Dengue fever in Thailand - symptoms, treatment, prevention. Dengue fever virus
Dengue fever is carried by mosquitoes that live in the following tropical countries:
- Singapore,
- Thailand,
- Philippines.
If a child is diagnosed with Dengue fever, which is also called tropical fever, this means only one thing: a few days ago the baby was bitten by a mosquito that carried one of the viruses.
In total, there are four types of viruses that can provoke the development of tropical fever in a representative of the younger generation. Immediately after recovery, the child develops immunity to the type of virus that caused the illness. Immunity is also formed to all other types. But in the first case we are talking about lifelong immunity, and in the second the body’s defenses will be resistant to viruses for only a few months.
Symptoms
Many parents mistakenly believe that the main symptom of dengue fever is a rash - small and all over the body. A rash is indeed a sign of the disease being discussed, but a sick child may not have one. But muscle pain in children infected with tropical fever always occurs under any circumstances. Moreover, these pains are quite significant.
The signs of classic Dengue fever in a child are very similar to the symptoms of ordinary and traditional flu in our area:
- increase in body temperature to forty degrees,
- pain in muscles and bones,
- red eye syndrome, a child complains that his eyes are itchy,
- the baby starts coughing and has a runny nose,
- A small, small rash may appear on the body,
- diarrhea.
Diagnosis of Dengue fever in a child
In this case, only two doctors can be diagnosticians:
- infectious disease physician
- lymphologist.
In some cases, a small patient and his attending physician may need to consult the following specialists:
- dermatologist,
- allergist.
After the doctor performs initial examination small patient, he will prescribe a number of important laboratory tests:
- general plasma analysis,
- PCR method, which allows you to determine the RNA of the virus,
- neutralization reaction,
- braking reaction,
- complement fixation reaction.
Based on the results of these laboratory research, and also taking into account the results of the examination of the child, the doctor diagnoses the disease.
Complications
The classic form of tropical fever is not fraught with serious consequences. Most likely, the child will get rid of it a week after infection. But if a representative of the younger generation develops tropical hemorrhagic fever, this can be dangerous for him with the following consequences:
- severe bleeding,
- jaundice,
- loss of consciousness,
- rapid breathing,
- rapid pulse,
- pale skin,
- death.
It is noteworthy that young people and children are especially susceptible to this form of the disease. However, we are not talking about tourists, but about residents who are indigenous to exotic countries.
Treatment
There is no cure or vaccine for Dengue fever. Modern medicine is not yet able to cope with this disease. However, despite such resistance to twenty-first century science, this disease is not dangerous. Can only result in death hemorrhagic type Dengue fever, which only affects local residents (natives of Singapore, Thailand and the Philippines).
What can you do
Finding yourself in a foreign country with a sick child in your arms, mom and dad should not panic. And that's why:
- in Thailand this disease is not treated at all; local doctors do not believe that tropical fever needs treatment;
- if the disease is not complicated in any way, then it will disappear on its own, without anyone’s help, after five to seven days;
- You need to be afraid of the hemorrhagic form of tropical fever, which attacks local residents, but you don’t need to be afraid of the classical form.
If mom and dad find themselves in a hopeless situation, they can independently help their child quickly overcome a disease that is unusual for our area. You can do this by following these recommendations:
- the baby should drink at least three liters of water during the day;
- especially useful in such a situation is beet juice which increases the level of platelets in the blood (before giving this juice to your child, you need to let it sit for four to five hours);
- I recommend that doctors use exclusively paracetamol-containing medications as an antipyretic;
- It is very useful to eat watermelons and pomelo during illness (in our country this is seasonal fruits, which are not so easy to find in winter, but in Thailand or the Philippines they are sold all year round and on every corner).
What can a doctor do?
- The doctor's primary task is to determine what type of fever has struck the little patient.
- When it comes to tropical hemorrhagic fever, early diagnosis is often life-saving for a child.
- Often young patients with classic dengue fever are hospitalized in a hospital medical institution. This is necessary so that the doctor has the opportunity to monitor the baby’s vital signs around the clock and monitor his health by analyzing the functioning of certain organs and systems of the body.
- In our country, children with tropical fever often receive blood transfusions. In countries where the fever occurs, this practice is absent due to ineffectiveness.
Prevention
Many people believe that it is possible to protect a child from tropical fever through vaccination. There is no vaccine (or medicine) for the disease under discussion. Parents should remember this the next time some charlatan tries to deceive them.
The only way to protect your child from Dengue fever is to use anti-mosquito drugs and Mosquito nets. Any bite can be destructive, so you must try to avoid every mosquito attack.
You should not take fumigators and other insect repellents purchased from a domestic supermarket with you to Thailand or Singapore. These funds do not in any way affect the small inhabitants of tropical countries, which means they are not able to protect the child and his parents. Protective equipment must be purchased locally. Ideally, immediately upon arrival.
You will also learn what can be dangerous untimely treatment the disease dengue fever in children, and why it is so important to avoid the consequences. All about how to prevent dengue fever in children and prevent complications.
