Fever in Common Infectious Diseases

Worldwide, diarrhoeal disease is the leading cause of death under 5 years of age. More than two million children die every year from gastroenteritis, almost all living in resource-constrained countries. In the absence of diarrhoeal diseases, the total infant and child mortality in the Third World would not differ significantly from that of developed countries. Data collected from 276 surveys on diarrhoea in 60 countries have shown that one-third of all deaths in children below 5 years of age were caused by diarrhoea. Approximately 1.5 billion diarrhoeal episodes and 4.6 million deaths in children occur per year (or 12,600 deaths/day), accounting for 21–29.3% of all childhood deaths [6].

In developing countries, bacterial (Escherichia coli, Salmonella, Shigella, Campylobacter and Yersinia enterocolitica) and parasitic (Entamoeba histolytica, Giardia lamblia, Cryptosporidium species) pathogens are the major causes of gastroenteritis, particularly in summer months (Table ). In developed countries, viruses are responsible for approximately 70% of the gastroenteritis. Viral GE causes shorter illness than bacterial GE and is associated with increased risk of vomiting and dehydration compared to bacterial GE. Rotavirus is the most common causative pathogen followed by norovirus and adenovirus. Enteric adenovirus is associated with longer-lasting diarrhoea.

Fever is common in both bacterial and viral gastroenteritis. High fever is commonly present in many bacterial causes (e.g. Shigella, Salmonella, Shiga toxin-producing E. coli). Fever is often absent or low-grade in other diseases (e.g. enteropathogenic E. coli, cholera). Other febrile conditions that cause diarrhoea and need to be differentiated from GE are shown in Table .

Bacteria or viruses acting as exogenous pyrogens can cause fever by inducing endogenous pyrogens which raises the hypothalamic thermoregulatory set-point. Clinical and laboratory findings, which can differentiate bacterial from viral aetiology of acute gastroenteritis, are shown in Table .

Dehydration, the most common cause of hyperthermia, leads to cutaneous vasoconstriction and decreased sweating, causing an increase in body temperature. In hypernatraemic dehydration, an increase in sodium pump activity needed to offset the high extracellular sodium concentration may further raise the body temperature. High sodium levels may also act directly upon the hypothalamus to increase the set-point. For every 1 °C increase of body temperature, there is an increase in insensible water loss of 10%. Table shows typical water losses based on caloric expenditure of 100 kcal/kg/day for an infant weighing 10 kg body weight.

Bacterial Gastroenteritis

Bacterial gastroenteritis is caused either by secretory pathogens (such as cholera, which causes watery diarrhoea through colonization and adherence to the small bowel mucosa) or invasive pathogens (such as Shigella, which cause inflammatory cell exudates in the distal bowel and/or colon). Secretory pathogens are likely to cause severe diarrhoea. Invasive organisms may cause watery or grossly bloody diarrhoea with cramps and tenesmus, but severe diarrhoea is infrequent.

Salmonellae are Gram-negative rods with over 1400 known species. The most common serotypes are S. typhimurium, S. enteritidis and S. infantis. In industrialized countries non-typhoidal salmonellae (NTS) infection is more common. This is usually a self-limiting and benign disease, and invasion beyond the gastrointestinal tract occurs in only about 5% of patients. In many African countries, bacteraemia is a major cause of death, and NTS account for 20–50% of cases, ranking second only to pneumococcal pneumonia as the leading bacterial cause of child mortality. Most human infections occur in late summer and early autumn and are caused by the ingestion of contaminated food (meat, poultry products, eggs) or water. Increased susceptibility to the infection occurs in children with sickle cell anaemia, impaired cellular immunity and achlorhydria. About 12–48 h following ingestion of contaminated ingestion of contaminated food, the onset is abrupt with nausea, fever, and crampy abdominal pain, followed by loose, watery diarrhoea, occasionally containing mucus, blood or both. The illness is indistinguishable from Shigella infection. Vomiting is a not a striking feature in salmonellosis. While salmonellosis in older children is usually self-limited disease requiring no antibiotic therapy, there is a significant incidence of bacteraemia (range 15–45%) and meningitis in infants younger than 3 months. Bacteraemia may occur in the absence of fever in this age group. The absence of fever usually excludes bacteraemia in older children.

Fever in Gastroenteritis

• Endotoxin is a complex lipopolysaccharide structure that constitutes the outside portion of the cell wall of Salmonella. Endotoxin releases IL-1 from macrophage into the circulation, accounting for the fever and other systemic manifestations of the disease. Cytokines are responsible for the symptoms and development of the protective mechanisms in the disease. Mean serum concentrations of TNF-alpha, TNF-gamma and IL-12 are increased during the acute phase of the disease. IL-8 and IL-10 are involved in the pathogenesis of rotavirus GE.

• Diarrhoea is usually more frequent in afebrile than in febrile cases.

• Children with bacterial GE are more likely to develop high fever than those with viral GE, and there is a significant relation higher fever and shigella GE.

• In a study from Finland [7] comprising 102 children salmonella gastroenteritis, 15 had a fever >40 °C, 66 had a fever of 38–39.9 °C and 21 had a temperature of <37.9 °C. There was a significant correlation between the degree of fever and the duration of organism excretion: a fever of >40 °C had the shortest and no fever the longest duration of excretion (Table ). Fever therefore appears to have a favourable prognostic influenza on the duration of salmonella excretion. The gastrointestinal tract acts as a major barrier against the potentially noxious substances, such as microbes. Immunological defences include secretory IgA, macrophage and activated T-lymphocytes in the Peyer patches and lamina propria. Fever is beneficial to the infected host by enhancing macrophage and T- and B-cell activity.

  Table 5.9

  Fever on admission and duration of bacterial excretion after salmonella gastroenteritis in 102 children (Ref [7])

  Degree of fever (°C)	No of children	Duration of salmonella excretion (weeks)
  		Range	Mean	Mean (SD)
  (A) > 40 0	15	0–10	0	1. 9 (2.9)
  (B) 38–38.9	66	0–18	3	4.1 (4.0)
  (C) <37.9	21	2–60	7	11.7 (15.1)

• Convulsion may occur during the diarrhoeal disease. About 10% develop febrile or afebrile seizures. Febrile seizures (FS) are particularly common with shigella infection. Occasionally, afebrile seizure may occur in association with dehydration, electrolyte imbalance, hypoglycaemia or hypocalcaemia. A third form of seizure is an afebrile seizure, particularly during viral GE, without dehydration of electrolyte imbalance. This type of seizure is usually benign. CSF and EEG are normal. Paracetamol has not been shown to prevent FS.

• Ibuprofen is an antipyretic that is frequently administered for febrile children with GE. Acute renal insufficiency may occur in association with ibuprofen and should therefore be avoided.

Typhoid fever includes infection with S. typhi and S. paratyphi A, B and C, rarely S. choleraesuis, S. heidelberg and S. typhimurium. The incidence of typhoid fever in the USA is 0.2 cases per 100,000 population, with a case fatality rate of 1.3% [8].

Elevated pro-inflammatory pyrogenic cytokines, particularly tumour necrosis factor-α and IL-6, are responsible for the prolonged fever, which is characteristic of the disease. High serum levels of these cytokines have been linked to disease severity. High level of IL-6 suggests poorer response to antibiotic therapy and its decline correlates with successful therapy. Vigorous antipyretic use may lead to shock.

In older children, presentation of a typical case follows the following steps:

Onset is insidious with fever (without shaking chills), which is present in all patients, and is associated with headache, cough and abdominal pain. Symptoms then gradually increase over 2–3 days. The child is often constipated, nauseated and anorexic. The temperature continues to rise in a stepwise fashion to reach 40–41 °C. In young children the onset of fever is more often abrupt, then becoming sustained or intermittent. The stepwise pattern of fever is less common. In all ages, fever may continue for many days despite successful antibiotic therapy, and the child does not become afebrile until the end of the therapy. At the end of the first week, patients remain febrile with hot, dry skin, abdominal tenderness, hepatosplenomegaly and relative bradycardia. Roseate spots may be detected in about 20–40%, characterized by a few discrete popular erythematous lesions confined to the anterior chest and abdomen. Delirium, convulsion, meningeal irritation, psychosis and ataxia may be noted. If untreated with antibiotics, fever remains continuous at 39–40.5 °C for 2–3 weeks before abating slowly. By the end of 2 weeks, perforation or haemorrhage (in about 5%) may occur due to typhoid ulceration and defects in coagulation. This serious complication is associated with 50% mortality. Typhoid bacilli persist indefinitely in the bile passage in about 3–5% who recover from the infection.

Laboratory findings include leucopenia, anaemia, thrombocytopenia and increased serum aspartate transaminase (SGOT). Elevated agglutination titres of O and H antigens at 1:160 are significant. The diagnosis is based on isolation of S. typhi or other salmonella strains from blood or bone marrow culture.

Shigellae are Gram-negative rods with worldwide distribution. Humans are the principal host for shigellosis (bacillary dysentery). The majority of patients are under 5 years of age; the infection is rarely seen in infants under 6 months of age.

Four serotypes are known: Shigella flexneri, S. dysenteriae, S. sonnei and S. boydii. The first two species are more common in developing countries, whereas S. boydii and S. sonnei usually cause a self-limiting febrile illness in developed countries. Shigella must penetrate the mucosa in order to cause dysentery.

The disease onset is usually acute with fever and malaise, often progressing to dysentery consisting of cramps, tenesmus and frequent stools composed largely of blood and mucosa. Severe dehydration is not a typical feature of the infection. High fever is common. Of 57 children with Shigella gastroenteritis, 27 (47%) had a fever greater than 40 °C at presentation, 21 (37%) had a fever between 38 and 40 °C and the remaining 9 (16%) were afebrile [9].

Complications include toxic megacolon, protein-losing enteropathy, hyponatraemia due to inappropriate antidiuretic hormone secretion, disseminated intravascular coagulation, renal failure, haemolytic uraemic syndrome and bacteraemia. Shigella bacteraemia occurs in 4.0% of patients. Neurological symptoms, particularly convulsion are among the most frequent extra-intestinal manifestations of shigellosis occurring with or without evidence of the production of Shiga toxin (neurotoxin). Death can occur in children with poor nutritional state.

Amoebic dysentery, caused by Entamoeba histolytica, may cause colitis simulating shigellosis. Virulence of E. histolytica depends on the trophozoites being able to bind to colonic epithelium. The infection tends to run a more chronic course with intermittent watery or semiformed diarrhoea (containing blood and mucosa) without or with a low-grade fever. Young children tend to present with acute symptoms similar to cases with Shigella infection. Liver abscess may occur a few months after the intestinal infection, causing discomfort over the liver, intermittent fever with chills and sweats and weight loss. Findings suggestive of amoebic liver abscess include an elevated right diaphragm, hepatomegaly and a history of colitis. The diagnosis of amoebiasis is confirmed by demonstration of E. histolytica in a stool (motile trophozoites during the diarrhoea, cyst if the diarrhoea is not present) or in tissues. The indirect haemagglutination (HA) test and enzyme-linked immunosorbent assays (ELISA) are positive in almost all patients with amoebic liver abscess and in majority of those with intestinal infection.

Escherichia coli cause either non-bloody diarrhoea (e.g. enterotoxigenic E. coli, ETEC; enteropathogenic E. coli, EPEC) or bloody diarrhoea (e.g. Shiga toxin-producing E. coli, STEC; enteroinvasive E. coli, EIEC). E. coli cause significant fluid loss and dehydration, but bloody stools are relatively infrequent.

