instead, some helpless disabled man was found at the “crime scene”, but without an alibi.

Ultimately, the published results of American military researchers lead us to the conclusion that the causes of the “Spanish” flu phenomenon cannot be revealed by a frontal attack on the genome of the H1N1 serotype virus. An analysis of publications on the following pandemics shows the presence of clinical forms of influenza similar to the Spanish flu already in the era of antibiotics, that is, when doctors had powerful means of combating secondary pneumonia. Similar clinical forms of influenza periodically appear during the epidemic spread of other serotypes of the virus.

THE MYSTERY OF PATHOLOGY

The fact that pneumonia was not the main cause of death during the pandemic of 1918-1919, but only accompanied it, is evidenced by the discrepancy between the intravital clinical picture and the actual lesion, repeatedly noted by pathologists of that time. lung tissue dead people.

Typically, pandemic researchers pay little attention to another important Spanish flu syndrome: cardiovascular disease. Rapidly growing lesion of cardio-vascular system, a sharp drop in blood pressure, confusion, and hemorrhages developed in patients even earlier than complications from the lungs. Contemporaries of the pandemic attributed these symptoms to the action of toxins from an unknown bacterial pathogen. But today it has been established that the genome of the influenza virus does not contain toxin genes with a similar mechanism of action. The mechanism of its pathogenic action is more complex and mediated by the host organism.

The question arises: when did the phenomenon itself, called the “Spanish” flu in 1918, appear?

A retrospective analysis of influenza pandemics suggests that "malignant" epidemics with hemorrhagic and pulmonary symptoms swept through England and Italy during the 1729 pandemic. Then in England, in terms of mortality among the population, it was compared with the “Great Plague of London of 1665.” The influenza pandemic of 1836-1837 manifested itself in a similarly cruel manner and with the same symptoms in London and Paris. Similar influenza epidemics were observed among the “natives” in 1843 in northern Siberia by Professor Middendorf and Doctor Kashin in 1859 near Irkutsk.

New Yorkers during the Spanish flu pandemic

Of course, these observations are not enough to establish the periodicity of the appearance of the Spanish flu, but they still allow us to assume that for its resumption a change of several generations of people is necessary, and not a change in the serotype of the influenza virus. In addition, there is another pattern in the epidemiology of the Spanish flu. The disease appears only in certain populations of the population, sometimes even in large ones, but never becomes universal. During the 1918-1919 pandemic in Russia, the “Spanish” flu was less dangerous than in European capitals and in certain regions of the USA. (The epidemic killed 675 thousand Americans. The demographic blow was so severe that it led to a decrease in average life expectancy in the United States by more than 10 years.)

Another oddity of the “Spanish flu” - the young age of the people who died, cannot be explained by the presence of immunity in people of the older generation remaining after the pandemic of 1889-1892, since, according to serological archeology, it was caused by a virus of the H2N2 serotype. The victims of the Spanish flu pandemic were mainly people who did not survive the flu during that pandemic (see figure).

THE SPANISH Flu PHENOMENON

Thus, the study of the epidemiology, clinical picture and pathomorphology of the “Spanish flu” did not provide a satisfactory explanation for the mysteries of the influenza virus that caused the 1918-1919 pandemic. But then we can only assume that the explanation for this phenomenon is hidden in the structure of the genome of the people who died in this pandemic.

“Spanish flu” is a hyperreaction of the host to the influenza pathogen, the epidemic severity of which depends on the frequencies of individual genes accumulated in the human population over a certain period of time. If we adhere to this point of view, then it becomes clear both the emergence of epidemics such as the “Spanish flu” (accumulation of genotypes highly sensitive to the influenza virus) and their cessation for a long period of time (elimination of these genotypes by the influenza virus).

The proposed hypothesis may be confirmed by a molecular study of the genomes of people who died during the Spanish Flu pandemic of 1918-1919. Apparently, the last word in solving the mystery of the “Spanish” flu will be said during the implementation of the international Human Genome Project.

P.S. Apparently, attempts to find explanations for the high mortality rate during the Spanish flu pandemic only by studying the characteristics of the causative agent of the disease were initially doomed to failure. There are two sides involved in the infection process, but only one of them has been studied.

But not only American, but also Russian scientists have the opportunity to reveal the mystery of the Spanish flu pandemic. In the archives of some Russian prosecturas that existed before 1918, macro- and micropreparations of tissues of people who died in that pandemic may still be preserved. It is known that in the early 1960s, Kiev pathologist N.E. conducted research with them. Boatswain. Moreover, he received samples from 6 prozecturas in Moscow and Odessa. All drugs were in good condition(see Botsman N.E., Pathomorphological manifestations of the “Spanish flu” of 1918-1920 and the Asian flu of 1957 / “Medical Affairs”, 1960, # 11, pp. 105-108).

However, molecular biologists' attention must now turn to variants in some human genes. After all, a study of historical material shows that the “Spanish flu” tends to return.

A severe viral infection that affects people regardless of gender or age. This is an acute disease, which is characterized by severe toxicosis, catarrhal symptoms in the form of rhinitis, nasal congestion. Often accompanied by a cough affecting the bronchi.
Influenza epidemics occur every year, usually during the cold season, and affect up to 15% of the world's population. Influenza and ARVI make up 95% of all infectious diseases in the world. Every year, up to 500 million people get sick in the world, 2 million of whom die. In Russia, from 27.3 to 41.2 million cases of influenza and other acute respiratory viral infections are registered annually.

Repeated periodically, the flu takes us about a year in total full life. A person spends these months in a helpless state, suffering from fever, general fatigue, headache, and poisoning of the body with poisonous viral proteins. In severe cases of influenza, irreversible damage to the cardiovascular system often occurs, respiratory organs, central nervous system, causing diseases of the heart and blood vessels, pneumonia, tracheobronchitis, meningoencephalitis.

From the history
The infamous “Spanish Flu” occurred between 1918 and 1920. This most severe known pandemic has claimed more than 20 million lives and affected 20 - 40% of the world's population. Death came quickly. A person could still be absolutely healthy in the morning, but by noon he would fall ill and die by night. Those who did not die in the first days often died from complications caused by the flu. In February 1957, a pandemic began in the Far East and quickly spread throughout the world, which was called the “Asian flu”. In the US alone, more than 70,000 people have died during this pandemic. In 1968 - 1969 A moderately severe "Hong Kong flu" occurred. Older people over 65 years of age have been hit the hardest by the virus. The total death toll from this pandemic is 33,800. In 1977 - 1978 A relatively mild pandemic occurred, called the “Russian” flu. The influenza virus that triggered this pandemic had already caused an epidemic in the 50s. Therefore, those born after 1950 were the first to suffer.

The causative agent of the disease, the influenza virus, was discovered in 1931. And it was first identified by English virologists in 1933. Three years later, influenza B virus was isolated, and influenza C virus was isolated in 1947.
Virus influenza A causes moderate to severe illness. It affects both humans and animals. It is influenza A viruses that are responsible for the emergence of pandemics and severe epidemics.
Viruses influenza B do not cause pandemics and usually cause local outbreaks and epidemics, sometimes affecting one or more countries. Outbreaks of influenza B may coincide with or precede influenza A. Influenza B viruses circulate only in the human population (more often causing illness in children).
Virus influenza C quite little studied. Infects only humans. Symptoms of the disease are usually very mild or do not appear at all. It does not cause epidemics and does not lead to serious consequences. Illnesses caused by influenza C virus often coincide with influenza A epidemics.

The influenza virus is very easily transmitted. The most common transmission route - airborne. It is also possible household way transmission, for example through household items. When coughing, sneezing, or talking, particles of saliva, mucus, and sputum with pathogenic microflora, including influenza viruses, are released from the nasopharynx of a patient or virus carrier. An infected zone with a maximum concentration of aerosol particles forms around the patient. Their dispersion range usually does not exceed 2-3 m.
The flu usually begins acutely. The incubation period usually lasts 2-5 days. Then the period of acute clinical manifestations. The severity of the disease depends on general health, age, depending on whether the patient has previously been in contact with this type of virus.

Depending on this, a person may develop one of forms of influenza:
- Lightweight; Medium-heavy; Heavy; Hypertoxic.

When light (including erased) form Influenza, body temperature remains normal or does not rise above 38°C, symptoms of infectious toxicosis are mild or absent.