And caring parents will find on the pages of the service full information about the symptoms of dengue fever in children. How do the signs of the disease in children aged 1, 2 and 3 differ from the manifestations of the disease in children aged 4, 5, 6 and 7? What is the best way to treat dengue fever in children?
Take care of the health of your loved ones and stay in good shape!
Specific timing of exacerbation of the epidemiological situation is predicted as follows:
The carrier of the infection is mainly the Egyptian biting mosquito - Aedesaegypti and some of its other relatives. And for breeding, this type of mosquito, like others, prefer to choose stagnant bodies of water or, as they often say, wetlands. (*But these can also be small tanks, as well as showers and toilets.) Thus, the peak of the epidemic coincides with the beginning of the rainy season - April May(but it’s better to focus on the rain), and subsequently the situation subsides a little, but there is still a chance of infection. The mosquito is only a carrier - there is no need to blame it for all the bad things. The source of the disease is humans and some primates. Therefore, when the number of carriers decreases due to the actions of doctors and natural processes then the epidemiological situation is decreasing.
There is no warning as such about the beginning of the epidemic, the locals already know. If they sit down and make a notification, they will say a couple of times on the news and that’s enough. Previously, this problem was more acute in Thailand, there was high mortality rate, not like now, then the notification was as needed. And now local medicine has learned to recognize and cope with this disease well.
How to protect yourself?
It’s very simple to protect yourself, avoid the carriers – the Egyptian biting mosquito – Aedesaegypti:
Egyptian biter, distinctive feature is the presence of white dots on the black body.
1. Most of all, the mosquito loves to be in a shady area.
2. Interesting feature The mosquito is that most of all it loves human blood and the blood of primates.
3. The most favorite breeding places for mosquitoes are places of stagnant water - wetlands or water filled with organic decay products, various leaves, grass, etc. But the most dangerous of them for humans can be the shower and toilet.
4. The increase in the population of this mosquito is facilitated by uncontrolled urbanization, accompanied by the emergence of urban areas without a centralized sewerage system, littered with household garbage, many components of which, for example, cans, serve as an excellent breeding ground for mosquitoes;
5. As a precaution, we recommend wearing long sleeves and using mosquito spray.
Currently, the range of new geographical regions visited by tourists has expanded significantly. In this regard, doctors of various profiles have to deal with unknown, including “exotic” infections, which include dengue fever.
Dengue fever- an acute arboviral disease that occurs with high body temperature, general intoxication, myalgia and arthralgia, exanthema, lymphadenopathy, severe leukopenia and relative lympho- and monocytosis. Some clinical forms of dengue fever occur with hemorrhagic syndrome. With repeated infection of adults, as well as with primary infection of newborns who have received antibodies from the mother, the disease can occur in hemorrhagic form. Refers to vector-borne zoonoses.
Spread of dengue fever
The source of infection is sick humans and monkeys, the carriers are mosquitoes Aedes aegypti in humans and Aedes albopictus in monkeys. The Aedes aegypti mosquito becomes infectious 8-12 days after feeding on the blood of a sick person and can remain infected for 3 months or more. The virus multiplies in the body of a mosquito at an air temperature of at least 22°C. Due to this, dengue fever is common in tropical and subtropical regions (42°N to 40°S). Behind last decades The incidence of dengue fever has increased significantly worldwide, with approximately 2.5 billion people, or every two in five people worldwide, at risk of contracting the disease. According to the latest WHO estimates, about 50 million cases of dengue infection occur annually worldwide. The disease began to be recorded more often in India, Vietnam, Singapore, Thailand, the Philippine Islands, as well as in European countries. Thus, in May 2010, 2 cases of dengue fever were identified in Tomsk in persons whose infection occurred on the island of Bali. Newcomers to an endemic region are most vulnerable to the disease.
Currently, the disease is endemic in more than 100 countries in Africa, America, the Eastern Mediterranean, South-East Asia and Western part Pacific Ocean. The disease is most common in Southeast Asia and the Western Pacific. Before 1970, epidemics of dengue hemorrhagic fever occurred in only nine countries, but by 1995 this number had more than quadrupled. In 2007, more than 890 thousand cases of dengue fever were registered on the American continent, of which 26 thousand cases developed the hemorrhagic form of the disease. In Venezuela alone, more than 80 thousand cases of dengue fever have been reported, including more than 6 thousand cases of the hemorrhagic form. As the disease spreads to new areas, not only does the number of sporadic cases increase, but new outbreaks occur.
Etiology
The causative agent of dengue fever belongs to viruses of the Togaviridae family, genus Flavivirus (arboviruses of antigenic group B). Contains RNA. It has a two-layer lipid shell made of phospholipids and cholesterol. The virion dimensions are 40-45 nm in diameter. It is inactivated by treatment with proteolytic enzymes, heating above 60°C, ultraviolet irradiation and exposure to disinfectants. There are 4 known types of dengue virus, different antigenically. Dengue viruses are antigenically related to viruses yellow fever, Japanese and West Nile encephalitis. They are cultivated on kidney cells of monkeys, hamsters, tissue cultures of HeLa, etc. In the blood serum of patients at room temperature, the causative agent of dengue fever persists for up to 2 months, and in dried material for up to 5 years.