• ETEC produce enterotoxins that cause copious, watery diarrhoea in developing countries. In severe form, the illness resembles cholera and is responsible for high mortality among young children. It is an uncommon cause of diarrhoea in industrial countries, but it is the most common cause of traveller’s diarrhoea. EPEC infection was in the past a common cause of outbreaks of infantile diarrhoea in industrialized countries, usually occurring in neonates and young children <2 years of age. Since the 1970s the infection has been reported less frequently, and the severity of the illness has lessened in children of these countries. It can cause protracted diarrhoea.

• EIEC and STEC produce Shiga toxins, causing a dysentery-like diarrhoea and haemolytic uraemic syndrome (HUS) by the strain 0157:H7.

Fever occurs frequently in the range of 38–40 °C. Fever, very often low-grade, is reported in only one third of patients in children infected with EIEC and STEC. EPEC usually does not cause systemic manifestations because the organisms remain confined to the bowel lumen. Fever was found in only 5 of the infected 49 children from Addis Ababa [10].

Campylobacter enteritis is an important cause of enteritis in both developed and developing countries. C. jejuni is the most important species. The enteritis is a zoonosis and a man-to-man transmission is unusual. Raw cow’s milk and incompletely cooked poultry meat have caused most of outbreaks in the UK. Contaminated water is another cause of outbreaks in developing countries.

Infection is usually self-limited in industrialized countries, lasting 2–4 days, following an incubation time that averages 5 days. Children present with an acute illness accompanied by fever, diarrhoea and bloody stools in about 90% of cases. Abdominal pain occurs almost universally, but vomiting is mild and occurs in about 30%. In a study from Canada, all 32 children with this infection who were older than 12 weeks develop fever up to 40.5 °C, whereas all five children who were younger than 12 weeks remained afebrile. In a study from Iraq, 202 children with diarrhoea, C. Jejuni was found in 13.86% and fever was detected in 82.14% [11].

Yersinia enterocolitica is an anaerobic, Gram-negative bacillus that causes an infection mostly in cooler climates such as Scandinavia and Canada. Serotype O:3 is the most common isolate. Transmission of Y. enterocolitica to humans occurs from ingestion of contaminated foods (particularly contaminated pork), water and milk.

Presentation is characterized by bloody diarrhoea in about one third of patients. The fever is usually mild, ranging between 38 and 39 °C. The associated abdominal pain sometimes mimics appendicitis (pseudo-appendicitis). The disease is usually mild although it can be prolonged (1 day to 3 weeks). A Canadian study of 181 children with Yersinia infection (45) reported that diarrhoea occurred in 98%, fever in 88%, abdominal pain in 64.5% and vomiting in 38% [12].

Rare complications are arthritis and erythema nodosum. Other rare complications include intestinal perforation, diffuse ulceration, ileocolic intussusception, peritonitis, glomerulonephritis, meningitis and peri-myocarditis. The infection can occur as septicaemia and patients then have high fever, toxic appearance and confusion.

Viral Gastroenteritis

Rotavirus infection is responsible for 30–60% of all cases of dehydration and diarrhoea in young children (peak age 3–15 months) in both developed and developing countries. The infection is prevalent in winter months. Approximately 125 million cases of rotavirus diarrhoea occur annually in developing countries, leading to an estimated 800,000–900,000 deaths a year [13]. Although viraemia is rare in healthy individuals, this was reported in 67% of immunocompetent children with rotavirus diarrhoea.

Nosocomial acquired outbreaks of rotavirus have occurred in newborn nurseries and paediatric hospital wards. The virus can be detected in oropharyngeal aspirates with or without diarrhoea. Spread occurs via the faecal-oral route. The virus is shed in faeces in high concentration, which allows its easy identification by electron microscopy.

There is often a preceding or accompanying upper respiratory tract infection or otitis media. Within 2 days of exposure, there is fever and vomiting, which last 1–3 days, and usually preceding the onset of watery diarrhoea, which lasts 4–7 days. Dehydration occurs as a result of marked faecal fluid loss.

Most children with rotavirus diarrhoea have fever. A study from Finland [14] reported that 14% of 336 infants had fever of 39–40.2 °C and 65% had less than 39 °C. Many cytokines, particularly IL-6, IL-10 and INF-γ, play an important role in the pathogenesis of as well as protection against rotavirus reinfection. IL-6 is elevated in children with fever.

Enteric adenovirus: Several studies have shown that adenovirus is second to rotavirus as the most common cause of viral gastroenteritis, occurring commonly during the first year of life. The infection was identified in 8.6% of 900 paediatric inpatients with diarrhoea, serotypes 40 and 41 being the most common isolates [15]. In contrast to enteric adenoviruses, other respiratory adenoviruses are not associated with diarrhoea. Watery diarrhoea is the most common presentation, usually followed by 1–2 days of vomiting. Illness typically lasts 5–12 days (mean 9 days). The duration of the diarrhoea usually lasts longer compared to that caused by rotavirus. Severe dehydration is less common compared to rotavirus infection.

A low-grade fever for 1–3 days is commonly recorded with adenovirus enteritis. A Canadian study [16] of 127 children with adenovirus enteritis found that 41% of them had a rectal temperature of >38 °C. The range of body temperature was 36.2–40.8 °C (mean 38 °C). The average duration of fever was 1.6 days (range 1–30 days).

The outcome of adenovirus gastroenteritis is generally good. Adenovirus is now more frequently diagnosed (due to PCR) in immunocompromised patients and is an important cause of mortality.

Other viruses: Norfolk virus and Norwalk-like viruses are major causes of small and large outbreaks of winter vomiting in older children and adults with or without diarrhoea. These outbreaks occur commonly in recreational camps, communities or schools in the USA. Presentation is similar to that of other types of viral gastroenteritis and includes anorexia, malaise, fever and abdominal cramps, followed within 48 h by vomiting and watery diarrhoea. Symptoms usually last 2–3 days and full recovery is the usual outcome. Astrovirus can also cause gastroenteritis. The infection is frequently asymptomatic in the newborn infants.

Treatment: Breast milk is the best prophylaxis against gastroenteritis, and exclusively breast-fed children remain remarkably free of severe diarrhoea in developed and developing countries.

The standard treatment of all diarrhoeal diseases is the replacement of fluid and electrolyte loss. This is best accomplished by oral rehydration solution (ORS) which has revolutionized the management of diarrhoeal diseases in developing countries. This is safe, cheap, convenient to use and superior to IV fluids because it can be started early at home. The sugar-electrolyte mixture recommended by the WHO contains (mmol/L water) sodium 90, chloride 80, potassium 20, sodium bicarbonate 30 and glucose 111, with an osmolality of 331 mosmol/L. A hypotonic solution with a sodium concentration of as low as 50–60 mmol/L and an osmolality of 224 mosmol/L has been shown in Finland to have clinical advantages over the standard ORS. Rice-based ORS compared with standard ORS reduced the 24 h stool volume. Intravenous electrolyte-glucose solution should be used for children with moderate to severe dehydration and persist vomiting.

Antibiotic therapy is usually not required for patients with gastroenteritis because it does not affect the clinical course of the majority of cases. Severe systemic manifestations associated with bacterial gastroenteritis (notably Shigella, Campylobacter, Yersinia and cholera) probably require antibiotics. Infants with salmonella gastroenteritis less than 3 months of age should be treated with an antibiotic, such as third-generation cephalosporin or a quinolone depending on the regional resistance pattern. Patients with typhoid fever and E. histolytica should also receive antibiotic treatment.

Viral fevers explained

Medical reviewer:Dr Ann Nainan

Last reviewed: 18/03/2021

Medically reviewed

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If you check your temperature and it’s higher than normal, you might have a fever – and viruses are a common cause.

Read on to learn more about viral fever symptoms, diagnosis and treatment, plus when you should see a doctor.

What is a viral fever?

A ‘normal’ body temperature varies from person to person and also changes throughout the day. But a high temperature, or fever, is generally thought of as a body temperature of 38C or more.

Several health conditions can cause a fever but it’s usually a sign that your body is fighting off infection by ‘microorganisms’, such as bacteria or viruses. A viral fever is a high temperature that’s caused by a virus.

What causes a viral fever?

Common viruses that cause fever include cold and flu viruses and viruses that infect your tummy and gut.

But any type of viral infection can cause a fever. This is because many viruses are sensitive to changes in temperature, so fever is one of your body’s ways of fighting the infection.

You can become infected by a virus in different ways. Cold and flu viruses, for example, can spread if you breathe in droplets from the cough or sneeze of an infected person. With tummy bugs such as norovirus, on the other hand, you get ill from eating food that has the virus in it. And some other viruses can be spread through insect bites.

Some viruses can cause fever and serious illness, which can lead to external and internal bleeding. This is called viral haemorrhagic fever. Viruses that can cause haemorrhagic fever include Ebola, dengue virus, hantavirus and the yellow fever virus.

What are the common viral fever symptoms?

Signs of a fever include:

• a temperature of 38C or higher
• a hot chest and back
• warm, red skin
• sweating
• shivering (chills)

You might also have other symptoms, but these will mainly be due to whatever’s causing the fever, rather than the fever itself. They can include:

• aches and pains
• headache
• tiredness and weakness

When to see a doctor

There are certain warning signs to watch out for when you have a fever. If you notice any of the following, you should see a doctor straight away:

• confusion
• severe headache
• stiff neck
• small, flat purplish red spots on your skin
• low blood pressure
• fast heart rate and/or breathing
• shortness of breath
• a temperature of more than 40C

You should also get medical advice if:

• you’re travelling in or have recently been to an area where a serious infectious disease is common
• you’re taking drugs that affect your immune system
• your fever lasts for more than 24 to 48 hours

How is a viral fever diagnosed?

If you have a fever, it’s likely that it’s caused by either a viral or bacterial infection. Your doctor may want to check if bacteria or a virus made you ill by looking at your medical history and doing a physical examination and sometimes simple tests, such as a urine test.

If it isn’t a bacterial infection, it’s often difficult to know exactly what virus has caused a fever. But the good news is that viral fevers usually go away without treatment. Unless your symptoms are severe, you probably won’t need further tests.

However, other tests may be needed if you live or work around certain animals or insects that carry diseases, or if you’ve recently been in areas where a particular virus is common.

What viral fever medicines and treatments are available?

A viral fever can usually be managed at home with self-care treatments to reduce symptoms, such as:

• resting as much as possible
• drinking plenty of fluids to avoid dehydration
• taking medication that reduces fever and pain, such common painkillers – ask your doctor or pharmacist about how to use these medicines safely

Please note that this advice is for adults only and doesn’t apply to children.

Should I get antibiotics for viral fever?

No – antibiotics can’t be used to treat viral infections.

Antibiotics are designed to fight bacteria, which are completely different organisms, so they won’t do anything to make you feel better if you have a viral fever. The only time you should take antibiotics with a viral infection is if your doctor thinks you also have a bacterial infection.

If you take antibiotics when you don’t need to, they may not work as effectively when they’re really needed.

Key points

• if you have a body temperature of 38C or more, you probably have a fever
• viruses and bacteria are common causes of fever
• a viral fever usually goes away on its own and doesn’t need specific testing or treatment
• certain other symptoms with a fever can suggest a more serious condition that needs treatment

Common cold – Symptoms and causes

Overview

The common cold is a viral infection of your nose and throat (upper respiratory tract). It’s usually harmless, although it might not feel that way. Many types of viruses can cause a common cold.