When moderate form flu temperature rises to 38.5 - 39.5 ° C, which is accompanied by classic symptoms of the disease:
- Intoxication ( profuse sweating, weakness, joint and muscle pain, headache).
- Catarrhal symptoms. - Respiratory symptoms (damage to the larynx and trachea, painful cough, chest pain, runny nose, hyperemia, dry mucous membrane of the nasal cavity and pharynx).

During development severe form Influenza, body temperature rises to 40 - 40.5°C. In addition to the symptoms characteristic of a moderate form of influenza, seizures, hallucinations, nosebleeds, and vomiting appear.

If the flu proceeds without complications, the febrile period lasts 2-4 days and the illness ends within 5-10 days. After suffering from the flu, symptoms of post-infectious asthenia persist for 2-3 weeks: weakness, headache, irritability, insomnia.

The clinical picture of influenza and acute respiratory diseases caused by various viruses has many similarities. The terms acute respiratory infections or acute respiratory viral infections cover a large number of diseases that are largely similar to each other. All of them are caused by viruses that enter the body along with inhaled air through the mouth and nasopharynx, and are characterized by the same set of symptoms. The patient has a fever, sore throat, cough and headache for several days. However, it is incorrect to call all acute respiratory infections and acute respiratory viral infections influenza. Influenza is caused directly by the influenza virus, which belongs to the orthomyxovirus family.

FLU(French grippe; syn. influenza) is a viral disease characterized by an acute onset, a short course with symptoms of general intoxication, and damage to the mucous membrane of the respiratory tract.

Story

G.'s diseases were known in ancient times. Hippocrates also described a disease whose main symptoms were persistent cough, inflammation of the pharynx, weakness, fever, and transient inflammation of the eyes. There is information about 126 epidemics and pandemics of G. over eight centuries (12-19). The pandemics of G. were especially large in 1889-1890 and 1918-1920. Both pandemics have affected every country in the world; in 1918-1920, according to incomplete data, St. died. 20 million people After the pandemic of 1918-1920. G. epidemics were observed on average every 2-4 years, but they never reached such intensity in terms of both morbidity and mortality of the population. Only in the pandemic of 1957-1959. and 1968-1969 the incidence was very high in all countries.

In Russia, the first descriptions of G.'s clinic were made in Moscow and St. Petersburg during the epidemic of 1729-1730, when the Medical Office issued a “Warning about diseases arising from contaminated air.” This unique document outlines the clinical picture, treatment of G. and its prevention. However, the abundance of the forms described by the wedge indicates that G. at that time, undoubtedly, did not stand out from among other acute respiratory diseases.

For a long time, the causative agent of G. was considered to be a bacillus isolated by R. Pfeiffer in 1892. The true history of the study of G. began with the establishment by R. Shoup in 1931 of the viral etiology of swine influenza and the discovery in 1933 by W. Smith et al. human G. virus. In the USSR, the G. virus was first isolated by A. A. Smorodintsev et al. in 1936. He was the first to propose a method specific prevention(1937) and treatment of G. with anti-influenza serum (1938).

Statistics

G. occupies a significant place in the general incidence of infectious diseases. Under the diagnosis of G., tonsillitis, rhinitis, pharyngitis, tracheobronchitis, etc. are often recorded; Therefore, in statistical analysis based on taking into account only clinically diagnosed diseases, total data on the incidence of various acute respiratory diseases (ARI) and influenza are used (Table).

INCIDENCE OF INFLUENZA AND ACUTE RESPIRATORY DISEASES IN THE USSR POPULATION

The incidence of G. and acute respiratory infections in the USSR exceeds the total incidence of all other infectious diseases. In some years, G. and acute respiratory infections accounted for more than 80% of all infectious pathologies, more than 60% of diseases in children.

The actual incidence of G. is slightly higher than that registered by appeal. During epidemics, it is especially high in preschool institutions and enterprises. The highest incidence rates are in large enterprises, the nature of production of which is associated with intensive contacts between workers. The incidence of G. in the rural population is approximately two times lower than in the urban population. Men and women get sick with the same frequency. A significant number of patients experience complications from the ENT organs and lungs (pneumonia). In 0.3% of cases, G. leads to the development of lesions of the nervous system.

Mortality from G., reaching during the pandemic of 1918-1920. high indicators, continuously decreased. An increase in mortality from G. is usually observed during epidemics caused by new antigenic variants of the influenza A virus.

Developed system of preventive, anti-epidemic, and treatment. measures against G. in our country have made it possible to stabilize mortality from this disease at low rates.

Mortality from G. is relatively low and hl is observed. arr. among children under 1 year of age and the elderly.

The damage to public health and the economy from G. epidemics is extremely great, which makes the problem of combating G. one of the primary health care tasks.

Etiology

The causative agents of G. are pneumotropic RNA-containing viruses of three antigenically distinct serolae, types A, B and C - belong to the family. Orthomyxoviridae (see Orthomyxoviruses).

G. pathogens are adsorbed on cells of various origins and are easily desorbed from their surface; have enzymatic (neuraminidase, RNA polymerase) and hemagglutinating activity. They are characterized by multiple reactivation (see Viruses), genetic recombination (see Recombination) and the formation of an incomplete virus (particles containing a defective genome and having reduced infectivity in the presence of high hemagglutinating activity). G. viruses have a round or oval shape with a particle diameter of 80-100 nm. Freshly isolated viruses are characterized by pleomorphism, the formation of filamentous (length up to 1000 nm with a diameter of 80-100 nm) and large (diameter up to 250 nm) rounded shapes.

Virions have a dense shell and are covered with protrusions 10-12 nm high. The core of the virus (nucleocapsid) consists of a helical strand of ribonucleoprotein (RNP) diameter. 9 nm. Chem. composition of G. viruses: RNA - 1.0%, protein - 70%, lipids - up to 24%, carbohydrates - up to 5%.

The RNA of G. viruses is single-stranded, with a predominance of uracil. The genome of the virus (see Genome) is fragmented and is a collection of several RNA molecules of different lengths, with a total mol. weighing 4-5 X 106 daltons.

Viral proteins are composed of seven types of polypeptides of different sizes. Four of them do not contain carbohydrates and are located in the central part of the virion. Two polypeptides have a mol. weight 81,000-94,000 daltons, their function is not clear; the third polypeptide is associated with RNA, they say. weight 53,000-65,000 daltons; fourth polypeptide - mol. weight 25,000 - 26,000 daltons - makes up the membrane covering the nucleocapsid.

The remaining three polypeptides contain carbohydrate groups and are glycoproteins with a mol. weighing 55,000-58,000, 46,000 - 50,000 and 25,000 - 29,000 daltons; they constitute the outer layer of the rim and are functionally associated with hemagglutinating and neuraminidase activities. Hemagglutinin is a glycoprotein of complex structure, consisting of two or three dimers, each of which in turn includes a heavy and light chain of polypeptides with a mol. weighing 46,000-50,000 and 25,000-29,000 daltons, respectively. Neuraminidase is a tetramer consisting of four polypeptides; in general, the functional complex has a pier. weight 220,000-250,000 daltons. The difference in mol. The weight of polypeptides depends on the strain, type of virus and isolation method. Hemagglutinin and neuraminidase are separated structurally, antigenically and functionally. Change them to natural conditions goes independently. Each of them can be isolated in purified form. In accordance with the nomenclature of the WHO Expert Committee (1971), human H. viruses have four antigenically distinct hemagglutinin subtypes (H0, H1, H2 and H3) and two neuraminidase subtypes (N1 and N2).

The polymerase (transcriptase) enzyme of G. viruses catalyzes the RNA-dependent process of incorporation of ribonucleotides into the daughter viral RNA (the mechanism of viral RNA synthesis - see Viruses).

Lipids are part of the intermediate layer of the virion. Like carbohydrates, they are structurally related to viral proteins; their synthesis and specificity depend on the cell genome. Internal proteins have type specificity and are immunologically designated as S-antigen (English: soluble). External glycoproteins have strain specificity and are immunologically designated as V-antigen (English: viral).

The synthesis of virus components occurs inside the infected cell, the “maturation” of the virus occurs on the cell membrane, and the virus is released by budding on transformed areas of the cell membrane.

It has been established that the genome of the G. virus is a complex composition of RNA fragments, each of which is closely connected to a protein; protein-associated fragments are connected to each other by labile bridges. The fragmentation of the genome of G. viruses and its separate synthesis during the process of reproduction determine the heterogeneity of the population characteristic of G. viruses, the formation of incomplete viruses with a defective genome, and also form the basis of genetic recombinations.