Pathogenesis
The virus enters the human body through the skin through the bite of an infected mosquito. At the site of the infection gate, after 3-5 days, limited inflammation occurs, where the virus multiplies and accumulates. Viremia begins in the last 12 hours of the incubation period and continues until 3-5 days of the febrile period. Clinical manifestations depend on the type of virus. The classic picture of dengue fever is usually caused by 1 or 2 types of the virus. Other types have pronounced vasotropic properties and cause the occurrence of hemorrhagic syndrome. Diseases caused by types 2, 3 and 4 of the dengue virus cause Philippine hemorrhagic fever. Under Singaporean hemorrhagic fever All 4 types of viruses were detected. Thai hemorrhagic fever has been linked to "new" types of viruses (types 5 and 6), but their existence is disputed.
In the hemorrhagic form of dengue fever, it primarily affects small vessels, where endothelial swelling, perivascular edema and mononuclear cell infiltration are observed. In more severe cases, multiple hemorrhages occur in the endo- and pericardium, pleura, peritoneum, gastric and intestinal mucosa, and in the brain.
The development of thrombohemorrhagic syndrome (THS) plays a major role in the pathogenesis of hemorrhagic fevers. TGS (M.S. Machabeli syndrome) is a symptom complex caused by the universal and nonspecific properties of blood, lymph, tissue fluid, cellular and intercellular structures to initiate coagulation. As a result of retraction, the blood is stratified into components of different states of aggregation.
TGS goes through four stages in its development:
I. (stage of hypercoagulation). Begins in the tissue cells of the damaged organ, which leads to the release of coagulative active substances, and the coagulation activation reaction spreads to the blood. The duration of the stage is usually short.
II. (stage of increasing consumption coagulopathy and inconsistent fibrinolytic activity). It is characterized by a decrease in the number of platelets and fibrinogen levels, as well as the consumption of other plasma factors of the body’s coagulation-lytic system. At this stage, disseminated intravascular coagulation (DIC) syndrome begins and increases (incomplete DIC syndrome).
III. (defibrinogenation-fibrinolytic stage), in which defibrinogenation and total, but not constant fibrinolysis are observed. Corresponds to complete DIC syndrome.
IV. (restorative stage or stage of residual thrombosis and occlusion). With a favorable course of THS, a return to physiological standards all factors of the coagulation-lytic system of the body.
In the hemorrhagic form of dengue fever, the primary pathological process develops at the cellular molecular level with the obligatory involvement of endothelial cells circulatory system, pluripotent stem cells bone marrow. The rate of development of the process is determined by the aggressiveness of the pathogen, its tropism towards sensitive cells (macrophages and monocytes) and the degree of maturity immune system. In the midst infectious process there is a change in the anatomical and morphological integrity and functional state microvasculature, vascular endothelium and hematopoietic organs. The development of hypoxia, deterioration of the trophism of organs and tissues and their universal functional failure are observed. Life threatening blood loss is extremely rare. Increased bleeding as a sign of changes in vascular permeability acts as one of the leading symptoms of hemorrhagic fevers.
The virus also has toxic effect, causing degenerative changes in the liver, kidneys and myocardium.
After past illness immunity lasts about 2 years. It is type-specific, so repeated illnesses are possible even in the same season (2-3 months later) due to infection with a different type of virus.
Clinical picture
Incubation period ranges from 3 to 15 days (on average 5-7 days). In most cases, the disease begins suddenly. Only some patients experience prodromal phenomena: mildly expressed, in the form of weakness and moderate headache 6-10 hours before the onset of the main symptoms. clinical manifestations. Usually, in the midst of complete health, chills and pain in the back, sacrum, spine, and joints (especially the knees) appear. Body temperature quickly rises to 39-40°C. Severe adynamia, nausea, dizziness, and insomnia are noted. The face is red, pasty, the vessels of the sclera are injected.
Depending on the characteristics of the clinical course, a distinction is made between the febrile form of dengue (classical) and hemorrhagic dengue fever.
To assess the severity of dengue hemorrhagic fever, WHO has suggested clinical classification, in which stage IV of the disease is identified:
Idegree- fever, symptoms of general intoxication, the appearance of hemorrhages in the elbow when a cuff or tourniquet is applied (“tourniquet test”). Thrombocytopenia and thickening are detected in peripheral blood.
IIdegree— stage I symptoms are accompanied by spontaneous bleeding (intradermal, from the gums, gastrointestinal, uterine). More pronounced hemoconcentration and thrombocytopenia are detected in the blood.
IIIdegree- Circular insufficiency and agitation are added. In the blood there is significant hemoconcentration and thrombocytopenia.
IVdegree- deep shock.
The severity of dengue hemorrhagic fever may be due to damage nervous system(meningitis, encephalitis); dehydration with the development of hypovolemic shock; kidney damage with the development of acute renal failure, kidney rupture; respiratory organs (pneumonia, pulmonary edema); development of infectious-toxic shock. The nature of the lesions determines the main direction pathogenetic therapy.
A number of complications of dengue fever may be caused by pneumonia, otitis media, mumps, etc., which are associated with secondary bacterial infections. This circumstance requires the prescription of antibiotics and other anti-inflammatory drugs.