Healthy adults can expect to have two or three colds each year. Infants and young children may have even more frequent colds.

Most people recover from a common cold in a week or 10 days. Symptoms might last longer in people who smoke. Generally, you don’t need medical attention for a common cold. However, if symptoms don’t improve or if they get worse, see your doctor.

Symptoms

Symptoms of a common cold usually appear one to three days after exposure to a cold-causing virus. Signs and symptoms, which can vary from person to person, might include:

• Runny or stuffy nose
• Sore throat
• Cough
• Congestion
• Slight body aches or a mild headache
• Sneezing
• Low-grade fever
• Generally feeling unwell

The discharge from your nose may start out clear and become thicker and yellow or green as a common cold runs its course. This doesn’t usually mean you have a bacterial infection.

When to see a doctor

For adults — generally, you don’t need medical attention for a common cold. However, seek medical attention if you have:

• Symptoms that worsen or fail to improve
• Fever greater than 101.3 F (38.5 C) lasting more than three days
• Fever returning after a fever-free period
• Shortness of breath
• Wheezing
• Severe sore throat, headache or sinus pain

For children — in general, your child doesn’t need to see his or her doctor for a common cold. But seek medical attention right away if your child has any of the following:

• Fever of 100.4 F (38 C) in newborns up to 12 weeks
• Rising fever or fever lasting more than two days in a child of any age
• Severe symptoms, such as headache, throat pain or cough
• Difficulty breathing or wheezing
• Ear pain
• Extreme fussiness
• Unusual drowsiness
• Lack of appetite

Causes

Although many types of viruses can cause a common cold, rhinoviruses are the most common cause.

A cold virus enters your body through your mouth, eyes or nose. The virus can spread through droplets in the air when someone who is sick coughs, sneezes or talks.

It also spreads by hand-to-hand contact with someone who has a cold or by sharing contaminated objects, such as eating utensils, towels, toys or telephones. If you touch your eyes, nose or mouth after such contact, you’re likely to catch a cold.

Risk factors

These factors can increase your chances of getting a cold:

• Age. Infants and young children are at greatest risk of colds, especially if they spend time in child care settings.
• Weakened immune system. Having a chronic illness or otherwise weakened immune system increases your risk.
• Time of year. Both children and adults are more likely to get colds in fall and winter, but you can get a cold anytime.
• Smoking. You’re more likely to catch a cold and to have more-severe colds if you smoke or are around secondhand smoke.
• Exposure. If you’re around crowds, such as at school or on an airplane, you’re likely to be exposed to viruses that cause colds.

Complications

These conditions can occur along with your cold:

• Acute ear infection (otitis media). This occurs when bacteria or viruses enter the space behind the eardrum. Typical signs and symptoms include earaches or the return of a fever following a common cold.
• Asthma. A cold can trigger wheezing, even if you don’t have asthma. If you have asthma, a cold can make it worse.
• Acute sinusitis. In adults or children, a common cold that doesn’t resolve can lead to swelling and pain (inflammation) and infection of the sinuses.
• Other infections. A common cold can lead to other infections, including strep throat, pneumonia, and croup or bronchiolitis in children. These infections need to be treated by a doctor.

Prevention

There’s no vaccine for the common cold, but you can take commonsense precautions to slow the spread of cold viruses:

• Wash your hands. Wash your hands thoroughly and often with soap and water for at least 20 seconds. If soap and water aren’t available, use an alcohol-based hand sanitizer that contains at least 60% alcohol. Teach your children the importance of hand-washing. Avoid touching your eyes, nose or mouth with unwashed hands.
• Disinfect your stuff. Clean and disinfect high-touch surfaces, such as doorknobs, light switches, electronics, and kitchen and bathroom countertops daily. This is especially important when someone in your family has a cold. Wash children’s toys periodically.
• Cover your cough. Sneeze and cough into tissues. Throw away used tissues right away, then wash your hands thoroughly. If you don’t have a tissue, sneeze or cough into the bend of your elbow and then wash your hands.
• Don’t share. Don’t share drinking glasses or eating utensils with other family members. Use your own glass or disposable cups when you or someone else is sick. Label the cup or glass with the name of the person using it.
• Stay away from people with colds. Avoid close contact with anyone who has a cold. Stay out of crowds, when possible. Avoid touching your eyes, nose and mouth.
• Review your child care center’s policies. Look for a child care setting with good hygiene practices and clear policies about keeping sick children at home.
• Take care of yourself. Eating well and getting exercise and enough sleep is good for your overall health.

What Is a Fever? How to Treat It & How Long It Lasts │ Vicks

Kids Health Information : Viral illnesses

A virus is a germ that causes infections such as the common cold, bronchiolitis, tonsillitis, ear infections, influenza, mumps and chickenpox. There are hundreds of different viruses.

Colds are very common in healthy children and on average, preschool children get at least six colds per year. It is common for healthy children to have up to 12 viral illnesses per year in the first few years of life. It is also common for children to get sick from one virus shortly after getting better from a different one, so it can seem they are sick all the time. As children get older, the frequency of catching viral illnesses usually reduces.

Viruses can easily spread when children have close contact with each other. Most viruses are mild, and the best treatment is rest at home.

Signs and symptoms of viruses

If your child has a virus, they may show a variety of symptoms, including:

• a blocked or runny nose
• red, watery eyes
• a sore throat
• fever
• rashes that turn white (blanch) for a second or so after you push on them with a finger (you could also press the side of a clear drinking glass over the rash and watch to see if it blanches)
• coughing or sneezing
• vomiting and/or diarrhoea
• wanting to sleep more (lethargy)
• not wanting to eat
• feeling generally unwell.

While most viruses are mild in children, infants under three months of age may become very ill quickly and need to be assessed by a doctor.

Care at home

Viruses cannot be treated with antibiotics. The best treatment is rest at home to allow your child’s immune system to fight the virus.

Here are some simple measures that can make your child more comfortable:

• Give your child small amounts to drink frequently when awake, such as a mouthful of water every 15 minutes or so. This helps to ease a sore throat by keeping it moist, and replaces the fluid lost due to having a fever, vomiting or diarrhoea. Water is best, but rehydrating icy poles are also a good way of providing fluids to your child.
• Giving enough fluid is particularly important in infants – this should be breastmilk or formula, or rehydration fluids such as electrolytes. See our fact sheet
  Dehydration.
• Do not be concerned if your child does not eat for a few days. When they feel better they will start eating again.
• Allow your child to rest.
• Use saline nasal (nose) drops to help clear a blocked nose in babies.  A baby with a clear nose will find it easier to feed.
• Give your child paracetamol or ibuprofen for pain, or if your child is miserable, irritable or lethargic. See our fact sheet
  Pain relief for children. Do not give your child aspirin. Carefully check the label for the correct dose and make sure you are not already giving your child any other products containing paracetamol or ibuprofen (such as some cough medicines and cold-and-flu preparations).
• Do not use paracetamol or ibuprofen just to reduce fever. Fever helps the body get better naturally.
• Do not use other remedies unless advised by a doctor or health care professional.

Your child is likely to feel better in a few days, but may be unwell for up to two weeks. A cough can linger for several weeks.

Most rashes are mild and do not cause your child any distress, although some rashes can cause a lot of itching. Talk to your local pharmacist about treatments that can help relieve itchy rashes. A rash often lasts a few days before going away on its own. Sometimes a rash appears when a fever goes away. When this rash appears, it means the child is getting better. See our fact sheet
Rashes.

When to see a doctor

If your child is not improving after 48 hours, or is getting worse, take them to see your GP. Also see your GP if your child has any of the following:

• pain that does not improve with paracetamol or ibuprofen
• persistent vomiting and diarrhoea (see our fact sheet
  Gastroenteritis)
• a high fever that is not improving after 48 hours
• refusal to drink or have an icy pole for six hours
• a rash or spot that does not blanch when you push on it
• less than half the usual number of wet nappies
• they are giving you concern for any other reason
• Poor feeding or fever in an infant aged three months or younger

Seek immediate care from your doctor or a hospital emergency department if your child:

• is very pale or hard to wake
• has trouble breathing
• has a rash and gets a headache, stiff neck or back pain
• is unwell with a fever and a skin rash (small bright red spots or purple spots or unexplained bruises) that does not turn to skin-colour (blanch) when you press on it (see our fact sheet
  Meningococcal infection)
• Poor feeding or fever in an infant aged one month or younger

Sometimes viruses can trigger asthma (if your child has a diagnosis of asthma) or a wheeze (whistling sound while breathing). If this happens, treat the asthma as you normally would. If the wheeze is new and your child is having difficulty breathing, take them to see your GP.

How are viral illnesses spread?

A virus can spread from person to person in tiny droplets from the nose (sneezing or a runny nose) and mouth (saliva or a cough). Viruses can also spread via vomit or faeces (poo), especially when someone has diarrhoea.

There is usually a delay between when a child is exposed to the virus and when they develop the illness. This delay is generally a few days, but some viruses may take up to two or three weeks before symptoms appear.

Good hygiene reduces the chance of getting viruses or passing them onto others. Good hygiene includes:

• regularly washing hands thoroughly
• not sharing cups or cutlery
• encouraging children to cough or sneeze into their elbow
• using tissues instead of hankies – teach your child to throw tissues into the bin as soon as they have used them and to wash their hands afterwards.

If your child is unwell with a virus, keep them home from child care, kindergarten or school until they are well again.

It is just about impossible to prevent your child from catching viruses, but you can help keep your child’s immune system in good shape by ensuring they have a balanced diet and plenty of sleep. Most children do not need to take vitamins on a daily basis. It is important to be up to date with your child’s immunisations to prevent viruses such as measles, mumps, rubella and chickenpox (varicella).

Key points to remember

• Viral illnesses are very common in children and are easily spread around child care, kindergarten or school.
• It is common for children to have up to 12 viral infections a year in the first few years of life, and it can seem like they are sick all the time.
• The best treatment is rest at home.  Antibiotics will not help treat viral illnesses.
• If your child does not improve after 48 hours, or their symptoms get worse, see your GP.

For more information

Common questions our doctors are asked

Do I need to see a doctor to have my child’s virus diagnosed?

If your child is only experiencing mild symptoms that are relieved by paracetamol or ibuprofen, and they seem to be getting better after 48 hours, there is no need to visit a doctor. Often, it is very difficult to determine which particular virus your child has, and it doesn’t matter anyway, as treatment is the same – rest at home, and no antibiotics, as antibiotics do not help viruses.

What natural remedies can I give my child to help them feel better when they have a cold?

We do not recommend giving treatments – whether medical or natural – to children without professional medical advice. As outlined in this fact sheet, you can usually care for your child at home when they have a cold by giving them plenty of fluids, allowing them to rest and providing simple
analgesia (e. g. paracetamol) if they are uncomfortable.

Over-the-counter products such as vitamins or supplements (e.g. vitamin C, multivitamins) are not necessary. These products generally have no or limited scientific evidence to prove their effectiveness in preventing or treating viruses such as colds.

Remedies that are usually passed down in families (e.g. staying warm, avoiding going to bed with wet hair, not going outside with bare feet or wet hair and staying indoors) have not been proven to prevent colds. These were developed before it was discovered that colds are caused by viruses.

Developed by The Royal Children’s Hospital General Medicine and Infectious Diseases departments and Victorian Department of Health and Human Services. We acknowledge the input of RCH consumers and carers.

Reviewed July 2020.

Kids Health Info is supported by The Royal Children’s Hospital Foundation. To donate, visit 
www. rchfoundation.org.au.