The international nomenclature of influenza A viruses provides a standard strain designation, including the following data: type of virus, host species, place of isolation, own strain designation or its number, last two digits of the year of isolation, envelope formula, i.e. abbreviated designation of the antigenic subtype of hemagglutinin and neuraminidase . When designating strains of human G. viruses, the type of host is omitted; When designating strains isolated from animals, the designation of the species of the natural host from which the strain was isolated is mandatory. When designating the antigenic formula of the envelope subunits, the subtypes of hemagglutinin and neuraminidase, characteristic of G. Animal viruses, in addition to the subtype number, are designated by the initial letters of the host species in which this antigen sample was first discovered: horse - eq (equine), pig - sw ( swine), birds - av (avian), etc.

For example, strain A/Hong Kong - 1/68 (H3N2) is a G. virus isolated from a person in Hong Kong in 1968, has hemagglutinin subtype 3 and neuraminidase subtype 2 of a human sample; strain A/horse/Miami - 2/63 (Heq2 Neq2) is a H. type A virus, strain No. 2, isolated from a horse in Miami in 1963, has hemagglutinin of subtype 2 of the horse sample and neuraminidase of subtype 2 of the horse sample .

The causative agents of pandemics and major epidemics of G. are antigenic variants of the type A virus, the division of which into serol, subtypes A (H0N1), A (H2N2) and A (H3N2) reflects the main stages of its evolution. The virus, first isolated in 1933 by Smith, C. Andrews and P. Laidlaw, was later classified as subtype A (H0N1). In 1947, A viruses appeared with a new hemagglutinin, but with the same subtype of neuraminidase A (H1N1), in 1957 new G. viruses were isolated - subtype A/Singapore - 1/57 (H2N2) and in 1968 - subtype A/Hong Kong - 1/68 (H3N2).

Strains of influenza virus type B were first isolated in 1940 independently by T. Francis in America and T. Magill in England. Epidemics of influenza type B occur once every 3-4 years, spread more slowly, are characterized by a protracted course and are limited to the territories of individual cities. The change in antigenic variants of a new subtype occurs with an interval of 10-20 years, the differences between them are expressed much less sharply than in the type A virus. The appearance of a new antigenic variant of the type B virus is accompanied by the gradual disappearance of previously circulating viruses, and therefore in one and the same In the same area, variants of the type B virus can be isolated that differ in antigenic properties.

Influenza virus type C differs from the two previous types by its greater constancy of its antigenic structure, which has remained almost unchanged since its isolation in 1947 by R. Taylor. Type C viruses infect Ch. arr. children; the outbreaks caused by it are strictly limited in distribution and are characterized by ease of wedge and flow.

A unified classification of influenza virus types B and C has not been created; hemagglutinin or neuraminidase subtypes are not included in the names of strains.

Experimental influenza infection is reproduced in white mice, African ferrets, white rats, and less often in hamsters, guinea pigs, and monkeys. In laboratory conditions, the simplest and most convenient model for cultivating the G. virus is 10-12-day-old developing chicken embryos. The propagation of some strains on primary trypsinized cultures of kidney tissue from human embryos, chickens, cows, young rhesus monkeys and green monkeys has been described. The presence of the G. virus in infected chicken embryos is detected by PHA, in tissue cultures by RHA and the hemadsorption reaction, based on the adhesion of erythrocytes of chickens or guinea pigs to the cells of the infected monolayer (see Hemagglutination, Hemadsorption), as well as by cytopathic action.

G. viruses are sensitive to external influences. They lose infectivity (in vitro) after heating for 20-30 minutes. at t°60° or 2-3 days at t° 37°, after UV irradiation, under the influence of formaldehyde, ether, ultrasound. The G. virus persists for a long time at t° -25°-70°. G.'s viruses quickly die in physiological solution, but persist in the presence of 10% skim milk solution, 6% peptone solution, 20% egg white solution or normal inactivated serum.

In the overwhelming majority, G. viruses are characterized by pronounced plasticity of antigenic and biol properties. The variability of surface antigens observed in natural conditions sharply distinguishes the influenza A virus from other viruses. It occurs in two forms: a) antigenic “drift” (partial displacement and renewal of antigenic determinants - active groups of antigens) of hemagglutinin or neuraminidase within one subtype; b) an “explosive” form of variability, designated as antigenic “shift” (complete replacement of a genome fragment encoding only hemagglutinin or hemagglutinin and neuraminidase), manifests itself in the emergence of a new subtype among influenza A viruses. Antigenic “drift” is based on the formation of mutants and their subsequent selection under the influence of immunol, population factors. The mechanism of occurrence of pandemic strains (“explosive” form of variability) is not clear enough. There are a number of hypotheses on this issue. One of them assumes the possibility of forming pandemic strains of G. viruses in the depths of previously circulating strains under the selective influence of immunol, protective factors; the second is the emergence of natural mutants; the third is the “splash” of G. viruses from animals into human society; the fourth - the most popular - is based on the possibility of genetic recombination between the human G. virus and the G. viruses of birds and animals.

Epidemiology

G. is found almost everywhere. Like none infection, G. is capable of epidemic and often pandemic spread in a relatively short time; it affects tens and hundreds of millions of people on all continents of the globe. This is determined by the following factors: a large number of mild forms of the disease and a short incubation period, which leads to a rapid increase in the number of patients (new sources of infection) among the population; airborne transmission of infection, ensuring simultaneous infection of many people from one patient; universal susceptibility of people to influenza; the appearance in each next epidemic (pandemic) of a new antigenic variant of the pathogen, to which the population has no immunity; short duration of post-infectious immunity, which entails the possibility of recurrent disease. Thus, in the USSR from 1957 to 1966, from 9 thousand to 21 thousand per 100,000 population were ill every year, and in just these 10 years, approx. 145 thousand per 100,000 population, i.e. on average approx. 1.5 diseases for every resident of the country (table). At the same time, one cannot fail to take into account that with a full-fledged general accounting of infectious patients in the USSR, a certain number lung patients forms G., undoubtedly, does not seek medical help and, therefore, is not included in the number of those taken into account.

The source of infectious agents in G. is only a sick person with a clinically pronounced or erased form of the disease. Already during the incubation period, the patient can release the G. virus into the environment through the upper respiratory tract (when coughing, sneezing, talking). Starting from the 7th day of illness, it is usually not possible to isolate the virus from the patient. Rare cases of isolation of type A virus on the 15-40th day in recovered patients have been described. However, the possibility of hron, carriage of the G. virus has not been proven.

Ways of spread of infection. From damaged cells villous epithelium of the respiratory tract, the virus is released into the air with drops of saliva, mucus, sputum when breathing, talking, screaming, crying, coughing, sneezing. The preservation of the G. virus in the air depends on the degree of dispersion of the aerosol containing viral particles, its exposure to light, moisture, heating, and the time of its settling. Droplets of respiratory tract secretions released into the air by a patient and containing viral particles, drying in a fraction of a second, form droplet nuclei that can long time remain in the air in the form of an aerosol. The G. virus survives in the air for up to several hours. Influenza virus type A is more stable than virus type B. It persists in dried and settled aerosol droplets: on bed linen - up to 2 weeks, in room dust - up to 5 weeks. In this regard, with influenza type A, the possibility of transmission of the virus through a secondary (dust) aerosol arises. However, the airborne route is the leading route in transmission of the G. virus. Infection is also possible through household items infected with the patient’s secretions (toys, pacifiers, dishes, towels, etc.).

According to V.A. Bashenin (1955), pandemic influenza of 1889-1890. claimed the greatest casualties among the elderly. During the pandemic of 1918-1920. The most affected were the flowering age (15-35 years). Usually, children are more likely to get sick with G., among whom young children suffer the most: from 6 months. up to 3 years. Children in the first six months of life have passive immunity received from their mother.

G.'s incidence is clearly seasonal. In our country, epidemics of G. occur, as a rule, in winter, but are also recorded in early spring or late autumn. Epidemics of G., which began in the spring, subside with the onset of summer, although the incidence of G. can significantly exceed the average level for the summer period, and in the fall the growth of diseases becomes stable, as was the case, for example, in 1957. Suggestions have been made about the influence of meteorol, factors on the incidence of G., but no convincing data have been obtained in this regard. On the other hand, factors such as population density and movement, crowding of people indoors and insufficient ventilation, and growing transport connections both within countries and on a global scale undoubtedly play a huge role. So, for example, if G., registered for the first time in Australia in 1946, reached the USSR only 3 years later, then in 1968 it spread throughout the globe in just six months.