Classic form of dengue fever
The classic form of dengue fever is more benign. With this form, characteristic pulse dynamics are revealed: in the first days of the disease, tachycardia is noted with a heart rate of more than 100 per minute, and from the 3rd-4th day bradycardia is recorded at less than 40 per minute. Significant leukopenia (up to 1.5-10 9 /l) with relative lymphocytosis and monocytosis, thrombocytopenia is observed. In most patients, peripheral lymph nodes are enlarged. By the end of 3 days, body temperature drops critically, then after 1-2 days it rises again, and the main symptoms of the disease appear. After 2-3 days, body temperature decreases. Thus, the total duration of fever ranges from 2 to 9 days.
A characteristic symptom of the disease is exanthema. It can appear during the first febrile wave (but more often during the second increase in body temperature), and sometimes during the period of apyrexia after the second wave - on the 6-7th day of the disease. Exanthema is profuse, maculopapular or urticarial, severely itchy; leaves behind pityriasis-like peeling. During the period of convalescence, asthenia, weakness, loss of appetite, insomnia, muscle and joint pain persist for a long time (up to 4-8 weeks).
The hemorrhagic form of dengue fever is more severe, especially caused by virus types 4 and 6. In addition to the indicated signs of the initial period, pronounced toxicosis appears. Most patients experience vomiting and significant enlargement of the liver (50-80% of patients). From the 2nd day of illness appears hemorrhagic syndrome with an abundant petechial rash (Fig. 1-3), sometimes confluent hemorrhages at the injection sites, increased fragility of blood vessels, and blood in the vomit. Often such patients experience severe gastrointestinal bleeding. The activity of aminotransferases increases, residual nitrogen increases, the amount of urine decreases, and protein appears in the urine. Some patients (up to 20-40%) develop collapse with severe cardiovascular failure, decreased blood pressure, and decreased pulse pressure to 20 mm Hg. Art. and below, cyanosis appears. Bleeding time increases, thrombocytopenia increases, and the amount of fibrinogen decreases. In severe cases, the disease can be fatal (mortality rate for hemorrhagic form is about 5%). This form is more often observed in children.
Rice. 1. Hemorrhagic form of dengue fever: skin lesions on the right hand
Rice. 2. Hemorrhagic form of dengue fever: skin lesions of the legs
Rice. 3. Hemorrhagic form of dengue fever: skin lesions of the left leg
Features of dengue fever caused by virus types 3 and 4 are the absence of liver enlargement, a more benign course, collapse rarely develops, hemorrhagic syndrome is manifested mainly by a hemorrhagic rash.
Complications: encephalitis, meningitis, psychosis, polyneuritis, pneumonia, mumps, otitis.
Diagnosis of dengue fever
In endemic areas, recognition of dengue fever is based on the characteristic clinical picture diseases (two-wave fever, exanthema, myalgia, arthralgia, lymphadenopathy). WHO has proposed clinical laboratory criteria for dengue fever, which include fever, hemorrhagic syndrome, hepatomegaly, thrombocytopenia and increased hematocrit. In the classical form of the disease, pronounced leukopenia (up to 1500 in 1 mm 3) with relative lympho- and monocytosis is typical. Differential diagnosis must be carried out with malaria, chikungunya fever, pappataci, yellow fever and other hemorrhagic fevers, less often it is necessary to differentiate from measles and scarlet fever.
The diagnosis can be confirmed by isolation of the virus from the blood (on the 2-3rd day of illness), as well as by a 4-fold or more increase in the titer of specific antibodies in paired sera with an interval of 10-15 days. Complement fixation reactions, hemagglutination inhibition and neutralization reactions are used.
Dengue fever treatment
Compliance required bed rest, the timing of which is determined by the severity of the patient.
At severe complications and the development of critical conditions, the patient is transferred to the department intensive care and resuscitation.
Great importance has an organization good care for the sick and providing therapeutic nutrition. Recommended diet No. 4 with limited mechanical and chemical irritants, containing 100 g of proteins, 70 g of fats and 250 g of carbohydrates. Products rich in fiber, broths, sauces, spices, etc. are excluded. The method of preparation is also important - boiled and stewed dishes are allowed. Food is served warm, in small portions (4-5 times a day). The amount of liquid you drink should be 1500-2000 ml per day. Can be used mineral water— Morshinskaya, Truskavetskaya, Essentuki No. 4 or Borjomi.
Treatment of patients with dengue fever is predominantly pathogenetic. The search continues for ways to influence the pathogen - antiviral drugs and immune serum. Interferon for the treatment of dengue hemorrhagic fever was ineffective.
Antimicrobial therapy can only be used when bacterial complications develop. The most severe and life-threatening is sepsis, which can be caused by various microorganisms, primarily staphylococci, pneumococci, Klebsiella, Escherichia, etc. Empirical therapy with antibacterial drugs in high doses should be prescribed without waiting for results microbiological research. If there is no effect within 48-72 hours, it is necessary to change the antibiotic. After bacteriological establishment of the etiology of sepsis, it is necessary to carry out correction antibacterial therapy taking into account the possible resistance of the pathogen.