Viral Infections – Sepsis Alliance

A virus is a tiny agent (germ) that lives inside living cells, or host cells. Viruses need living cells to be able to replicate or reproduce. There are thousands of viruses, some more common than others. For example, the common cold and the flu are viruses, but so are Ebola and HIV. Viral infections that may be minor in normal, healthy individuals can be quite severe for people who have a weakened immune system. Almost any virus can lead to sepsis.

Sometimes called blood poisoning, sepsis is the body’s often deadly response to infection. Sepsis kills and disables millions and requires early suspicion and treatment for survival.

Sepsis and septic shock can result from an infection anywhere in the body, such as pneumonia, influenza, or urinary tract infections. While bacterial infections are the most common cause of sepsis, viral infections can cause sepsis too. Like strokes or heart attacks, sepsis is a medical emergency that requires rapid diagnosis and treatment.  Worldwide, one-third of people who develop sepsis die. Many who do survive are left with life-changing effects, such as post-traumatic stress disorder (PTSD), chronic pain and fatigue, organ dysfunction (organs don’t work properly), and/or amputations.

Examples of viral infections

Viruses “hijack” normal, living cells in your body. They use these cells to replicate and multiply, eventually destroying the host cell – this is what makes you sick. Unlike bacterial infections that respond to antibiotics, viral infections are not so easy to treat. Many, like colds, run their course and your body heals on its own, but others, like HIV, do not.

Some of the more common viruses include:

• COVID-19, caused by a novel coronavirus
• Influenza (the flu)
• HIV, which can lead to AIDS
• Meningitis (there is also bacterial meningitis)
• Pneumonia (there is also bacterial pneumonia)
• Human papillomavirus (HPV)
• Herpes
• Rotavirus
• Chicken pox

Symptoms of viral infections

The signs and symptoms of a viral infection depend on what virus you have and how it affects your body. Here are a few examples:

Influenza:

• Fever
• Muscle ache
• Cough
• Sore throat
• Headache

Meningitis:

• Stiff neck
• Headache
• Fever
• Nausea and vomiting
• Rash
• Sensitivity to light (photophobia)
• Confusion

Prevention

Viruses are spread in different ways, depending on the virus. Hepatitis C, a liver disease, is spread through body fluid. On the other hand, influenza can be spread by coming in contact with the virus that has been left behind on an object, like a phone, or through droplets in the air, if someone with the flu sneezes or coughs in front of you. Not all viral infections can be prevented, but you can reduce your risk of contracting a virus in a few ways:

• Stay up-to-date with all recommended vaccines, even adults (To learn more about vaccines, visit Sepsis Prevention: Vaccinations)
• Wash your hands frequently
• Avoid contact with people who are ill
• Don’t share personal items

Treatment

For most viruses, treatment is for the symptoms, such as using over-the-counter pain relievers to ease pain and reduce fever, rest for fatigue, etc. , until the virus is gone. But the viruses themselves are not easy to treat. For example, treatment for hepatitis C, a liver disease, involves a strict medication regimen that can take from several weeks up to a few months before the virus is cleared from your body. Other viruses don’t have a cure, but there are medications that may speed healing if they are taken early enough after your exposure to the virus. These include medications for influenza and shingles (herpes zoster). Medications for other viruses, such as HIV, keep the virus in check, but aren’t a cure. They can prevent the virus from replicating and causing more damage.

Complications

Sometimes, people who have viral infections, such as influenza, can develop severe bacterial infections, in addition to the viral infection. For example, influenza and other respiratory viral illnesses, could lead to pneumonia.

If you suspect sepsis, call 9-1-1 or go to a hospital and tell your medical professional, “I AM CONCERNED ABOUT SEPSIS. ” 

Would you like to share your story about sepsis or read about others who have had sepsis? Please visit Faces of Sepsis, where you will find hundreds of stories from survivors and tributes to those who died from sepsis.

Updated June 10, 2021.

Dengue and severe dengue

Dengue is a mosquito-borne viral disease that has rapidly spread in all regions of WHO in recent years. Dengue virus is transmitted by female mosquitoes mainly of the species Aedes aegypti and, to a lesser extent, Ae. albopictus. These
mosquitoes are also vectors of chikungunya, yellow fever and Zika viruses. Dengue is widespread throughout the tropics, with local variations in risk influenced by rainfall, temperature, relative humidity and unplanned rapid urbanization.

Dengue causes a wide spectrum of disease. This can range from subclinical disease (people may not know they are even infected) to severe flu-like symptoms in those infected. Although less common, some people develop severe dengue, which can be any number
of complications associated with severe bleeding, organ impairment and/or plasma leakage. Severe dengue has a higher risk of death when not managed appropriately. Severe dengue was first recognized in the 1950s during dengue epidemics in the Philippines
and Thailand. Today, severe dengue affects most Asian and Latin American countries and has become a leading cause of hospitalization and death among children and adults in these regions.

Dengue is caused by a virus of the Flaviviridae family and there are four distinct, but closely related, serotypes of the virus that cause dengue (DENV-1, DENV-2, DENV-3 and DENV-4). Recovery from infection is believed to provide lifelong immunity against
that serotype. However, cross-immunity to the other serotypes after recovery is only partial, and temporary. Subsequent infections (secondary infection) by other serotypes increase the risk of developing severe dengue.

Dengue has distinct epidemiological patterns, associated with the four serotypes of the virus. These can co-circulate within a region, and indeed many countries are hyper-endemic for all four serotypes. Dengue has an alarming impact on both human health
and the global and national economies. DENV is frequently transported from one place to another by infected travellers; when susceptible vectors are present in these new areas, there is the potential for local transmission to be established.

Global burden of dengue

The incidence of dengue has grown dramatically around the world in recent decades. A vast majority of cases are asymptomatic or mild and self-managed, and hence the actual numbers of dengue cases are under-reported. Many cases are also misdiagnosed as
other febrile illnesses ^[1].

One modelling estimate indicates 390 million dengue virus infections per year (95% credible interval 284–528 million), of which 96 million (67–136 million) manifest clinically (with any severity of disease) ^[2]. Another study on
the prevalence of dengue estimates that 3.9 billion people are at risk of infection with dengue viruses. Despite a risk of infection existing in 129 countries ^[3], 70% of the actual burden is in Asia ^[2].

The number of dengue cases reported to WHO increased over 8 fold over the last two decades, from 505,430 cases in 2000, to over 2.4 million in 2010, and 5.2 million in 2019. Reported deaths between the year 2000 and 2015 increased from 960 to 4032.

This alarming increase in case numbers is partly explained by a change in national practices to record and report dengue to the Ministries of Health, and to the WHO. But it also represents government recognition of the burden, and therefore the pertinence
to report dengue disease burden. Therefore, although the full global burden of the disease is uncertain, this observed growth only brings us closer to a more accurate estimate of the full extent of the burden.

Distribution and outbreaks of dengue

Before 1970, only 9 countries had experienced severe dengue epidemics. The disease is now endemic in more than 100 countries in the WHO regions of Africa, the Americas, the Eastern Mediterranean, South-East Asia and the Western Pacific. The America, South-East
Asia and Western Pacific regions are the most seriously affected, with Asia representing ~70% of the global burden of disease.

Not only is the number of cases increasing as the disease spreads to new areas including Europe, but explosive outbreaks are occurring. The threat of a possible outbreak of dengue now exists in Europe; local transmission was reported for the first
time in France and Croatia in 2010 and imported cases were detected in 3 other European countries. In 2012, an outbreak of dengue on the Madeira islands of Portugal resulted in over 2000 cases and imported cases were detected in mainland Portugal
and 10 other countries in Europe. Autochthonous cases are now observed on an almost annual basis in many European countries. Among travellers returning from low- and middle-income countries, dengue is the second most diagnosed cause of fever after malaria.

In 2020, dengue affected several countries, with increased number of cases in Bangladesh, Brazil, Cook Islands, Ecuador, India, Indonesia, Maldives, Mauritania, Mayotte (Fr), Nepal, Singapore, Sri Lanka, Sudan, Thailand, Timor-Leste and Yemen. In 2021,
dengue continues to affect Brazil,  Cook Islands, Colombia, Fiji, Kenya, Paraguay, Peru and Reunion island.

The COVID-19 pandemic is placing immense pressure on health care and management systems worldwide. WHO has emphasized the importance of sustaining efforts to prevent, detect and treat vector-borne diseases such as dengue and other arboviral diseases during
this crucial period, as case numbers increase in several countries, exposing urban populations at highest risk for both diseases. The combined impact of  COVID-19 and dengue epidemics can potentially result in devastating consequences for the populations at risk.

The largest number of dengue cases ever reported globally was in 2019. All WHO Regions were affected, and dengue transmission was recorded in Afghanistan for the first time.

The American Region alone reported 3.1 million cases, with more than 25,000 classified as severe. Despite this alarming number of cases, deaths associated with dengue were fewer than in the previous year. 

High number of cases were reported in Bangladesh (101,000), Malaysia (131,000) Philippines (420,000), Vietnam (320,000) in Asia.

The year 2016 was also characterized by large dengue outbreaks with the Region of the Americas reporting more than 2.38 million cases. During that year, Brazil alone contributed approximately 1.5 million cases, approximately three times higher than in
2014; 1032 dengue deaths were also reported in the region. In the same year, the Western Pacific Region reported more than 375,000 suspected cases of which the Philippines reported 176 411 and Malaysia 100 028 cases, representing a similar burden
to the previous year for both countries. The Solomon Islands declared an outbreak with more than 7000 suspected. In the African Region, Burkina Faso reported a localized outbreak of dengue with 1061 probable cases.

In 2017, a significant reduction was reported in the Americas – from 2 177 171 cases in 2016 to 584 263 cases in 2017. This represents a reduction of 73%. Panama, Peru and Aruba were the only countries that registered an increase in cases during 2017.

Similarly, a 53% reduction in severe dengue cases was also recorded during 2017. The post-Zika outbreak period (after 2016) saw a decline of cases of dengue and the exact factors leading to this fall are still unknown.

Transmission

Mosquito-to-human transmission

The virus is transmitted to humans through the bites of infected female mosquitoes, primarily the Aedes aegypti mosquito. Other species within the Aedes genus can also act as vectors, but their contribution is secondary to Aedes aegypti.

After feeding on an DENV-infected person, the virus replicates in the mosquito midgut, before it disseminates to secondary tissues, including the salivary glands. The time it takes from ingesting the virus to actual transmission to a new host is termed
the extrinsic incubation period (EIP). The EIP takes about 8-12 days when the ambient temperature is between 25-28°C ^[4-6]. Variations in the extrinsic incubation period are not only influenced by ambient temperature; a number of factors
such as the magnitude of daily temperature fluctuations^{[7, 8]}, virus genotype ^[9], and initial viral concentration ^[10] can also alter the time it takes for a mosquito to transmit virus. Once infectious, the mosquito
is capable of transmitting virus for the rest of its life.

Human-to-mosquito transmission

Mosquitoes can become infected from people who are viremic with DENV. This can be someone who has a symptomatic dengue infection, someone who is yet to have a symptomatic infection (they are pre-symptomatic), but also people who show no signs of illness
as well (they are asymptomatic) ^[11].

Human-to-mosquito transmission can occur up to 2 days before someone shows symptoms of the illness ^{[5, 11]}, up to 2 days after the fever has resolved ^[12].

Risk of mosquito infection is positively associated with high viremia and high fever in the patient; conversely, high levels of DENV-specific antibodies are associated with a decreased risk of mosquito infection (Nguyen et al. 2013 PNAS). Most people
are viremic for about 4-5 days, but viremia can last as long as 12 days ^[13].