The ecology of influenza viruses studies the relationship of influenza pathogens with their habitat and the consequences of this interaction both for the virus and for natural hosts, including humans. Particular attention is paid to the study of the evolution of the virus occurring under these conditions and its prediction.

The need to use ecology approaches to solving the problem of G. arose in connection with new ideas that G. may need to be considered as a zoonotic infection. Under natural conditions, the influenza virus type A affects not only humans, but also a number of mammals - pigs, horses, cattle, dogs, apparently fur seals, as well as numerous species of domestic (Chickens, ducks, turkeys), wild (pheasants , quails, ducks, terns, loons, gulls, etc.) and synanthropic (crows, etc.) birds. Strains of influenza A viruses circulating among different types of hosts differ from each other not only in biological characteristics, but also radically in the antigenic and protein composition of hemagglutinin and neuraminidase. In known H. viruses of humans and animals, 15 subtypes of hemagglutinin and 9 subtypes of neuraminidase have been identified. Of the 15 antigenic subtypes of hemagglutinin, 4 were discovered for the first time in strains isolated from humans and belong to the human subtype, 1 to the porcine subtype, 2 to the equine subtype, and 8 to the avian subtype. Of the 9 known antigenic subtypes of neuraminidases, 2 are human, 2 are equine, and 5 are avian. However, all 9 known subtypes of neuraminidases are found in avian H. viruses. At the same time, subtype 1 of neuraminidase, designated as human, was found in a strain isolated from chickens in 1902, i.e., 31 years before the discovery of the human G. virus.

The epidemic process characteristic of type A influenza is cyclical. The periodic replacement of previously circulating antigenic variants with new ones is of great importance. The emergence of new subtypes of the virus, capable of overcoming previously established immunity, can lead to the emergence of epidemics or pandemics of G., when a significant part of the susceptible population becomes ill and the epidemic subsides. In the next epidemic season (1.5-2 years from the appearance of the variant), the second wave of G. usually occurs, during which people who were not affected by the first wave are mostly ill, but repeated diseases are also possible in people who have not developed strong immunity, especially for children. In subsequent years, the introduced variant causes Ch. arr. local outbreaks, then disappears. The emergence of epidemics (see) is associated with the spread of variants that have changes in hemagglutinin or neuraminidase within the antigenic “drift”. There may be several such variants in one subtype; some become more widespread, while others become more limited in certain areas of the globe. A new pandemic cycle (see Pandemic) begins after the appearance of the next subtype of the virus, which, according to preliminary observations, occurs after 11-18 years.

It is believed that previously circulating variants of the virus may return in 60-80 years. Confirmation of this was obtained on the basis of serol examinations of elderly people, since, according to the theory of Francis (1960), the first infection with the G. virus in a person’s life leaves the strongest immunological trace and antibodies to this variety persist throughout life. In this way, it was established that varieties of the virus similar to the A(Hong Kong)68 variety had already had an epidemic, spreading in 1890, and the A(Hsw1N1) variety, known as the causative agent of swine influenza, was the cause of the Spanish Flu pandemic in 1918. 1920s The isolation of strains similar to this virus from people during the G. outbreak in the USA in 1976 shows the fundamental possibility of a return of this type of virus.

The epizootic process in domestic animals (mammals and birds) largely depends on the properties of the strain, population density and the intensity of interspecific contacts. The most pathogenic for poultry are strains of the virus with hemagglutinin of the first avian subtype, previously designated as true avian plague.

The circulation of G. viruses among people, as well as in animal populations, occurs through the transmission of infection from a sick individual or carrier to a healthy one. Besides airborne transmission of pathogens, in animals there is a fecal-oral transmission route, as well as transmission of pathogens with the participation of an intermediate host. Thus, swine G. is transmitted directly from one individual to another, as well as through pulmonary roundworms, which, when infected with the G. virus in the body of a sick pig, transmit pathogens transovarially. Infected roundworm eggs are hatched in external environment, are absorbed by earthworms or remain in the soil. At the same time, the G. virus located in eggs retains its activity.

Long-term persistence of the G. virus in roundworms and earthworms leads to the emergence of endemic foci of infection and contributes to its transition to other host populations, for example, to wild birds.

Human pathogens, in particular the Hong Kong variety of the virus - type A, can be naturally transmitted from humans to dogs, cattle, pigs, chickens, synanthropic and migratory birds, and possibly other animal species. Infections caused by human G. viruses in chickens, pigs, and cows are benign, but in the presence of additional factors (cooling, vitamin deficiency, bacterial and mycoplasma infections), severe forms with widespread illness and death are observed. Young animals suffer more often. Therefore, during epidemics of G., when carrying out anti-epidemic and anti-epizootic measures in rural areas, it is necessary to pay special attention to preventing the introduction of G. to animals from the personnel serving them.

Wild birds are an important link in the natural circulation of influenza A viruses among animals and in their spread between continents. There is no evidence of direct transfer with preservation of the pathogenicity of G. viruses from animals to humans. Antigenic variants affecting livestock, poultry, or wild birds do not cause epidemics in humans.

However, the possibility of hybridization of human and animal G. viruses, as well as the appearance in natural conditions of epidemically active varieties that have antigenic similarity with avian and equine G. viruses in terms of neuraminidase or hemagglutinin, has been experimentally proven. This gives reason to believe that the reverse influence of epizootic processes on epidemic ones can be carried out indirectly through the processes of genetic recombinations that stimulate the natural evolution and variability of human G. viruses, contributing to the formation of pandemically dangerous viruses. In this process, G. viruses of mammals and especially birds are donors of additional genetic information. Epizootic processes in populations of different species of natural hosts can be carried out independently, but it is assumed that in nature the influenza A virus has a common cycle that includes many species of living beings.

Pathogenesis

The G. virus, entering the upper respiratory tract, multiplies in epithelial cells, causing their necrosis and desquamation. An important role in the development of the disease belongs to intoxication caused by the resorption of toxic proteins of the pathogen and the influence of toxins on the walls of blood vessels. In mild forms of G., the lesions are limited to the upper respiratory tract; in more severe forms, the process moves to the trachea and quickly spreads to the bronchi, causing dystrophic and necrotic changes, acquiring the features of a generalized infection.

Due to the desquamation of altered epithelial cells, the mucous membrane of the respiratory tract becomes permeable to the virus, which under these conditions penetrates the bloodstream along with the decay products of the affected cells, as well as various bacteria that intensively multiply in the respiratory tract tissues affected by the virus.

The virus is found in the blood even in the absence of its discharge from the nose, and is also often isolated from the blood from the 2nd to the 14th day of illness, not only in patients with fever, but also in patients with normal temperature. According to Meers (R. D. Meers, 1969), Dudgeon (J. A. Dudgeon, 1969) et al., among other factors in the pathogenesis of G., the allergic component, caused both by the pathogen proteins themselves and by antigen-antibody complexes, is also important and antigen - damaged tissue of the patient (see Autoallergy).

Pathological anatomy

Morphol. changes in G. are expressed by damage to the respiratory organs and toxic damage to other organs and systems. The severity of these changes depends on the virulence of the pathogen, the state of specific and nonspecific immunity, as well as on the nature of concomitant diseases and bacterial complications.

Local changes in G. are characterized by mucous and vacuolar degeneration of the epithelium, its partial death along the respiratory tract, followed by reactive changes.

Serous, catarrhal-purulent, hemorrhagic and necrotizing rhinitis (see), laryngitis (see) and tracheobronchitis (see Tracheitis) are characteristic. Imprint smears from the middle turbinate reveal a large number of dystrophied columnar epithelial cells, in the cytoplasm of which oxyphilic inclusions are often found. The most severely affected areas are the subglottic region of the larynx, trachea and large bronchi (Fig. 1), as well as the mucous membrane of the tongue. The mucous membrane is fiery red, with frequent pinpoint hemorrhages and yellowish islands (foci of necrosis). In more severe cases, the mucous membrane of the trachea and large bronchi throughout is grayish-yellow in color, with small areas of hemorrhage (tsvetn. fig. 2 and 3). Histologically, the epithelium of the trachea and bronchi takes the form of arcade-shaped structures that arise due to edema (see), vacuolization (see) and detachment of the surface layers of cells containing viral antigen. The formation of fuchsinophilic cytoplasmic inclusions (Fig. 2) and the development of regenerative (pseudometaplastic) processes are often observed. Under the influence of the G. virus, bronchial epithelial cells lose villi, and the number of granules in them decreases sharply. Cytoplasmic inclusions are autophagosomes formed in the zone of partial necrosis of the cytoplasm due to the reproduction of the G. virus (Fig. 3). Sharp plethora, edema and round cell infiltration of the subepithelial layers are combined with thickening of the basement membrane and increased secretion of mucus-forming glands. In other places, there is death of the epithelium, pronounced plethora and leukocyte infiltration of the subepithelial layer of the bronchi and purulent exudate with colonies of microbes in the lumen of the respiratory tract. Such foci of purulent-necrotic tracheobronchitis serve as a source of bacterial lesions of the lung tissue.