Empirical therapy usually involves the use of two drugs. The following combinations are appropriate:
- Cephalosporins of II-III generations and metronidazole.
- Inhibitor-protected penicillins and aminoglycosides of II-III generations.
- Carbapenems and aminoglycosides of II-III generations.
Pneumonias that complicate the course of hemorrhagic fever are classified as nosocomial pneumonias. They often develop during the use of corticosteroid drugs. For etiotropic therapy, the drugs of choice are cefepime, ceftazidime or cefoperazone in combination with aminoglycosides or fluoroquinolones. Alternative drugs are carbapenems, aztreonam, vancomycin. In the absence of bacterial complications, antibiotics are not prescribed.
The central link in the pathogenesis of hemorrhagic fevers is the development of THS. In this regard, in the pathogenetic therapy of patients important has anticoagulant therapy - controlled hypocoagulation. It allows you to prevent the consequences of hypercoagulation, that is, the transition of increased blood clotting to intravascular coagulation. In addition to the use of anticoagulants, disaggregants (acetylsalicylic acid) are also used to prevent thrombosis. Heparin preparations are used as anticoagulants.
At severe forms For hemorrhagic fevers with pronounced THS, it is advisable to use hourly administration of heparin (intravenously) at 40-50 thousand units per day. For mild forms of hemorrhagic fever and for the prevention of thrombosis, it is better to use low-molecular-weight heparin preparations: enoxaparin, nadroparin or dalteparin.
Enoxaparin sodium, obtained from standard heparin by depolymerization, is highly active against thrombokinase and does not affect bleeding time and blood clotting time. To prevent thrombosis, the drug is prescribed subcutaneously at a dose of 20 mg (0.2 ml of solution) once a day for 7-10 days.
Dalteparin sodium refers to direct-acting anticoagulants, isolated from the mucous membrane small intestine pigs. Binds plasma antithrombin and does not affect blood clotting time. Can be prescribed to patients with acute renal failure. To prevent thromboembolic complications, the drug is administered subcutaneously at a dose of 2.5 thousand IU once a day (in the morning). The course of treatment is 5-7 days. Contraindicated if present gastrointestinal bleeding.
Nadroparin calcium, a low molecular weight heparin, is used to prevent blood clotting during hemodialysis.
Among the disaggregants for the treatment of patients with hemorrhagic fevers, acetylsalicylic acid is used at a dose of 0.75-1.5 g per day for 7-10 days. There is no data in the literature on the effectiveness of other antiplatelet agents (pentoxifylline, dipyridamole) in the treatment of patients with hemorrhagic fevers.
To the most active means Pathogenetic therapy for patients with hemorrhagic fevers includes glucocorticosteroids. Their effectiveness has been proven in the treatment of patients with dengue hemorrhagic fever, Marburg, etc. The dose and duration of therapy with drugs in this group depends on the clinical form and severity of the disease.
- Severe course with the threat of developing severe renal failure: anuria for 24 hours or more, repeated vomiting, abdominal pain, hemorrhagic manifestations, leukocytosis more than 14.0-10 9 /l. Prednisolone is prescribed parenterally at a daily dose of 0.5-1 mg/kg. After polyuria appears, the daily dose begins to be reduced. Course duration is 3-5 days.
- A prolonged oliguric period, when at the onset of the disease the signs of a severe course are not clearly expressed, but the development of polyuria is delayed until 12-14 days of illness. Prednisolone is prescribed at 0.5-1 mg/kg. Course duration is 3-5 days.
- Development of acute vascular failure or infectious-toxic shock. Daily dose prednisolone is 120-240 mg or more (up to 10-20 mg/kg), hydrocortisone - up to 500-1000 mg, followed by a dose reduction. Course duration is 7-10 days.
For mild forms of hemorrhagic fever, glucocorticosteroids are not prescribed.
The prescription of protease inhibitors is pathogenetically justified. One of these drugs is aprotinin, which inactivates proteinases in plasma, blood cells and tissues. The activity of the drug is expressed in kallikrein-activating units (KIU). 50 thousand KIU per hour are administered intravenously. The daily dose is 300-500 thousand KIU. Course duration is 5-7 days. In case of developed DIC syndrome, the drug is contraindicated.
For desensitization purposes, it is prescribed antihistamines. IN last years new antihistamines appeared II- III generation, the use of which deserves attention.
Of the second generation antihistamines, we can recommend terfenadine 1 tablet (60 mg) 2 times a day for 5-7 days. III generation antihistamines cetirizine 10 mg (1 tablet) once a day or ebastine 10 mg 1-2 times a day for 5-7 days are more effective. The drugs do not have significant side effects and can be combined with other medicines, including antibiotics.
Patients with dengue fever may develop critical conditions requiring treatment in intensive care units and intensive care units. The most dangerous are:
- acute renal failure;
- dehydration, hypovolemic shock;
- infectious-toxic shock;
- pulmonary edema, acute respiratory failure.
The length of a patient's stay in hospital is determined by the severity of the disease, the presence of complications and epidemiological data.
The patient is discharged from the hospital after the clinical manifestations of the disease disappear and the main laboratory parameters normalize. In severe forms - no earlier than 3-4 weeks from the onset of the disease.