Other modes of transmission

The primary mode of transmission of DENV between humans involves mosquito vectors. There is evidence however, of the possibility of maternal transmission (from a pregnant mother to her baby). While vertical transmission rates appear low, with the risk
of vertical transmission seemingly linked to the timing of the dengue infection during the pregnancy ^[14-17]. When a mother does have a DENV infection when she is pregnant, babies may suffer from pre-term birth, low birthweight, and fetal
distress ^[18].

Vector Ecology

The Aedes aegypti mosquito is considered the primary vector of DENV. It lives in urban habitats and breeds mostly in man-made containers. Ae. aegypti is a day-time feeder; its peak biting periods are early in the morning and in the evening
before sunset
^[19]  Female Ae. aegypti frequently feed multiple times between each egg-laying period ^[20]. Once a female has laid her eggs, these eggs can remain viable for several months, and will hatch when they in contact
with water.

Aedes albopictus, a secondary dengue vector in Asia, has spread to more than 32 states in the USA, and more than 25 countries in the European Region, largely due to the international trade in used tyres (a breeding habitat) and other goods (e.g.
lucky bamboo). Ae. albopictus is highly adaptive. Its geographical spread is largely due to its tolerance of colder conditions, as an egg and adult ^{[21, 22]}.   Aedes albopictus has been implicated as the primary vector
of DENV in a limited number of outbreak, where Aedes aegypti is either not present, or present in low numbers ^{[23, 24]}

Disease characteristics (signs and symptoms)

Dengue is a severe, flu-like illness that affects infants, young children and adults, but seldom causes death. Symptoms usually last for 2–7 days, after an incubation period of 4–10 days after the bite from an infected mosquito ^[25].
The World Health Organization classifies dengue into 2 major categories: dengue (with / without warning signs) and severe dengue. The sub-classification of dengue with or without warning signs is designed to help health practitioners triage patients
for hospital admission, ensuring close observation, and to minimise the risk of developing the more severe dengue (see below).

Dengue

Dengue should be suspected when a high fever (40°C/104°F) is accompanied by 2 of the following symptoms during the febrile phase:

• severe headache
• pain behind the eyes
• muscle and joint pains
• nausea
• vomiting
• swollen glands
• rash.  

Severe dengue

A patient enters what is called the critical phase normally about 3-7 days after illness onset. It is at this time, when the fever is dropping (below 38°C/100°F) in the patient, that warning signs associated with severe dengue can manifest. Severe
dengue is a potentially fatal complication, due to plasma leaking, fluid accumulation, respiratory distress, severe bleeding, or organ impairment.

Warning signs that doctors should look for include:

• severe abdominal pain
• persistent vomiting
• rapid breathing
• bleeding gums
• fatigue
• restlessness
• blood in vomit. 

If patients manifest these symptoms during the critical phase, close observation for the next 24–48 hours is essential so that proper medical care can be provided, to avoid complications and risk of death.

Diagnostics

Several methods can be used for diagnosis of DENV infection. These include virological tests (that directly detect elements of the virus) and serological tests, which detect human-derived immune components that are produced in response to the virus).
Depending on the time of patient presentation, the application of different diagnostic methods may be more or less appropriate. Patient samples collected during the first week of illness should be tested by both serological and virological methods
(RT-PCR).

Virological methods

The virus may be isolated from the blood during the first few days of infection. Various reverse transcriptase–polymerase chain reaction (RT–PCR) methods are available. In general, RT–PCR assays are sensitive, but they require specialised
equipment and technical training for staff implementing the test, therefore they are not always available in all medical facilities. RT–PCR products from clinical samples may also be used for genotyping of the virus, allowing comparisons with
virus samples from various geographical sources.

The virus may also be detected by testing for a virus-produced protein, called NS1. There are commercially-produced rapid diagnostic tests available for this, because it takes only ~20 mins to determine the result, and the test does not require specialized
laboratory techniques or equipment.

Serological methods

Serological methods, such as enzyme-linked immunosorbent assays (ELISA), may confirm the presence of a recent or past infection, with the detection of IgM and IgG anti-dengue antibodies. IgM antibodies are detectable ~1 week after infection and are highest
at 2 to 4 weeks after the onset of illness. They remain detectable for about 3 months. The presence of IgM is indicative of a recent DENV infection. IgG antibody levels take longer to develop than IgM, but IgG remain in the body for years. The presence
of IgG is indicative of a past infection.

Treatment

There is no specific treatment for dengue fever.

Fever reducers and pain killers can be taken to control the symptoms of muscle aches and pains, and fever.

• The best options to treat these symptoms are acetaminophen or paracetamol.
• NSAIDs (non-steroidal anti-inflammatory drugs), such as ibuprofen and aspirin should be avoided. These anti-inflammatory drugs act by thinning the blood, and in a disease with risk of hemorrhage, blood thinners may exacerbate the prognosis.

For severe dengue, medical care by physicians and nurses experienced with the effects and progression of the disease can save lives – decreasing mortality rates from more than 20% to less than 1%. Maintenance of the patient’s body fluid volume is
critical to severe dengue care. Patients with dengue should seek medical advice upon the appearance of warning signs.

Vaccination against dengue

The first dengue vaccine, Dengvaxia® (CYD-TDV) developed by Sanofi Pasteur was licensed in December 2015 and has now been approved by regulatory authorities in ~20 countries. In November 2017, the results of an additional analysis to retrospectively
determine serostatus at the time of vaccination were released. The analysis showed that the subset of trial participants who were inferred to be seronegative at time of first vaccination had a higher risk of more severe dengue and hospitalizations
from dengue compared to unvaccinated participants. As such, use of the vaccine is targeted for persons living in endemic areas, ranging from 9-45 years of age, who have had at least 1 documented dengue virus infection previously.

WHO position on the CYD-TDV vaccine

As described in the WHO position paper on the Dengvaxia vaccine (September 2018) the live attenuated dengue vaccine CYD-TDV has been shown in clinical trials to be efficacious and safe in persons who have had a previous dengue virus infection (seropositive
individuals). However, it carries an increased risk of severe dengue in those who experience their first natural dengue infection after vaccination (those who were seronegative at the time of vaccination). For countries considering vaccination as
part of their dengue control programme, pre-vaccination screening is the recommended strategy. With this strategy, only persons with evidence of a past dengue infection would be vaccinated (based on an antibody test, or on a documented laboratory
confirmed dengue infection in the past). Decisions about implementing a pre-vaccination screening strategy will require careful assessment at the country level, including consideration of the sensitivity and specificity of available tests and of local
priorities, dengue epidemiology, country-specific dengue hospitalization rates, and affordability of both CYD-TDV and screening tests.

Vaccination should be considered as part of an integrated dengue prevention and control strategy. There is an ongoing need to adhere to other disease preventive measures such as well-executed and sustained vector control. Individuals, whether vaccinated
or not, should seek prompt medical care if dengue-like symptoms occur.

Prevention and control

If you know you have dengue, avoid getting further mosquito bites during the first week of illness. Virus may be circulating in the blood during this time, and therefore you may transmit the virus to new uninfected mosquitoes, who may in turn infect other
people.

The proximity of mosquito vector breeding sites to human habitation is a significant risk factor for dengue as well as for other diseases that Aedes mosquito transmit. At present, the main method to control or prevent the transmission of dengue
virus is to combat the mosquito vectors. This is achieved through:

• Prevention of mosquito breeding:
• Preventing mosquitoes from accessing egg-laying habitats by environmental management and modification;
• Disposing of solid waste properly and removing artificial man-made habitats that can hold water;
• Covering, emptying and cleaning of domestic water storage containers on a weekly basis;
• Applying appropriate insecticides to water storage outdoor containers;

• Personal protection from mosquito bites:
• Using of personal household protection measures, such as window screens, repellents, insecticide treated materials, coils and vaporizers. These measures must be observed during the day both inside and outside of the home (e. g.: at work/school)
  because the primary mosquito vectors bites throughout the day;
• Wearing clothing that minimises skin exposure to mosquitoes is advised;

• Community engagement:
• Educating the community on the risks of mosquito-borne diseases;
• Engaging with the community to improve participation and mobilization for sustained vector control;

• Reactive vector control:
• Emergency vector control measures such as applying insecticides as space spraying during outbreaks may be used by health authorities;

• Active mosquito and virus surveillance:
• Active monitoring and surveillance of vector abundance and species composition should be carried out to determine effectiveness of control interventions;
• Prospectively monitor prevalence of virus in the mosquito population, with active screening of sentinel mosquito collections;

In addition, there is ongoing research amongst many groups of international collaborators in search of novel tools and innovative strategies that will contribute in global efforts to interrupt transmission of dengue, as well as other mosquito-borne diseases.
The integration of vector management approaches is encouraged by WHO to achieve sustainable, effective locally adapted vector control interventions.

WHO response

WHO responds to dengue in the following ways:

• supports countries in the confirmation of outbreaks through its collaborating network of laboratories;

• provides technical support and guidance to countries for the effective management of dengue outbreaks;

• supports countries to improve their reporting systems and capture the true burden of the disease;

• provides training on clinical management, diagnosis and vector control at the country and regional level with some of its collaborating centres;

• formulates evidence-based strategies and policies;

• support countries in the development of dengue prevention and control strategies and adopting the Global Vector Control Response (2017-2030)

• reviews the development of new tools, including insecticide products and application technologies;

• gathers official records of dengue and severe dengue from over 100 Member States; and

• publishes guidelines and handbooks for surveillance, case management, diagnosis, dengue prevention and control for Member States.

Cited references

 [1] Waggoner, J.J., et al., Viremia and Clinical Presentation in Nicaraguan Patients Infected Wi1. Waggoner, J.J., et al., Viremia and Clinical Presentation in Nicaraguan Patients Infected With Zika Virus, Chikungunya Virus, and Dengue Virus. Clinical Infectious Diseases, 2016. 63(12): p. 1584-1590. 

 [2] Bhatt, S., et al., The global distribution and burden of dengue. Nature, 2013. 496(7446): p. 504–507.

 [3] Brady, O.J., et al., Refining the global spatial limits of dengue virus transmission by evidence-based consensus. PLOS Neglected Tropical Diseases, 2012. 6(8): p. e1760.

 [4] Tjaden, N.B., et al., Extrinsic Incubation Period of Dengue: Knowledge, Backlog, and Applications of Temperature Dependence. Plos Neglected Tropical Diseases, 2013. 7(6): p. 5.

[5] Siler, J.F., M.W. Hall, and A.P. Hitchens, Dengue: Its history, epidemiology, mechanism of transmission, etiology, clinical manifestations, immunity and prevention. 1926, Manila: Bureau of Science.

[6] Watts, D.M., et al., Effect of Temperature on the vector efficiency of Aedes aegypti for Dengue 2 virus. American Journal of Tropical Medicine and Hygiene, 1987. 36(1): p. 143-152.

[7] Carrington, L.B., et al., Fluctuations at low mean temperatures accelerate dengue virus transmission by Aedes aegypti. PLOS Neglected Tropical Diseases, 2013. 7(4): p. e2190.

[8] Lambrechts, L., et al., Impact of daily temperature fluctuations on dengue virus transmission by Aedes aegypti. Proceedings of the National Academy of Sciences of the United States of America, 2011. 108(18):
p. 7460-7465.