On macroscopic examination, sharp plethora of blood, edema, foci of acute emphysema are observed in the lungs (see Pulmonary Emphysema), often areas of intense red compaction with a smooth cut surface, as well as purulent bronchitis (see) and bronchiolitis (see), areas of purulent, abscessed pneumonia and pleurisy (tsvetn. Fig. 3), usually developing in cases of bacterial, often staphylococcal, infection (“variegated” influenza lungs). Histologically, foci of atelectasis, thickening of the interalveolar septa due to protein impregnation and plethora, degeneration and desquamation of alveolocytes are often detected. In the lumen of the alveoli, in addition to collapsing alveolocytes, a few macrophages and leukocytes are found suspended in the serous fluid, in places disintegrating leukocytes or edematous fluid with colonies of microbes.

On the 6-10th day of illness, along with severe circulatory disorders and dystrophic changes, regenerative processes occur in the mucous membrane of the upper respiratory tract. Suppurative processes often develop in the lungs due to bacterial infection, which is facilitated by disturbances in the drainage function of the bronchi due to damage to the muscular layer of the bronchial wall and metaplastic processes in the mucous membrane. Often there are phenomena of purulent bronchitis and bronchiolitis with complete destruction of the epithelial lining and subsequent obliteration of the lumen of bronchioles or the development of bronchiectasis.

Post-influenza changes in the respiratory organs (days 11-30) are characterized by proliferation and differentiation of proliferating bronchial epithelial cells. In areas of atelectasis, small cavities are formed, corresponding to the alveoli, lined with cuboidal epithelium with eosinophilic cytoplasm. The lumens of such cavities contain mucus, neutrophilic leukocytes with an admixture of dead cells and microbial flora. The formation of such structures can contribute to the development of post-influenza bacterial pneumonia. Subsequently, differentiation of epithelial growths occurs unevenly, and more later in the lungs you can see islands of cuboidal epithelium resembling giant cells (Fig. 4). This, apparently, gave reason to call pneumonia occurring during this period giant cell pneumonia of unknown etiology.

In other internal organs, especially in severe G., various dystrophic changes associated with circulatory disorders are observed. There is acute swelling of the brain (see Edema and swelling of the brain), expressed by symptoms of stasis, hemorrhages (color Fig. 1) and dystrophic changes in cortical cells, sometimes with lymphoid infiltration. These phenomena, previously mistakenly considered as influenza encephalitis, are regarded as the result of influenza neurotoxicosis. Dystrophic changes are detected in the sympathetic ganglia and peripheral nerve trunks.

In the heart during G., dystrophic changes in muscle fibers and nerve cells intramural ganglia. Dystrophic and inflammatory changes in blood vessels are sometimes combined with vein thrombosis (see Thrombosis). In the liver, along with dystrophic changes in hepatocytes, diffuse hyperplasia and proliferation of Kupffer cells, round cell infiltration of connective tissue layers are often observed.

Death in G. is most often associated with the addition of bacterial suppurative processes, as well as with viral toxicosis itself, expressed in sudden and acute circulatory disorders.

Immunity

A person does not have innate immunity to G. Only newborns have antibodies to G., received during intrauterine development from the mother and disappearing by the 7th month. life. Acquired immunity in G. is type- and strain-specific. Antigenic variants of influenza A virus induce only partial cross-immunity. Antibodies to the pathogen appear within 2-3 days. from the onset of the disease and reach the most high level on the 10-14th day. Acquired immunity for influenza type C apparently lasts for life, immunity to influenza type B lasts 3-5 years, and immunity to influenza type A lasts 1-2 years. To homologous strains of influenza type A, immunity is stronger and longer lasting. Acquired immunity is provided by two types of factors - local (secretory) and general (humoral). Nonspecific immunity factors include cofactors (see Antiviral immunity), serum inhibitors (see) and interferon (see), which reduce the likelihood of G.

Clinical picture

The incubation period for influenza type A is from several hours to two days, for influenza type B - up to three days.

Some patients experience so-called harbingers of the disease, manifested by mild malaise, chilling, aching joints and muscles, a short-term increase in body temperature to 37.1 - 37.5°.

The onset of the disease is often acute - a practically healthy person turns into a seriously ill person within a few hours. In G.'s clinic, two main syndromes are distinguished: intoxication and catarrhal.

The first symptoms of the disease are signs of intoxication: chills, fever, dizziness, headache, weakness, muscle and joint pain. Catarrhal phenomena (nasal discharge, cough, sore throat, pain when swallowing, etc.) often appear towards the end of 1-2 days. or do not appear at all. The headache has a characteristic localization in the forehead, temples, brow ridges, and eyes. Dizziness and a tendency to faint are more often observed in adolescence and old age, as well as in persons suffering from hypertension or cerebral atherosclerosis. Fever is one of the main symptoms of G. The maximum temperature in most patients is observed on the first, less often the second, day of illness. The duration of fever is 2-5 days. The decrease in temperature in some patients occurs critically, in others - accelerated lysis. Some patients may have a two-humped type of temperature curve, which is caused by exacerbation of hron, foci of infections, the occurrence of inflammatory complications, viral superinfection (see Infection). Non-febrile forms of G. are extremely rare.

Following or along with the early symptoms of the disease, other signs of intoxication begin to appear: adynamia, general weakness, flushing of the facial skin, insomnia, delirium, nausea, vomiting, convulsions, meningeal symptoms. Hemorrhages (nosebleeds, bleeding gums, blood in sputum, etc.) are often observed.

Catarrhal syndrome manifests itself in the form of pharyngitis (see), rhinitis (see), tracheitis (see), less often laryngitis and bronchitis. Pharyngitis is more common, manifested by hyperemia of the pharynx, with characteristic granulation of the posterior pharyngeal wall and occasionally hemorrhages. From the 3rd day of illness, the mucous membrane of the pharynx begins to turn pale, and the granulations begin to flatten, leaving a pronounced vascular pattern in the form of a mesh. Rhinitis in the first days of the disease is manifested by difficulty in nasal breathing, caused by hyperemia of the mucous membrane of the nasal passages. Rhinorrhea occurs on the second - third day of illness in 1/2-1/3 of patients. The cough is usually dry, hacking, accompanied by pain in the chest, sneezing is observed in 1/2 of patients. Conjunctivitis, photophobia and lacrimation are relatively rare. Herpetic rashes usually appear no earlier than the 3-4th day of illness.

The severity of G.’s course is determined by a complex of clinical signs and, above all, intoxication syndrome (fever, headache, disturbance cardiovascular activity, addition of hemorrhages).

From the cardiovascular system, muffled heart sounds and hypotension are observed; with rentgenol. examination on the 2-3rd day sometimes reveals an increase in the pulmonary pattern, indicating pulmonary hyperemia. A pneumotachometer examination (see Pneumotachography) reveals a decrease in bronchial patency, more pronounced with influenza type A. Changes in the kidneys correspond to the severity of intoxication and are characterized by a decrease in the volume of urine excreted, proteinuria (see), less often microhematuria (see Hematuria). Enlargement of the liver with G. is rare. Under the influence of the toxin of the pathogen G., disturbances in the activity of the liver are sometimes observed, up to toxic influenza hepatitis, impaired renal activity, as well as a decrease in the function of the pituitary-adrenal system. The leukocyte formula in the first days of the disease is characterized by a pronounced band shift, and later leukopenia appears. The average duration of the disease is 6 days, with severe forms - 11-13 days (epidemics of 1968-1969 and 1972-1973).

Complications. The most common and serious complication of G. is pneumonia of viral, bacterial or viral-bacterial origin (see Pneumonia).