Dispensary observation of convalescents is carried out for one year. The first examination (1 month after discharge) is carried out by the attending physician at the hospital, the subsequent examinations (3, 6, 9 and 12 months after discharge) are carried out by a doctor at the infectious diseases office.
The prognosis in most cases is favorable, but in hemorrhagic forms it is serious. Recovery may take several weeks due to severe asthenia.
The first outbreak of dengue was recorded in 1635 in the Caribbean; over the next three centuries, epidemics were recorded in many countries with tropical and subtropical climates. The role of mosquitoes in the spread of the disease was proven in 1907, the pathogen was isolated and studied by Sabin in 1944. The hemorrhagic form of the disease was described in 1953 in the Philippines, but cases of a fatal course of the disease with the development of shock were described earlier. Currently, dengue fever is one of the widespread arboviral infectious diseases.
Dengue fever is a mosquito-borne disease caused by a flavivirus. Dengue fever usually results in sharp increase fever, headache, myalgia, arthralgia and swollen lymph nodes, accompanied by a rash that appears with the 2nd increase in temperature after a period without fever. Respiratory tract lesions such as cough, as well as tonsillitis and rhinorrhea may occur. Dengue can also cause a potentially fatal hemorrhagic fever with bleeding and shock. Diagnosis includes serological analysis and PCR. Treatment is symptomatic and for dengue hemorrhagic fever includes transfusion therapy.
Dengue is endemic to tropical regions of the world at latitudes ranging from approximately 35° north to 35° south. Outbreaks are most common in Southeast Asia, but have also occurred in the Caribbean, including Puerto Rico and the US Virgin Islands, Oceania and the Indian subcontinent; Recently, the incidence of dengue fever has increased in Central America and South America. Every year, it is estimated that 100-200 cases are brought into the US by returning tourists, but about 50-100 million cases occur worldwide, with approximately 20,000 deaths.
The causative agent, a flavivirus with 4 serological groups, is transmitted by the bite of Aedes mosquitoes. The virus circulates in the blood of infected people for 2-7 days; Aedes mosquitoes can acquire the virus while feeding on humans.
Epidemiology of dengue fever
Natural foci exist in tropical and subtropical regions of America, Africa, South and Southeast Asia, Oceania and Australia. During epidemics, the main source of the virus is a sick person, the carrier is the Aedes aegypti mosquito. Epidemics in cities and populated areas are explosive in nature, their epicenter most often being hospitals and schools. Immunity is short-term, type-specific. At re-infection another serotype or presence against it innate immunity SSD often develops.
Causes of dengue fever
The causative agent is an RNA-containing virus of the flavivirus family, genus Flavivirus, has a size of 40-45 nm, is poorly resistant in environment. By antigenic structure There are four serotypes of the virus - I, II, III, IV. Its antigenic structure is similar to yellow fever, West Nile fever and Japanese encephalitis viruses. Has a cytopathic effect. Its replication occurs in the cytoplasm of the affected cell. Heat labile, sensitive to formaldehyde and diethyl ether.
From the site of introduction, the virus penetrates into regional lymph nodes and vascular endothelium, where it replicates during the incubation period. Viremia then develops. In this case, the virus affects many organs and tissues. Damage to the vascular endothelium is accompanied by increased permeability. During primary infection, the “classic” benign form of the disease develops. When re-infected with another (usually II) serotype of the virus or in children under 1 year of age who have passive immunity, the formation of the “anti-dengue-Ig-dengue virus” immune complex occurs, which is fixed by the Fc receptors of mononuclear cells.
As a result, relatively resistant cells (monocytes, histiocytes, Kupffer cells) are infected by the virus. This leads to a sharp increase in the intensity of viremia, vascular damage, increased intoxication, plasmorrhea with blood thickening, thrombohemorrhagic syndrome and the development of SSD, which is usually observed in residents (children) of endemic regions.
In those who died from the hemorrhagic form of dengue, hemorrhages are found in the skin, epicardium, and myocardium. Pronounced dystrophic changes are found in the liver, kidneys, heart, and brain matter. Pathology of blood vessels, especially small ones, is characteristic: swelling and destruction of the endothelium. The death of patients occurs as a result of ITS, accompanied by blood thickening and thrombohemorrhagic syndrome.
Symptoms and signs of dengue fever
Fever, chills, headache, postorbital pain when moving the eyes, lumbar back pain and severe general weakness. Severe pain in the legs and joints is felt during the first hours, which gives dengue fever its traditional name - bone crushing fever, swaying fever, fever with inflammation of the joints. The temperature quickly rises to 40 °C with relative bradycardia. Bulvar and palpebral conjunctival injection and intermittently flaring or pale pink macular rash (especially on the face). Cervical, axillary and inguinal lymph nodes are often enlarged.
Fever and other symptoms persist for 48-96 hours, accompanied by a rapid decrease in temperature from profuse sweating. Patients then feel well for approximately 24 hours, after which the fever may begin again (pathological lordosis pattern), usually with a lower peak temperature than the first time. At the same time, a pale maculopapular rash spreads throughout the body to the limbs and face.