[9] Anderson, J.R. and R. Rico-Hesse, Aedes aegypti vectorial capacity is determined by the infecting genotype of dengue virus. American Journal of Tropical Medicine and Hygiene, 2006. 75(5): p. 886-892.

[10] Ye, Y.X.H., et al., Wolbachia Reduces the Transmission Potential of Dengue-Infected Aedes aegypti. PLOS Neglected Tropical Diseases, 2015. 9(6): p. e0003894.

[11] Duong, V., et al., Asymptomatic humans transmit dengue virus to mosquitoes. Proceedings of the National Academy of Sciences of the USA, 2015. 112(47): p. 14688–14693.

[12] Nguyen, N.M., et al., Host and viral features of human dengue cases shape the population of infected and infectious Aedes aegypti mosquitoes. Proceedings of the National Academy of Sciences of the United States
of America, 2013. 110(22): p. 9072-9077.

[13] Gubler, D.J., et al., Viraemia in patients with naturally acquired dengue infection. Bulletin of the World Health Organisation, 1981. 59: p. 623-630.

[14] Basurko, C., et al., Estimating the Risk of Vertical Transmission of Dengue: A Prospective Study. American Journal of Tropical Medicine and Hygiene, 2018. 98(6): p. 1826-1832.

[15] Mazarin, N., J.M. Rosenthal, and J. Devenge, Mother infant dengue transmission during the 2009-2010 dengue epidemic: Observation of four cases. Archives De Pediatrie, 20141.  Waggoner, J.J., et al., Viremia
and Clinical Presentation in Nicaraguan Patients Infected With Zika Virus, Chikungunya Virus, and Dengue Virus. Clinical Infectious Diseases, 2016. 63(12): p. 1584-1590.

[16] Sinhabahu,
V.P., R. Sathananthan, and G.N. Malavige, Perinatal
transmission of dengue: a case report. BMC Research Notes, 2014. 7(795).

[17] Basurko,
C., et al., Maternal and foetal
consequences of dengue fever during pregnancy. European Journal of
Obstetrics & Gynecology and Reproductive Biology, 2009. 147(1): p. 29-32.

[18] Pouliot,
S.H., et al., Maternal Dengue and
Pregnancy Outcomes A Systematic Review. Obstetrical & Gynecological
Survey, 2010. 65(2): p. 107-118.

[19] Trpis,
M., et al., DIEL PERIODICITY IN LANDING
OF AEDES-AEGYPTI ON MAN. Bulletin of the World Health Organization, 1973. 48(5): p. 623-629.

[20] Scott,
T.W., et al., Longitudinal studies of
Aedes aegypti (Diptera: Culicidae) in Thailand and Puerto Rico: Blood feeding
frequency. Journal of Medical Entomology, 2000. 37(1): p. 89-101.

[21] Medlock,
J.M., et al., Analysis of the potential
for survival and seasonal activity of Aedes albopictus (Diptera: Culicidae) in
the United Kingdom. Journal of Vector Ecology, 2006. 31(2): p. 292-304.

[22] Romi,
R., F. Severini, and L. Toma, Cold acclimation
and overwintering of female Aedes albopictus in Roma. Journal of the
American Mosquito Control Association, 2006. 22(1): p. 149-151.

[23] Paupy,
C., et al., Comparative role of Aedes
albopictus and Aedes aegypti in the emergence of dengue and chikungunya in
Central Africa. Vector-Borne and Zoonotic Diseases, 2010. 10(3): p. 259-266.

[24] Metselaar,
D., et al., AN OUTBREAK OF TYPE-2 DENGUE
FEVER IN THE SEYCHELLES, PROBABLY TRANSMITTED BY AEDES-ALBOPICTUS (SKUSE).
Bulletin of the World Health Organization, 1980. 58(6): p. 937-943.

[25] World
Health, O., Dengue: Guidelines for
Diagnosis, Treatment, Prevention and Control. Dengue: Guidelines for
Diagnosis, Treatment, Prevention and Control. 2009, Geneva: World Health
Organization. 1-147.

Lassa Fever

Background

The virus that causes Lassa disease was first described in the 50s of the last century, but was identified only in 1969. The virus contains single-stranded RNA and belongs to the arenaviruses (Arenaviridae) family.

Approximately 80% of people infected with the Lassa virus have no symptoms. In every fifth case, the infection leads to the development of a serious illness in which the virus infects several organs, in particular the liver, spleen and kidneys.

Lassa fever is a zoonotic disease, meaning that humans become infected through contact with infected animals. The animal reservoir, or carrier, of the Lassa virus is the rodent of the species Mastomys, commonly known as the “multi-nipple rat.” Mastomys rats infected with the Lassa virus do not get sick themselves, but are capable of transmitting the virus through urine and droppings.

Due to the large discrepancies in the clinical picture, the identification of the disease in patients is difficult. However, once the disease is confirmed in an individual community, an outbreak can be controlled by immediate isolation of patients, adequate infection control and infection control measures, and careful contact tracing.

It is known that Lassa fever is endemic in Benin (the first case of infection was reported in November 2014), Guinea, Ghana (the first case was diagnosed in October 2011), Liberia, Mali (the first case was diagnosed in February 2009), Sierra Leone and Nigeria, but it is possible that cases are occurring in other West African countries.

Lassa fever symptoms

The incubation period for Lassa fever lasts from 6 to 21 days.Early symptoms of illness, such as high fever, general weakness, and malaise, usually begin gradually. After a few days, headache, sore throat, muscle aches, chest pains, nausea, vomiting, diarrhea, cough, and abdominal pain may appear. In severe forms of the disease, swelling of the face may develop, fluid may appear in the pulmonary sinuses, bleeding from the mouth, nose, vagina or gastrointestinal tract, and blood pressure may drop. Protein can be found in the urine.Later, shock, seizures, tremors, disorientation, and coma may occur. Deafness develops in 25% of cured patients. Half of these patients experience partial return of hearing after 1–3 months. During the recovery period, temporary hair loss and gait disturbances may occur.

In fatal cases, death usually occurs within 14 days of the onset of symptoms. The disease is particularly severe in the later stages of pregnancy, with maternal mortality and / or fetal loss rates exceeding 80% during the last trimester.

Transmission

Typically, humans become infected with the Lassa virus through contact with the urine or droppings of infected Mastomys rats. Lassa virus can also be spread from person to person through direct contact with the blood, urine, faeces, or other secretions of a person infected with Lassa fever. There is no epidemiological data confirming the transmission of the Lassa virus by airborne droplets from person to person. Human-to-human transmission occurs in both communities and healthcare settings through the use of infected medical equipment, in particular through repeated use of needles.There is evidence of sexual transmission of the Lassa virus.

Lassa fever affects both women and men of all age groups. People living in rural areas, where Mastomys rats tend to be found, are at greatest risk, especially in communities with poor sanitation or cramped living conditions. Health care workers who care for patients with Lassa fever in the absence of appropriate barrier and infection control techniques are at risk.

Diagnostics

Due to the varied and nonspecific symptoms of Lassa fever, clinical diagnosis, especially in the early stages of the disease, is often difficult. Lassa fever is difficult to distinguish from other viral haemorrhagic fevers, such as Ebola virus disease, and many other diseases that cause fever, including malaria, shigellosis, typhoid fever, and yellow fever.

To establish a final diagnosis, testing is necessary, which is possible only in specialized laboratories.Laboratory specimens can be hazardous and therefore must be handled with the strictest precautions. A definitive diagnosis of Lassa virus infection can only be made in the laboratory with the following tests:

• Enzyme-linked immunosorbent assay (ELISA)
• Antigen detection tests
• Reverse transcription polymerase chain reaction (RT-PCR) method
• Isolation of the virus by cell culture.

Treatment and vaccines

In the early stages of clinically manifest disease, the antiviral drug ribavirin is considered an effective treatment for Lassa fever. There is no information on the effectiveness of ribavirin as a post-exposure prophylactic agent for Lassa fever.

There is currently no vaccine for Lassa fever.

Prevention and control

Prevention of Lassa fever is based on good hygiene practices at the community level in order to control the entry of rodents into dwellings.Effective measures include storing grain and other food in containers that are not accessible to rodents, removing waste disposal sites from homes, keeping homes clean, and keeping cats. Since the population of Mastomys in endemic areas is very large, their complete eradication is not possible. Family members should always take precautions to avoid contact with blood and body fluids when caring for sick people.

When caring for patients in healthcare settings, regardless of the presumptive diagnosis, healthcare providers should always follow standard infection prevention and control measures.These measures include basic hand hygiene, respiratory hygiene, use of personal protective equipment (against splashing or other contact with infectious materials), safe injection techniques, and safe burials.

Healthcare professionals caring for patients with suspected or confirmed Lassa fever need to take additional infection control measures to prevent contact with patients’ blood and body fluids, and with infected surfaces or materials such as clothing and bedding.For close contact with patients with Lassa fever (within one meter), healthcare providers need face protection (face shield or medical mask and goggles), a clean, non-sterile long-sleeved gown and gloves (some procedures require sterile gloves).

Laboratory workers are also at risk. Human and animal specimens for the study of Lassa virus infection should be handled by trained personnel and the study should be conducted in laboratories with maximum biosecurity.

On rare occasions, travelers from areas endemic for Lassa fever bring the disease to other countries. Although cases of malaria, typhoid fever, and many other tropical infections are much more common, Lassa fever must be assumed when diagnosing fever patients returning from West Africa, especially from rural areas or hospitals in countries where Lassa fever is endemic. Upon admission of patients with suspected Lassa fever, healthcare providers should immediately contact local and state experts for guidance and arrange laboratory testing.

WHO activities

The Ministries of Health of Guinea, Liberia and Sierra Leone, WHO, the United States Office for Disaster Relief, the United Nations and other partners have worked together to create a network for Lassa haemorrhagic fever control within the Mano River Basin Union. The program is supporting the three countries to develop national strategies for the prevention of Lassa fever and improve laboratory diagnosis of Lassa fever and other dangerous diseases.It also includes specialized training in laboratory diagnostics, clinical patient management and environmental monitoring.

Clinical guidelines ARVI

Clinical recommendation:

“Acute respiratory viral infection (ARVI) in children. ICD 10: J00 / J02.9 / J04.0 / J04.1 / J04.2 / J06.0 / J06.9

Year of approval (revision frequency): 2018 (revision every 3 years)

Professional associations: Union of Pediatricians of Russia

Approved by: Union of Pediatricians of Russia

Appendix B. Patient Information

ARVI (acute respiratory viral infection) is the most common disease in children.

The cause of the disease is a variety of viruses. The disease develops more often in autumn, winter and early spring.

How to get infected with an infection that causes ARVI: most often by contact with the nasal mucosa or conjunctiva from hands contaminated by contact with a patient (for example, through a handshake) or with virus-infected surfaces (rhinovirus persists on them for up to a day).

Another route – airborne – by inhaling saliva particles released when sneezing, coughing or in close contact with a patient.

The period from infection to the onset of illness: in most cases – from 2 to 7 days. The allocation of viruses to patients (infectiousness for others) is maximum on the 3rd day after infection, sharply decreases by the 5th day; low shedding of the virus can persist for up to 2 weeks.

Signs of ARVI: The most frequent manifestation of ARVI in children is nasal congestion, as well as nasal discharge: transparent and / or white and / or yellow and / or green (the appearance of yellow or green nasal discharge is not a sign of adhesion bacterial infection!).The rise in temperature often lasts no more than 3 days, then the body temperature decreases. With some infections (influenza and adenovirus infection), the temperature above 38ºC remains longer (up to 5-7 days).