In 1968-1969 and 1972-1973, according to individual clinics, X-ray examination of a significant number of patients with G. revealed interstitial small-focal, large-focal and lobar pneumonia. More often they were localized in the lower lobe of the right lung. Bilateral pneumonia was also observed. In more than 0.5 inpatients, G. pneumonia was diagnosed in the first 3 days of illness. Pneumonia in G. is in the vast majority of cases viral-bacterial and, in particular, influenza-staphylococcal. Often they take a protracted course, turning into chronic, form or pulmonary suppuration. Fulminant hemorrhagic pneumonia is relatively rare. Pneumonia is more common in young children and the elderly. There is an opinion that virus A causes pneumonia more often than virus B.

Acute otitis media, damage to the paranasal sinuses, and acute catarrhal laryngotracheitis are detected in approximately 1/3 of patients.

Complications from the nervous system are observed in 1/4 of seriously ill patients. Most of them experience early neurological complications in the form of cerebral edema and increased intracranial pressure(see Hypertensive syndrome). In a smaller number of cases, late neurol symptoms are observed: neuralgia, radiculitis, plexitis, as well as the so-called. asthenovegetative syndrome (see Asthenic syndrome). Acute mental disorders with insomnia and disorientation are sometimes noted in children and adolescents (see Infectious psychoses).

Diagnosis

Diagnosis of G., especially early, is sometimes difficult. There is often a discrepancy between wedge and serol diagnoses. The basis for early diagnosis of G. is a characteristic wedge, picture, anamnesis, assessment of epidemics, the situation (indication of contact with a febrile patient, the presence of disease outbreaks or epidemics in the locality), objective examination and laboratory data.

Clinical signs characteristic of G.: acute onset, manifested by a rapid increase in symptoms of intoxication, the appearance of fever, headache with typical localization in the forehead, brow ridges, eyeballs, especially when they move; the presence of adynamia, symptoms of meningism, nausea, vomiting, hemorrhagic phenomena; typical blood picture; frequent complications, in particular pneumonia.

Differential diagnosis. The similarity of the wedge, the picture of acute respiratory infections (parainfluenza, adenovirus, rhinovirus and respiratory syncytial infections, etc.) with G. often complicates their differential diagnosis.

G., unlike acute respiratory infections, has a more acute onset. Severe symptoms of intoxication with G. increase and reach their maximum very quickly, sometimes within several hours. With acute respiratory infections, they reach their maximum on the 2-3rd day of illness and are moderately or weakly expressed. The temperature during G., as a rule, reaches 38° and higher in 1-2 days. from the moment of illness; with acute respiratory infections, the temperature often remains at low-grade levels, and sometimes even normal. Catarrhal symptoms (runny nose, conjunctivitis, pharyngitis, cough, etc.) with G. occur within 1-2 days. later than symptoms intoxication and are mildly or moderately expressed, while with acute respiratory infections they appear simultaneously with the first signs of the disease, are often pronounced and form the main symptomatology of the disease.

ARIs vary significantly depending on their ability to primarily affect one or another part of the respiratory tract. With G., along with damage to the entire respiratory tract, the most pronounced symptoms of tracheitis are observed, manifested by a dry cough and pain along the trachea. With parainfluenza (see Parainfluenza diseases), the larynx is predominantly affected and symptoms of laryngitis occur: aphonia or hoarseness. Adenoviral diseases (see) are manifested by damage to the mucous membranes of the eyes (conjunctivitis), nose (rhinitis), pharynx (pharyngitis), tonsils (tonsillitis with a pronounced exudative component). Rhinovirus diseases (see Rhinovirus disease) are predominantly manifested by rhinitis and rhinorrhea. With respiratory syncytial disease in children (see Respiratory viral diseases), asthmatic bronchiolitis often occurs (see Bronchial asthma), with swelling and spasm of the smooth muscles of the smallest bronchi, while in adults pharyngitis often occurs. Acute respiratory infections of mycoplasma etiology are accompanied by dryness and sore throat and an annoying dry cough. Isolated damage to the larynx is observed in G. rarely. With parainfluenza, the leading catarrhal symptom is mild laryngitis (sore throat, dry cough and hoarseness), which occurs in isolation in the vast majority of patients, although patol, the process can sometimes spread to the trachea.

In adenoviral diseases accompanied by damage to the upper respiratory tract, a number of patients experience abdominal pain, intestinal dysfunction and enlarged liver, and in 1/3 patients painless, slight or moderate enlargement of lymph nodes, mainly cervical, submandibular and much less frequently axillary and inguinal ; Sometimes a rash is noted on the skin of the body.

It is generally accepted that the most characteristic of G. is rhinopharyngolaryngotracheitis, for parainfluenza - rhinopharyngolaryngitis, for adenoviral infection - rhinopharyngolaryngotonsillitis (isolated) in combination with conjunctivitis and rhinopharyngoconjunctivitis. Respiratory syncytial disease with damage to the upper respiratory tract occurs in half of the patients as nasopharyngitis. In the group of patients with damage to the lower respiratory tract due to this infection, as a rule, nasopharyngobronchitis is observed - independent and with pneumonia. However, with every acute respiratory infection there are also common catarrhal syndromes.

Laboratory diagnostics

Virol., Serol, and Cytol methods are used.

The G. virus is released in the first days of the disease from the discharge of the nasal passages and pharynx of patients. The most effective method is infection of chicken embryos into the amniotic and allantoic cavities, followed by incubation at t° 32-37°. You can use, especially for the H. virus type B, infection of primary trypsinized cultures from the kidneys of a chick embryo, young monkeys or human embryo. To indicate the virus in the allantoic or amniotic fluids of a chicken embryo, as well as in the culture fluid, the hemagglutination reaction is used (see). The presence of the virus in the infected monolayer is determined by the hemadsorption reaction (adhesion of red blood cells to the monolayer of infected cells), less often by the presence of a cytopathic effect (granular degeneration of cells and rarefaction of the monolayer). If there is no virus in the first passage, additional passages are made.

Identification of isolated viruses is carried out by RSC, RTGA, neutralization reaction (PH) and precipitation reaction in agarose gel. The belonging of hemagglutinin to one or another serotype (A, B, C) is established using type-specific diagnostic sera, after which strain-specific sera are used to determine the antigenic variant within a given serotype. The antigenic specificity of neuraminidase of isolated G. viruses is established in the reaction of suppression of neuraminidase activity (RPNA). After contact of the virus with various antisera, the residual neuraminidase activity of the mixture is determined. The effect of neuraminidase is assessed by its ability to cleave N-acetylneuraminic acid from ovomucin or fetuin.

Serol, G.'s diagnosis is based on detecting an increase in antibodies in the sera of convalescents by 4 or more times according to RSC, RTHA, PH, or indirect hemagglutination reaction (IRHA). The RSC uses type-specific antigens from influenza viruses type A and B. This makes it possible to distinguish influenza type A from influenza type B, but does not provide identification of the antigenic subtype that caused the epidemic. In the last three reactions, epidemically active antigenic variants of G. viruses of types A and B are used. The high strain specificity of the antigen is especially important when studying the blood serum of young children who have had G. for the first time, containing strictly specific anti-influenza antibodies.

The staging of RTGA is often complicated by the presence of nonspecific inhibitors in sera that simulate the action of antibodies and distort the specificity of the reaction. To destroy them, the serum is treated with destructive enzymes of bacterial origin or rivanol, as well as carbon dioxide, potassium or sodium periodate, and also adsorbed with koalin. Inhibitor-resistant variants of strains are used to produce antigens.

PH on chicken embryos, tissue cultures, or a color test is a sensitive, but more labor-intensive method for diagnosing G. than X-ray. In PH it is necessary to use inhibitor-resistant strains of the G. virus or remove nonspecific inhibitors from the serum.

As a diagnostic tool for RNGA, special preparations are used, which are preserved red blood cells with viruses fixed on their surface. Red blood cells sensitized by viruses are specifically agglutinated under the influence of anti-influenza antibodies. RNGA can be placed using the drip method. The results of RNGA are not affected by nonspecific inhibitors.

Express (or early) diagnosis of G. during the first days of illness is carried out by cytol, using a method using fluorescent antibodies. The method is based on the ability of fluorochrome-labeled anti-influenza antibodies to specifically bind to the G. virus and detect its presence in columnar epithelial cells when viewing fingerprint smears from the nasal cavity in a fluorescent microscope.

For early diagnosis of G., the method of rhinocytoscopy, based on the study of morphology, changes in the epithelial cells of the nasal mucosa of sick people, is much less often used. One of characteristic features G. - viral inclusions located in columnar epithelial cells or extracellularly.