Mild forms of fever usually do not have swollen lymph nodes. With more severe illness, asthenia may last several weeks. Death is rare. Immunity to the infecting strain is long-lasting, while broader immunity to other strains lasts only 2-12 months.
In most patients, against the background of erythema, a profuse, pinpoint rash appears, which during the second wave becomes maculopapular in nature. The rash is accompanied by itching; after a few days, peeling of the skin appears during the period of convalescence. A constant symptom is polyadenopathy. Lymph nodes are soft and painless. In addition to arthralgia, pain is noted when moving in the joints, especially the knees. Patients are immobilized or their joints and spine are spared when walking. On the first day, tachycardia appears, which is replaced by bradycardia. The tongue is coated soft palate Enanthema is often found in the form of small vesicles. Possible disturbances of consciousness, delirium. After a decrease in body temperature, prolonged asthenia is noted. When examining blood from the 2-3rd day, leuko- and neutropenia is detected, when examining urine - transient proteinuria. An abortive course of the disease is possible. In this case, the fever lasts no more than 3 days, the rash is ephemeral, and there is no polyadenopathy.
In contrast to classic dengue, myalgia, arthralgia and osteoalgia occur rarely. Polyadenopathy and liver enlargement are often noted. A decrease in body temperature on the 3-4th day of illness is accompanied by a progressive deterioration of the patient's condition. Already in the febrile period, the first signs of increased bleeding appear - petechiae, nosebleeds, and a positive “tourniquet” symptom. After a decrease in body temperature, they sharply intensify. Petechiae, ecchymoses, bleeding gums, gastrointestinal and pulmonary hemorrhage, metrorrhagia. They are combined with clinical signs shock, kidney damage. Those who survive this difficult period experience full recovery within a few weeks.
- Degree I. Characterized by general symptoms and a positive “tourniquet” test (“tourniquet” symptom).
- Degree II. Characterized by the appearance of signs of spontaneous bleeding.
- Grade III. SSD develops, along with the signs present in stage II, circulatory insufficiency and agitation appear.
- Grade IV. Characterized by the development of decompensated shock (BP is not determined).
With all degrees of hemorrhagic dengue, progressive thrombocytopenia and hemoconcentration are detected. Hypoalbuminemia, increased aminotransferase activity, and creatinine and urea concentrations are also characteristic. Prothrombin activity of the blood decreases, hypofibrinogenemia develops, fibrin degradation products appear in the blood, and the complement system is depleted.
Diagnosis of dengue fever
- Serological analysis in acute period and during the recovery period.
Dengue fever may be suspected in patients in endemic areas if they present with sudden onset of high-grade fever, headache, myalgia, and adenopathy, especially with a characteristic rash or recurrent fever. Evaluation should rule out alternative diagnoses, especially malaria and leptospirosis. Diagnostic tests include serological analysis, antigen detection and blood PCR. Serologic testing includes hemagglutination inhibition or complement fixation assays using paired sera, but cross-reactions with other flavivirus antibodies are possible. Antigen detection is available in some parts of the world (not the US), and PCR is usually only done in specialty testing laboratories. Although rare and labor intensive, test cultures can be performed using mosquitoes or special cell lines in specialized laboratories.
A complete blood count may show leukopenia by the 2nd day of fever; by day 4 or 5, the white blood cell count may be 2,000-4,000/ml with only 20-40% granulocytes. Urinalysis may show mild albuminuria.
During outbreaks, clinical diagnosis is typically straightforward. To identify atypical and sporadic cases, PCR and isolation of a virus culture from the blood followed by typing, serological methods (RN, RSK, RTGA, ELISA, etc.) are used.
Differential diagnosis is carried out with phlebotokal fever (pappatachi), yellow and other hemorrhagic fevers, malaria, meningococcemia, rickettsiosis, measles, scarlet fever, and influenza.
Dengue fever treatment
- Supportive care
Treatment is symptomatic. Acetaminophen may be used, but nonsteroidal anti-inflammatory drugs, including aspirin, should be avoided because of the risk of bleeding. Aspirin increases the risk of Reye's syndrome in children and should be avoided for this reason.
Conduct pathogenetic treatment, anti-shock measures.
Forecast. The prognosis for classic dengue fever is favorable, mortality is less than 1%; for dengue hemorrhagic fever of I-II degrees, the prognosis is also favorable. With the development of SSD, the mortality rate reaches 10% or more.
Prevention of dengue fever
Residents of endemic areas should avoid mosquito bites. To prevent further transmission of the virus by mosquitoes, patients with dengue fever should be kept under a mosquito net until the 2nd episode of fever is over. Vaccines are being developed.
The main Direction is the fight against mosquito vectors, the use of mosquito repellents. It is important to kill mosquitoes in vehicles, arriving from dengue-endemic areas. For vaccination, a recombinant vaccine against dengue caused by type II virus is used.