With ARVI, there may also be: sore throat, cough, redness of the eyes, sneezing.

Examinations: in most cases, additional examinations are not required for a child with ARVI.

Treatment: ARVI, in most cases, is benign, resolved within 10 days and does not always require medication.

Decrease in temperature: of a febrile child should be opened, wiped off with water T ° 25-30 ° C. In order to lower the temperature in children, it is permissible to use only 2 drugs – paracetamol or ibuprofen. Antipyretic drugs in healthy children ≥3 months are justified at temperatures above 39 – 39.5 ° C. With a less pronounced fever (38-38.5 ° C), temperature-lowering agents are indicated for children under 3 months of age, for patients with chronic pathology, as well as for temperature-related discomfort.Regular (course) intake of antipyretics is undesirable, a repeated dose is administered only after a new rise in temperature.

The alternation of these two drugs or their use in combination does not lead to an increase in the antipyretic effect.

Acetylsalicylic acid and nimesulide are not used for antipyretic purposes in children. It is highly undesirable to use metamizole in children due to the high risk of agranulocytosis.In many countries of the world, metamizole has been banned for use more than 50 years ago.

Antibiotics – do not affect viruses (the main cause of ARVI). Antibiotics are considered if a bacterial infection is suspected. Antibiotics must be prescribed by a doctor. Uncontrolled use of antibiotics can promote the development of resistant microbes and cause complications.

How to prevent the development of ARVI:

A sick child should be left at home (not taken to kindergarten or school).Measures to prevent the spread of viruses are of paramount importance: washing hands thoroughly after contact with a sick person.

It is also important to wear masks, wash surfaces in the patient’s environment, adhere to the ventilation regime. Getting the flu vaccine every year from 6 months of age reduces the risk of this infection. It has also been proven that vaccination of children against influenza and pneumococcal infection reduces the likelihood of developing acute otitis media in children and a complicated course of ARVI. There is no reliable evidence of a decrease in respiratory morbidity under the influence of various immunomodulators.The prophylactic efficacy of herbal preparations and vitamin C, homeopathic preparations has also not been proven.

Contact a specialist if:

– the child refuses to drink for a long time – you see changes in behavior: irritability, unusual drowsiness with a decrease in reaction to attempts to contact the child

– the child has difficulty breathing, noisy breathing, rapid breathing, retraction of the intercostal spaces, jugular fossa (the place located in front of the neck and chest)

– the child has convulsions against the background of an increased temperature – the child has delirium against the background of an increased temperature

– high body temperature (more than 38.4-38.5ºC) persists for more than 3 days

– nasal congestion persists without improvement for more than 10-14 days, especially if at the same time you see a “second wave” of an increase in body temperature and / or a deterioration in the child’s condition

– the child has ear pain and / or discharge from the ear – the child has a cough that lasts more than 10-14 days without improvement

90,000 In India, the possible cause of an unknown fatal disease was named

https: // ria.ru / 20210831 / bolezn-1747920229.html

India named a possible cause of an unknown fatal disease

India named a possible cause of an unknown fatal disease – RIA Novosti, 08/31/2021

India named a possible cause of an unknown fatal disease

the disease, which killed several dozen people in India last week, may be due to dengue fever. This is the opinion of the state authorities of RIA Novosti, 08/31/2021

2021-08-31T07: 24

2021-08-31T07: 24

2021-08-31T10: 56

in the world

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Southeast Asia

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NEW DELHI, Aug 31 – RIA Novosti. An unknown viral disease that killed several dozen people in India last week may be caused by dengue fever. This is the opinion of the authorities of the state of Uttar Pradesh, where the outbreak occurred. As told in the local Ministry of Health, most of the infected had a high fever, dehydration and a drop in the level of platelets in the blood was recorded.Other patients presented with severe migraines, muscle pain, nausea and swollen lymph nodes. Local officials previously reported that 70 people, including 12 children, had died from an unknown fever in Uttar Pradesh. State Health Minister Jai Pratap Singh denied the claim and clarified that 32 children and seven adults have died of the disease. Dengue fever is a viral infection transmitted by mosquito bites. It is widespread in Southeast Asia. According to the WHO, there is no special treatment, and the vaccine can only be applied to those people who have already had one illness.

https://radiosputnik.ria.ru/20210407/bolezn-1727265702.html

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in the world, india, carriage , uttar pradesh, southeast asia

07:24 08/31/2021 (updated: 10:56 31.08.2021)

In India, they named a possible cause of an unknown fatal disease

Rospotrebnadzor monitors cases of an unknown disease in India

An outbreak of an unknown disease has been reported in northern India. The country’s authorities report that the focus of the viral fever of unknown origin is the city of Firozabad, Uttar Pradesh state. Over the past week, at least 68 people have died of the disease there, including 40 children. The largest number of cases of the disease was detected in the districts of Agra, Mathura and Mainpuri, that is, in the western part of the state, writes the Times of India.

90,004 68 deaths are only an approximate number of deaths. The exact number cannot be determined, as rural areas have been most severely affected, from where some patients are transported to major cities. Health department teams also deliver medicines to villagers, but there is no record of those dying in private hospitals and in their homes.

At Firozabad Medical College, 72 out of 135 hospitalized children are in critical condition and are fighting for the lives.More than 50% of them have symptoms of dengue virus infection, officials said.

Dengue fever is a consequence of infection with the RNA virus of the same name, it is carried by mosquitoes, mainly in tropical countries.Over the past 20 years, the virus has become one of the most common pathogens and has mutated into almost 50 strains. Every year around 390 million people are infected with the dengue virus worldwide, and most of its varieties are asymptomatic or subclinical.

The first symptoms of fever usually appear 3 to 14 days after infection. Patients have fever, headaches, vomiting, and a characteristic rash on the body. In advanced cases, the disease passes into the hemorrhagic stage and leads to serious consequences up to death.But in most cases, the disease in those infected is asymptomatic or mild.

As for the “mysterious fever” that is now spreading in India, then it, tentatively, has nothing to do with SARS-CoV-2. In hospitals where patients are admitted, all patients are tested for coronavirus, and so far everything indicates that none of the cases of the unknown virus is associated with COVID-19, Indian doctors emphasize. At the same time, health authorities accuse citizens of non-compliance with sanitary and hygienic requirements and complain about mosquitoes.

“Due to heavy rains and waterlogging (dangerous mosquitoes breed and live there. – Gazeta.Ru), dengue and malaria cause high fever among children,” says Chandra Vijay Singh, an official from Firozabad.

For the most part, patients complain of high fever and dehydration, they are also diagnosed with a sharp drop in the number of platelets in the blood – this is the most common cause of death. Some have also been diagnosed with comorbidities.

“Patients with viral fever are admitted to COVID-19 patient rooms. Doctors and paramedics are on the alert. The severity of the fever is worrying and it takes children two weeks to recover, ”said Chief Medical Superintendent (CMS) of Firozabad College of Medicine, Dr. Hansraj Singh, who confirmed that the humidity and temperature in the regions remain above normal, which is the“ ideal ”environment for spread vector-borne diseases.

In Russia, it is believed that the risk of an unknown fever in the country is practically zero, since the Russian Federation does not have a land border with India.Nevertheless, Rospotrebnadzor continues to closely monitor the situation, noting that India is known for the appearance of various infectious diseases.

“Measures for the sanitary protection of the territory of the Russian Federation currently allow to minimize the import of infectious diseases into the country from India. There is practically no risk of spreading the alleged disease into Russia, ”a spokesman for the department’s press service told TASS.

90,000 2.1 Complaints and anamnesis / ConsultantPlus

A patient or parents (legal representatives) may complain of acute rhinitis and / or cough and / or conjunctival hyperemia (catarrhal conjunctivitis) in combination with symptoms of rhinitis, pharyngitis.

The disease usually begins acutely, often accompanied by an increase in body temperature to subfebrile numbers (37.5 ° C – 38.0 ° C). Febrile fever is more common for influenza, adenovirus infection, enterovirus infections. The increased temperature in 82% of patients decreases on the 2nd – 3rd day of illness; longer (up to 5 – 7 days) febrile condition persists with influenza and adenovirus infection [7]. An increase in the level of fever during the course of the disease, the symptoms of bacterial intoxication in a child should be alarming for the addition of a bacterial infection.A repeated rise in temperature after a short-term improvement often happens with the development of acute otitis media against the background of a prolonged runny nose.

Nasopharyngitis is characterized by complaints of nasal congestion, discharge from the nasal passages, discomfort in the nasopharynx: burning, tingling, dryness, often accumulation of mucous discharge, which in children, flowing down the back of the pharynx, can cause a productive cough.

When inflammation spreads to the mucous membrane of the auditory tubes (eustachitis), clicking, noise and pain in the ears appear, hearing may decrease.

Age features of the course of nasopharyngitis: in infants – fever, discharge from the nasal passages, sometimes – anxiety, difficulty feeding and falling asleep. In older children, typical manifestations are symptoms of rhinitis (peak on day 3, duration up to 6 – 7 days), in 1/3 – 1/2 of patients – sneezing and / or cough (peak on day 1, average duration – 6 – 8 days), less often – headache (20% in the 1st and 15% – up to the 4th day) [8].

Hoarseness is a symptom that can diagnose laryngitis.At the same time, there is no difficulty in breathing, other signs of stenosis of the larynx.

With pharyngitis, hyperemia and swelling of the posterior pharyngeal wall, its granularity, caused by hyperplasia of the lymphoid follicles, are noted. There may be a small amount of mucus on the back of the throat (catarrhal pharyngitis) [8], and pharyngitis is also characterized by an unproductive, often obsessive cough. This symptom causes extreme anxiety for parents, gives unpleasant sensations to the child, since the cough can be very frequent.Such a cough does not respond to treatment with bronchodilators, mucolytics, inhaled glucocorticosteroids.

Laryngitis, laryngotracheitis are characterized by a rough cough, hoarseness. With tracheitis, coughing can be intrusive, frequent, exhausting the patient. Unlike croup syndrome (obstructive laryngotracheitis), there are no laryngeal stenosis and no respiratory failure.

On average, ARVI symptoms can last up to 10-14 days [9].

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West Nile Virus

West Nile Virus (WNV) was discovered in 1937 in Africa, near the river
Nile.The virus belongs to the flavivirus family and it is relatively simple
arranged viruses that contain a small RNA molecule. Virus particle
about 60 nanometers in size, it consists of RNA, three proteins and a lipid membrane.
This structure of the viral particle is typical for all flaviviruses, and today
about 70 species are known. Most flaviviruses are capable of causing severe
diseases of humans and domestic animals. Most significant to humans
flavivirus infections are associated with Dengue, yellow fever, Japanese
encephalitis, West Nile and tick-borne encephalitis.These five viruses cause
annually up to 200 million human cases in various countries of the world.
Moreover, mortality from some of the most dangerous flaviviruses can reach
60%. A characteristic feature of these viruses is that they are
natural focal diseases, and a person, as a rule, becomes infected through a bite
mosquito or tick. Flaviviruses are also capable of forming foci of infection in
large cities and residents of large cities very often become victims
these serious infectious diseases.

For a long time, it was believed that VZV was not capable of causing significant outbreaks
diseases in humans, and is common only in Africa. Description of the first outbreaks
diseases of West Nile fever (WNF) in Israel was the impetus for
studies of the spread of this virus and it soon became clear that the virus
widespread in Africa, southern Europe and Asia. The virus was transmitted
a person through a mosquito bite and caused a benign viral fever,
which ended in recovery after a few days.