Treatment

Before prescribing medications, the doctor must isolate the patient from other family members, neighbors in the dorm, apartment, and establish mandatory bed rest for illness of any severity.

To treat G., complex therapy is used, aimed at suppressing the reproduction of the virus in the body, neutralizing influenza toxin, and eliminating catarrhal and other symptoms. Treatment of a patient with a typical wedge, picture of G. is carried out at home. Patients with severe and complicated forms of G. are hospitalized, as are patients with concomitant severe cardiovascular or other somatic diseases.

Patients are recommended to eat a dairy-vegetable diet, enriched with vitamins, with plenty of liquid (warm milk, hot tea, fruit juice, fruit juice, etc.). Frequent ventilation of the patient's room, toileting the oral cavity, and monitoring bowel function should be recommended.

Drug treatment is carried out depending on the severity of the disease, as well as the presence of certain complications. For patients with a mild or moderately severe course, rimantadine 50 mg 3 times a day is prescribed in the first two days of the disease, 3 times a day, for 3-5 days, sometimes in combination with ascorbic acid. It is advisable to inhale 0.5 ml of anti-influenza serum into each nostril 2-3 times a day for 2-3 days. In addition to these drugs, the patient is prescribed pathogenetic and symptomatic drugs in various combinations.

To relieve headaches, muscle and joint pain, use acetylsalicylic acid, amidopyrine, analgin or other antipyretic and analgesic drugs (askofen, pyraminal, novocephalgin, novomigrofen, etc.); for agitation and insomnia - phenobarbital, barbamyl and other drugs in sedative or hypnotic doses; for severe cough, codeine, ethylmorphine hydrochloride, expectorants, mustard plasters, alkaline heat-moisture inhalations are recommended; to eliminate dryness and sore throat - warm drink (warm milk with Borjom); for rhinitis - injection into the nose after 3-4 hours of 2-5% solution of ephedrine, naphthyzine or other vasoconstrictor drugs. For rhinitis, oxolin (oxolinic ointment) is used, which, along with prophylactic, also has curative properties. action. Oral cordiamine is useful for the prevention of cardiovascular disorders.

For uncomplicated G. of mild and moderate severity, antibiotics and sulfonamide drugs are not prescribed, with the exception of elderly or weakened persons concomitant diseases. This group of patients is shown with for preventive purposes tableted antibiotics (tetracycline, vitacycline, rondomycin, oletethrin, etc.) or sulfonamide drugs for treatment. doses Some patients are prescribed physical therapy: aeroion therapy using devices for individual (AIR-2) and group (AF-2) use, UV irradiation, UHF, inductotherapy.

In severe cases with severe intoxication syndrome, donor anti-influenza gamma globulin is administered intramuscularly in a dose of 3.0 ml. Usually after administration of gamma globulin 6-12 hours later. the temperature decreases, the symptoms of intoxication decrease or disappear, and the patient’s condition improves. If this does not happen, it is recommended to re-inject the drug at the same dose; You can also administer donor anti-measles gamma globulin or serum polyglobulin 3.0 ml intramuscularly according to the same scheme as anti-influenza gamma globulin. Specific polyglobulin is effective against parainfluenza, adenovirus, respiratory syncytial and other influenza-like diseases. Gamma globulin does not have a noticeable effect on the course of catarrhal syndrome. Leukocyte interferon is used with treatment. aiming at early stage disease, when the first wedge, symptoms of G. appear.

Biological drugs should be administered to seriously ill patients repeatedly, until the temperature decreases and severe intoxication disappears.

At the first signs of cardiovascular failure, glucose with corglycone, strophanthin or other cardiac glycosides is administered intravenously, and oxygen inhalation is prescribed.

In order to prevent pneumonia, patients with severe G. are prescribed tableted antibiotics. If pneumonia is suspected of being associated with G., antibiotics are administered intramuscularly, and in severe cases, intravenously. The following treatment regimen for pneumonia is recommended. Anti-influenza gamma globulin (or polyglobulin) is administered intramuscularly, Morphocycline or olemorphocycline is administered intravenously, oletethrin or sigmamycin tablets, anti-inflammatory, desensitizing, cardiac, expectorant, and cupping medications are administered orally. In 2-3 days. intravenous administration antibiotics are stopped. Antibiotic aerosols are prescribed in combination with enteral administration of terramycin, kanamycin, etc.

If there is no effect, 5-7 days after the start of treatment, semi-synthetic Penicillins (methacillin, oxacillin) or antibiotics of the zeporin series (zeporin, etc.) are used intramuscularly; If blood appears in the sputum, calcium chloride is added intravenously.

Treatment with hypertoxic, extremely severe forms of G. should be carried out especially vigorously according to the following approximate diagram: repeated administration of anti-influenza gamma globulin and others antiviral agents to combat viral toxemia; drip administration of isotonic (200 to 500 ml) solution of glucose or sodium chloride for the purpose of detoxification; intravenous administration of morphocycline or olemorphocycline; intramuscular administration (4-5 times a day) of methicillin, oxacillin or ceporin, i.e. antibiotics with anti-staphylococcal action; intravenous and then intramuscular administration of hydrocortisone, norepinephrine, metazone, ephedrine to eliminate vascular disorders; for cardiovascular failure - intravenous administration of strophanthin or korglykon, subcutaneous administration of cordiamine; prescribing oxygen or placing the patient in an oxygen tent to combat hypoxia. If necessary, other drugs are added to this. measures, in particular the antihemorrhagic complex to lay down. Means for identifying hemorrhagic syndrome; dehydration therapy for pronounced cerebral symptoms (intravenous administration of hypertonic glucose solutions, intramuscular novuritis, lumbar puncture, etc.).

Forecast

The prognosis for severe and especially complicated forms of G. in the elderly and children is serious.

Prevention

Prevention is provided by the sanitary and hygiene complex. and anti-epidemic measures aimed at protecting the population from G. infection and limiting the spread of infection.

For the purpose of timely and effective organization of preventive measures, forecasting the expected epidemic of G. and establishing the dynamics of its spread throughout the country plays an important role. At the All-Russian Research Institute of Influenza M3 of the USSR, modeling of the nature and scale of emerging epidemics of G. is carried out with sufficient success, which makes it possible to correctly and timely organize preventive measures and provide medical care to those who are sick.

During the epidemic of G., activities are aimed at the early identification of patients and their separation from healthy individuals, which is achieved by isolating patients in families or communities. For these purposes, outpatient and hospital care sick people with primary repeated care of patients at home, for which additional vehicles are allocated.

When treating a sick person at home, caregivers are recommended to wear 4-6-layer gauze masks. The patient's household items are disinfected, wet cleaning is carried out daily and the room where the patient is located is regularly ventilated.

To reduce the risk of G.'s spread during the epidemic, the work of outpatient institutions is reorganized. The number of local doctors to serve patients at home is increasing; if necessary, doctors of other specialties, nursing staff, and senior medical students are also involved for this purpose. Inst. In the premises of clinics and children's consultations, wet cleaning of the premises is carried out 2-3 times a day using 0.5% clarified bleach solution or 0.2% chloramine solution, followed by ventilation. To disinfect the air, it is recommended to irradiate rooms with bactericidal ultraviolet lamps.

Patients with severe and complicated forms, as well as persons suffering from severe concomitant diseases. Patients must be isolated from dormitories and other groups.

Specialized departments for hospitalization of seriously ill patients are opened in hospitals, and additional beds are deployed. In lech. institutions install anti-epidemics. regime (see Isolation of infectious patients) that limits the spread of influenza diseases.

The pharmacy network creates a reserve of medicines and disinfectants in advance for the uninterrupted supply of the population and treatment. institutions.

During the epidemic, entertainment and other public events are limited, especially for children. Mandatory wearing of gauze bandages is being introduced for employees of medical, transport, trade, household and other enterprises related to serving the population.

The implementation of these activities is facilitated by a wide sanitary clearance. work among the population with propaganda on radio, television, in cinema about the rules of personal hygiene, the importance of timely access to a doctor, etc.

Specific prevention of G. is based on active immunization with influenza vaccine. There are two types of influenza vaccines (live and inactivated), which began to be developed in 1937. In the USSR, for active immunization against G., the live influenza vaccine (LAV) proposed by A. A. Smorodintsev is used, which is administered into the upper respiratory tract. In the USA, Great Britain, France and other countries, inactivated egg vaccine is used for subcutaneous or intramuscular administration.