The content of the article
Dengue fever(disease synonyms: joint fever, bone crush disease, giraffe fever) is an acute natural focal zoonotic disease, which is caused by the arbovirus of the same name and is transmitted by mosquitoes. There are classic and hemorrhagic forms of the disease.Historical Data of Dengue Fever
Endemic outbreaks of the disease in countries with hot climates have been recorded since the 18th century. until now. It was first described under the name joint fever by D. Bylon in 1779 on the island. Java and called relapsing fever by W. Ruch in 1780 in Philadelphia. In 1869, the London Medical College of Physicians gave the disease its current name, which comes from the English. dandy - dandy due to the peculiar gait of patients. The transmission of dengue fever pathogens through mosquitoes was established in 1906 p. T. Bancroft, P. Ashburn et al. in 1907 he proved the viral nature of the disease, but only in 1944 p. A. Sabin isolated and studied the virus.Etiology of Dengue fever
The causative agent of dengue fever is Dengue virus, which belongs to the genus Flavivirus, family Togaviridae. There are four known serovars of the virus: 1, 2, 3, 4. They contain RNA, heat-stable and heat-labile antigens. The virus is sensitive to ether, thermolabile, dies at a temperature of 50 ° C. When dried and frozen in the patient's blood serum at a temperature of - 70 ° C, it persists for 8-10 years.Epidemiology of Dengue fever
The source of infection is sick humans and monkeys. In the latter, the course of the disease may be latent. There are natural (jungle) and anthropourgic (urban) centers of the disease.The carriers of the virus are mosquitoes of the genus Aedes, which are capable of transmitting the virus from 8-12 days after infection and remain infected for life (1-4 months). In endemic foci, it is mainly children and people arriving from other areas who get sick. After the illness, type-specific immunity remains for up to 2-3 years. The disease is recorded between 40°S. w. and 42 ° N. w. - In the countries of America, Africa, Southeast Asia, Spain, Greece. Not registered in Ukraine.
Pathogenesis and pathomorphology of Dengue fever
After infection, the virus replicates in the cells of the mononuclear phagocyte system. After 5-15 days, viremia occurs, the virus is carried with the blood into the vascular endothelium, connective tissue, muscles, liver, kidneys, brain, endocardium, where it leads to cytolytic and degenerative changes. Due to cytolysis of damaged cells, secondary viremia occurs, accompanied by a second wave of fever. Morphological changes in the typical form of the disease have not been sufficiently studied due to the favorable course of the disease. In hemorrhagic form, except dystrophic changes detect multiple hemorrhages and hemorrhages in various tissue organs.Dengue Fever Clinic
The incubation period lasts 5-15, more often 3-7 days. In 20% of patients, prodromal signs are possible - headache, pain in muscles and joints.There are two clinical forms of the disease:
1) classic (benign)
2) hemorrhagic.
Classic shape
The classic form of the disease begins acutely, with chills and an increase in body temperature to 39-40 ° C. Patients complain of intense headaches, as well as pain in muscles and joints, which increases significantly with movements. The patient moves on straight legs, without bending them at the knee joints (dandy gait, giraffes). During Peshi days of illness, hyperemia and puffiness of the face with burning cheeks, scleritis, and conjunctivitis are observed. On the 2-3rd day of illness, a pinpoint roseola rash appears on the skin of the trunk and limbs, intense on the extensor surface of the joints, which can merge into larger elements different shapes to continuous erythema, disappears after a decrease in body temperature, leaving itching and peeling. Peripheral lymph nodes are enlarged, sometimes moderately painful. The liver may become enlarged. At the beginning of the disease, tachycardia appears, which changes from the 2-3rd day to relative bradycardia.On the 3-4th day of illness, body temperature drops critically to normal with profuse sweating. Arthralgia and myalgia persist. Within 1-3 days, the body temperature rises again, and the symptoms of the disease worsen. The entire febrile period lasts 7-10 days. After an illness, asthenia, arthralgia, myalgia, decreased performance, and asthenovegetative symptoms persist longer.
On the blood side, leukopenia with relative lymphocytosis is observed.
Hemorrhagic form
The hemorrhagic form of the disease often develops in people with hypersensitivity to the pathogen as a result of re-infection with the same serovars of the virus, often when infected with two serovars of it (usually the first and second).The disease begins suddenly, body temperature with chills rises to 39-40 ° C, manifestations of intoxication quickly increase, and signs characteristic of the classic form of fever appear. From the 2-3rd day of illness, a petechial rash appears, and in severe cases, severe hemorrhagic syndrome develops - hemorrhagic purpura, hemorrhages in the skin and various organs, nasal, gastrointestinal, uterine bleeding, hematuria. During the height of the disease (3-5 days), dengue shock syndrome may develop, tachycardia, low blood pressure, oligoanuria, and azotemia are detected.
There is no second febrile wave; the duration of the febrile period is 4-8 days. Microcirculation in the adrenal glands, kidneys, lungs, liver and other organs is disrupted as a result of blockade of capillaries by loose masses of fibrin and blood cell aggregates (DIC syndrome).
Complications are rare- polyneuritis, meningoencephalitis, psychosis, thrombophlebitis, orchitis, pneumonia, otitis, mumps.
The prognosis is favorable(mortality rate 0.1-0.3%), but if the disease is caused by dengue 2 virus, it may predominate hemorrhagic manifestations with development state of shock(dengue shock syndrome) with a mortality rate of 5-20%.