Today it is believed that the history of the spread of the modern VZN genovariant
started with an outbreak in Algeria in 1994 with 50 cases
diseases and 8 people died from severe viral encephalitis. Next
an outbreak of WNV was reported in Romania in 1996. Doctors recorded
453 cases of the disease and 9% of cases died. And “modern fame” came to
VZN in 1999. This year, a large outbreak of WNV was recorded in
Volgograd and Astrakhan, as well as fundamentally important that it was then
the appearance of WNV was also recorded on the American continent (an outbreak in
central New York in the United States).It took only three years for VZN to
spread almost throughout the United States and the southern regions
Canada. Such a high rate of distribution of WZN in new geographic
areas was due to the fact that many species of birds were susceptible to
a new WNV genovariant, and the virus spread to new territories of the Northern
America with the speed of a bird. And in 2006-2007. VZN has already appeared in the countries
South America and reached the southern coast of this continent.Today in the North
America (USA and Canada) every year there are thousands of cases of severe
human diseases caused by this virus.

A similar picture was observed in our country. Employees of “Vector” already in
In 2002, the appearance of VZN was registered in the south of the Novosibirsk region near
migratory birds. This has been confirmed many times in the following years. Moreover, in
2004 the first cases of human disease were detected in our region. V
samples collected on the territory of the Primorsky Territory and the city of Vladivostok in
2002-2004, WZN was also identified. This actually meant that the virus,
appeared in countries located near the Mediterranean in the mid-90s
years, for several years made an almost round the world trip and
widely, if not universally, spread in America, Africa, Asia and Europe.

These unusual findings stimulated active research into genetic
the structure of the RNA of the pathogen. Genetic analysis quickly allowed
to reconstruct the WZN propagation path.It was found that modern
VZN variant appeared in 1996 in Romania, then was identified in Israel, crossed
ocean and was discovered in the United States and Canada, followed by the countries of Central and
South America. Another branch of the spread of the virus was directed to the south of Russia
and further to the Pacific coast of Asia. Almost at the same time it was found out
that the Kunjin virus, previously considered a typical Australian virus, is
just a kind of VZN. This allowed us to conclude that under the conditions
modern civilization, practically before our very eyes, VZN won practically
all continents, except perhaps Antarctica, within just a few
years with the help of migratory birds.But the registration of the death of polar bears from VZN in
Canada allows us to say that the emergence of this virus can be expected even in
Arctic and Antarctica.

This behavior is completely atypical for viruses, the circulation of which requires
the formation of a natural focus of the disease, and a person gets sick, only
invading this natural hearth, and at the same time is not a further
the distributor of the virus. Unusual success of WZN in the formation of new natural
foci of this infection on different continents of the planet are associated with a number
circumstances: this is the ability of the virus to reproduce in hundreds of bird species, in
dozens of mosquito and tick species, dozens of mammalian species and even
reptiles; these are climatic and natural changes; is creating conditions for
breeding mosquitoes in rural and urban areas.Even a small increase
the average summer temperature for several weeks is enough to share
mosquitoes infected with WNV increased significantly and an outbreak occurred.

The main route of human infection is a mosquito bite. Therefore, most
diseases are recorded in the second half of summer and autumn. Incubation
the period of the disease is 6-8 days and the disease begins with an increase
temperature. Most often, viral fever of varying severity develops
and duration.This form of the disease is very similar to the usual viral
flu and very often the correct diagnosis is simply not made. 10-20 percent
patients develop viral encephalitis and meningoencephalitis, these are severe forms
diseases and they require treatment in a hospital setting. Clinic of the disease
very similar to tick-borne encephalitis and in this form of the disease
mortality can reach 10% or more. Correctly differentiate tick-borne
encephalitis and WNV are possible only with the help of laboratory methods.Especially
poor prognosis in older and elderly people, children get sick
much easier.

A very important point of this infection is associated with the fact that many people after
the bite of an infected mosquito, the disease does not develop or disappears
asymptomatic form. The reasons for this are not entirely clear. As a rule, one
sick there are 4-5 people with an asymptomatic form of the disease. This people
may pose a threat to others if they donate blood or
using their organs for transplantation.Many deaths described,
when WNV developed after a blood transfusion or organ transplant. it
forced the US to introduce a compulsory VZN test for blood and organ products
for transplantation, since it is usually possible to establish the fact of infection only with
using laboratory diagnostic methods.

In our country, cases of WIP were usually associated with the Caspian Sea region and
the Volga delta. Selective serological studies suggest that
the majority of the local population has been ill with PWN in one form or another.Officially
in this region, from several dozen to several
hundreds of cases of WNV. These are, of course, severe forms of the disease that require treatment in
hospital conditions. Selective serological studies in the south of Siberia and
Primorsky Krai show that up to 20% of the local population were infected with WNV
or have had WNV. Unfortunately, cases of correct diagnosis of WNV remain
single. To solve this problem, the specialists of “Vector” in collaboration with
CJSC “Vector Best” have developed and are producing diagnostic kits for
diagnostics of WNV in patients and monitoring the circulation of WNV in nature.Sets
are used in various regions of the country with good reviews about their quality. AND
if the problems of diagnosing this new disease for us are already practically
are solved, the problems of treatment and prevention of WNV are still far from being solved. it
the problem is not only for our country, there is simply no money in the whole world now
vaccination and immunization of this new disease. Of course, in many
laboratories of the world are conducting intensive research to develop
vaccines and means of immunoprophylaxis of WNN.The staff of the Vector also proposed
a new method for the prevention and treatment of this infection based on gene therapy.
However, it is too early to expect its immediate implementation into practice. Would need
additional testing of the drug and the creation of technology for its
production, which requires several more years of intense research.

Without a doubt, the West Nile virus is now a real threat to
domestic animals and the population of vast regions of the south of our country.Appearance in
our area of ​​this new virus was an unpleasant surprise and today in
the list of highly pathogenic flaviviruses circulating in the south of Siberia is
tick-borne encephalitis virus, Omsk hemorrhagic fever virus and new for
us West Nile virus. Many flaviviruses are carried by birds, which
makes possible the appearance in the south of Siberia and other dangerous flaviviruses. These
the facts require continued monitoring of WNV and other flaviviruses in their
natural foci, assessing the direction of their evolution, genetic variability,
improving methods of diagnosis, prevention and treatment of these dangerous
infectious diseases.

Head of the Department of Molecular Virology
flaviviruses and viral hepatitis

SSC VB “Vector”,

Professor, Doctor of Biological Sciences,

full member of the Russian Academy of Natural Sciences

Valery Borisovich Loktev

90,000 Ebola – DZM

Ebola fever – causes, symptoms, diagnosis, treatment (V.I. Pokrovsky, 2007)

acute, presumably zoonotic disease from the group of viral hemorrhagic fevers, occurring with severe hemorrhagic syndrome, has a high mortality rate.Refers to especially dangerous viral infections .

Etiology
The causative agent of Ebola is an RNA genomic virus of the Filovirus genus of the Filoviridae family. Identified 3 virus strains – Zaire, Sudan, Renston – differing in antigenic structure. Clear differences were found between the Zaire and Sudan strains in terms of genetic, biological and biochemical properties.
In vitro, cultures of the pathogen are maintained by passage through the liver or blood of monkeys.
The Ebola virus is moderately resistant to the environment.

Ebola virus

Epidemiology
The reservoir and source of infection in nature is poorly understood, most likely, it is mainly represented by various rodents.
The role of monkeys as sources of infection is not excluded.
A sick person is very dangerous to others, 5-8 consecutive transmission of the virus from the patient and the occurrence of nosocomial outbreaks of the disease are known.It was noted that during the first transmissions, mortality was the highest (100%), then it decreased.
The virus is detected in various organs, tissues and secretions: blood (7-10 days), nasopharyngeal mucus, urine, semen.
The patient presents a high danger within 3 weeks from the onset of the disease; during the incubation period, the sick virus does not emit.

Transmission mechanism Ebola varied.
The polytropy of the virus, the variety of ways of its excretion from the body determine the possibility of infection through contact with the blood of patients, through sexual and aerosol routes, when using common household items and eating together.It has been established that infection with Ebola fever is mainly realized through direct contact with infected material. The disease is very contagious and is transmitted when the virus enters the skin and mucous membranes . The most dangerous is blood. The greatest risk of infection is exposed to medical personnel when caring for patients, as well as personnel involved in capturing, transporting and caring for monkeys

Natural susceptibility of people to Ebola high.

Post-infectious immunity is stable.

Recurrences are rare; their frequency does not exceed 5%.

Main epidemiological signs:

foci of Ebola virus circulation are located in the tropical rainforest zone of Central and West Africa (Zaire, Sudan, Nigeria, Liberia, Gabon, Senegal, Kenya, Cameroon, Ethiopia, Central African Republic).

Ebola outbreaks occur in endemic foci mainly in spring and summer.

Pathogenesis
During the incubation period Ebola virus reproduces in regional lymph nodes, spleen and possibly other organs.

Acute onset of the disease with fever coincides with the development of intense viremia with multiple organ dissemination of the pathogen.
The damage to cells and tissues of various organs is presumably due to both the direct cytopathic effect of the virus and autoimmune reactions.

The development of microcirculation disorders and blood rheological properties is manifested by capillarotoxicosis with hemorrhagic syndrome, perivascular edema, and disseminated intravascular coagulation.

Disseminated intravascular coagulation is the leading syndrome diagnosed histologically.
Pathological changes in organs in the form of focal necrosis, disseminated hemorrhages in the clinical picture are manifested by signs of hepatitis, interstitial pneumonia, pancreatitis, orchitis, etc.

The reactions of cellular and humoral immunity are reduced, antiviral antibodies are rarely found in those who died in the early stages of the disease, and they appear late in convalescents.

Clinical presentation
The incubation period varies from several days to 2-3 weeks. The onset of the disease is acute, with an increase in body temperature to 38-39 ° C, headache, myalgia and arthralgia, malaise, nausea.
During the first days, most patients experience symptoms of angina; inflammation of the tonsils causes a painful “ball in the throat” sensation.
In the midst of the disease, indomitable vomiting, abdominal pain and diarrhea of ​​a hemorrhagic nature with feces in the form of melena join. Hemorrhagic syndrome develops rapidly with manifestations of skin hemorrhages, organ bleeding, and bloody vomiting. Signs of encephalopathy are often observed in the form of agitation and aggressiveness of patients; in cases of recovery, they persist for a long time and during the period of convalescence
On the 4-6th day from the onset of the disease, approximately half of the patients develop exanthema of a confluent nature.
Death in Ebola occurs, as a rule, at the beginning of the 2nd week of illness. Its main causes are bleeding, intoxication, hypovolemic and infectious toxic shocks.
In cases of recovery, the acute phase of the disease lasts 2-3 weeks.
The period of convalescence is delayed up to 2-3 months, accompanied by asthenia, anorexia, weight loss, hair loss, and sometimes the development of mental disorders.

Differential diagnosis

It presents significant difficulties due to the absence of specific clinical signs and the transience of the development of the disease.Ebola fever can be brought into our country from the countries of Central and West Africa.

Laboratory diagnostics

Provides for the use of PCR, ELISA, immunofluorescent methods, serological tests (RN, RSK, RNGA). The methods are available only in well-equipped virological laboratories with a strict anti-epidemic regime. In the field, you can use a complex diagnostic kit for RIF or solid-phase immunoassay test systems to detect antigens of the Ebola and Marburg viruses, as well as antibodies to them.