Live influenza vaccine is produced from the allantoic fluid of developing chicken embryos infected with weakened strains of the G virus. The drug is produced in the form of influenza mono-vaccines of types A and B. The effectiveness of LAIV largely depends on the compliance of the vaccine strains with the G virus causing the current epidemics. Therefore, the composition of LAIV for vaccine strains identical in the properties of hemagglutinin and neuraminidase to epidemiologically relevant pathogens of G. is updated once every 3-4 years. Thus, vaccine strains of the type A virus were replaced in 1957, 1965, 1969 and 1973. Type B virus strains are replaced after 5-10 years. The need to periodically replace vaccine strains complicates vaccine prevention of G. and reduces the effectiveness of this measure during the emergence of new subtypes of the G. virus, when old composition LAIV is not specific enough.

To obtain vaccine strains of the G. virus that are harmless to humans, the method of successive passages in developing chicken embryos is used. A decrease in virulence occurs after 15-25 passages. Vaccine strains obtained under these conditions are highly reactogenic for children under 15 years of age.

The main requirements for LAIV include its high activity, i.e. the ability to stimulate anti-influenza immunity. It is administered in 0.25 ml doses into the nasal passages using liquid sprays with adjustable dispersion or a dispenser spray.

The ability of LAIV to stimulate secretory immunity at the site of entry into infection is an advantage of this drug, which distinguishes it from the inactivated influenza vaccine; parenteral administration causes a predominant accumulation of antibodies in the blood. Antibodies in respiratory tract secretions have more wide range specific activity.

Immunization against G. is carried out annually in the autumn-winter period. They vaccinate healthy adults over 16 years of age who work in large factories and factories, transport, communications, utilities and healthcare. institutions, trade, police.

Vaccination is carried out routinely three times with an interval of 10-14 days. The effect of vaccinations largely depends on the vaccination technique, which requires very careful administration of the vaccine using a nebulizer.

Preventive vaccinations are allowed at the beginning of the G. epidemic, reducing the interval between revaccinations to 5-7 days. In this case, vaccines first stimulate the formation of interferon, a nonspecific protective factor of anti-influenza immunity, and after 2-3 weeks. specific immunity is formed.

Intranasal LAIV is not used for the prevention of G. in children due to its increased reactogenicity when administered into the respiratory tract.

A.K. Alekseeva and O.G. Andzhaparidze (1968) developed tissue LAIV for oral administration, which is produced on a primary culture of embryonic kidneys of chickens or quails. The drug is harmless for adults and children, has interferonogenic and protective activity. FH, administered in liquid form through the mouth, does not cause vaccination reactions, but stimulates the formation of antibodies, which makes it possible to use it for the prevention of G. in children.

Modern inactivated influenza vaccines are a highly concentrated suspension of the G. virus, purified from ballast substances, grown on chicken embryos and inactivated with formaldehyde.

In the USSR, purified and concentrated preparations of inactivated influenza vaccine are used to vaccinate donors in order to obtain hemagglutinin with a high content of anti-influenza antibodies.

Vaccine prevention reduces the incidence of G. in vaccinated people compared to unvaccinated people during epidemics by 1.5-3 times, sometimes by 4-5 times.

For individual emergency prevention of G., leukocyte interferon obtained in the culture of human leukocytes is used. This drug has a wide spectrum of antiviral action, directed not only against the G. virus, but also other respiratory viruses - causative agents of acute respiratory infections of a non-influenza nature. Leukocyte interferon is administered intranasally by instilling 5 drops into the nose or inhalation 1-3 times a day daily throughout the epidemic.

Flu in children

Influenza in children is more severe than in adults, with frequent complications in the form of pneumonia, otitis, pyelonephritis, etc. Flu in children aggravates the course of other diseases, reduces the reactivity of the child’s body and has a significant share among the causes of child mortality. Children of all age groups are susceptible to G. Cases of intrauterine infection of the fetus from a sick mother have been described. The disease begins with high temperature(39-40°), short-term fever (2-5 days) and quickly developing symptoms intoxication. There is a predominance of the syndrome of general intoxication associated with damage to c. n. pp., over local catarrhal manifestations of the respiratory tract. The main and early symptoms of intoxication include headache, dizziness, repeated vomiting, abdominal pain, hyperesthesia, agitation or adynamia, drowsiness, nosebleeds observed in older children. With high fever, some children experience confusion, delirium, hallucinations, meningeal symptoms, muscle pain, and chills.

G. in children early age often begins with convulsions, loss of consciousness, vomiting, and less commonly symptoms of meningism. Convulsions usually occur against a background of high temperature and are clonic-tonic in nature (see Convulsions).

G. in newborns and children in the first months of life is characterized by an erased wedge and symptoms. Against the background of normal or subfebrile temperature, they have difficulty nasal breathing, restlessness or lethargy, breast refusal, regurgitation without worsening stool. In some cases, a short-term increase in stool without patol or impurities is possible. The uniqueness of the wedge, the course of G. in this age group is due to the reduced reactivity of the body, and in some cases, the presence of trans-placental anti-influenza antibodies.

Catarrhal symptoms from the respiratory system are absent or very mild in approximately 20-30% of cases. Other patients experience moderate hyperemia of the pharynx, nasal congestion or slight mucous discharge, dry cough, sometimes rough, tracheal, sore throat, laryngitis. Laryngitis may be accompanied by symptoms of stenosis, giving a picture of croup (see).

Lesions of the lungs in G. often occur without pronounced wedge symptoms and are often detected only radiographically, and are unstable. Characteristic are peculiar “segmental lesions” in the form of homogeneous large shadows corresponding to the location of the segment, less often the lobe of the lung. These changes appear from the onset of the disease and usually disappear after a few days. In the blood picture in the first days of the disease, leukocytosis, neutrophilia with band shift, eosinopenia or aneosinophilia and toxic granularity of neutrophils are noted. In the following days - leukopenia, lymphocytosis. ROE is within normal limits or moderately accelerated.

The duration of G.'s disease without complications is 3-8 days. After 1-3 days of normal temperature, it may rise in the absence of complications (second wave).

Diagnosis of G. in children with a pronounced wedge, the picture is facilitated during the epidemiological period. It is necessary to remember the presence of mild and asymptomatic forms of the disease. When diagnosing such forms, it is necessary to take into account epidemiol, data and results of laboratory research methods.

Treatment of children in severe forms of G. it is based on the early administration of specific donor anti-influenza gamma globulin, 1-3 ml intramuscularly. At the early stage of the disease, the administration of leukocyte interferon in the form of an aerosol of 0.25 ml into each nasal passage 4-5 times a day for 3-4 days is also indicated. At the same time, nonspecific pathogenetic and symptomatic therapy is carried out. For hyperthermia - intramuscular administration of amidopyrine or analgin, combined administration of a daily dose of chlorpromazine, diphenhydramine or pipolfen with novocaine solution ( lytic mixture), cold on the head, to large vessels. Cocarboxylase is indicated to combat acidosis. For convulsions, magnesium sulfate, phenobarbital is administered intramuscularly or by enema - daily dose diluted in 10 ml of 2% warm solution of sodium hydrochloride, 20% solution of GHB intravenously or intramuscularly; in case of prolonged convulsions and the presence of meningeal symptoms - spinal puncture (see). To eliminate meningoencephalitic syndrome, along with hypothermic and anticonvulsants, diuretics are used, hormonal drugs intramuscularly, intravenously; for the purpose of dehydration and detoxification - low-molecular solutions (hemodez, polyvinol, rheopolyglucin, albumin) and osmotic diuretics (15% mannitol, 20% sorbitol) intravenously. From cardiovascular drugs - corglucon, strophanthin, digoxin, mezaton. In mild and moderate forms of G., along with general activities(bed rest, drinking plenty of fluids) carry out symptomatic and stimulating therapy (analgin, diphenhydramine, vitamins, expectorant mixtures, mustard plasters, cupping, hot foot baths, etc.). Prescribing antibiotics for uncomplicated G. is not recommended. The exception is children under 2 years of age, who often experience complications; they are prescribed antibiotics from the first day of illness. Sulfonamides are not indicated.

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D. M. Zlydnikov; G. I. Alexandrova, L. Ya. Zakstelskaya, Yu. G. Ivannikov, G. I. Karpukhin, T. Ya. Luzyanina, A. S. Shadrin (etiol., epid., laboratory), G.I. Ilyin (pat. an.), E.A. Sirotenko (ped.).