THE CONCEPT OF INFECTIOUS PROCESS AND INFECTIOUS DISEASES. PRINCIPLES OF DIAGNOSIS, PREVENTION AND IMMUNOPROPHYLAXIS OF INFECTIOUS DISEASES. SARS (INFLUENZA, PARAINFLUENZA, ADENOVIRAL, RYNOVIRAL, RESPIRATORY-SYNCYTIAL INFECTIONS). IMMUNOPROPHYLAXIS OF FLU.

CHILDREN INFECTION IN ADULTS. MEASLES, RUBELLA, MUMPS, SCARLET FEVER. IMMUNOPROPHYLAXIS OF THESE DISEASES.

 

Influenza (flu). Other ARVI (acute respiratory viral infections): parainfluenza, adenoviral disease, respiratory-syncytial infection, rhinoviral infection.

Definition

Influenza is acute infectious disease which occurs in epidemics and is caused by a virus, it is characterized by an abrupt onset and such manifestations as general intoxication and  affection of the respiratory tract mucosa.

http://www.cdc.gov/flu/other_flu.htm

Together with the diseases of the cardiovascular system and tumors, influenza takes the leading position in the human pathology. Influenza and other acute respiratory diseases constitute about 75% of all infectious diseases, and 85 – 90% in epidemics, thus resulting in great social and economic damage. Thus, in Ukraine in the epidemic period 1968 – 1972 the economic damage equaled about $120 million. The main thing is that besides relatively mild cases of the disease, there are severe cases resulting in disability and sometimes death when children or old people contract a disease. According to the USA statistics influenza takes the tenth position concerning fatal outcomes.

http://virus.stanford.edu/uda/

History

The first pandemic which spread from Asia to Europe and America was registered in 1580. There have been 23 great epidemics and pandemics since that time. During the pandemic of 1780 – 1782 the modern term «flu» or «influenza» appeared (from the French word «Gripper» meaning catch, envelope, Latin «influere», Italian «influenza» meaning penetrate, invade, instill).

In the manuscripts of the 14 – 15^th centuries eight epidemics are mentioned, their names are “mass epidemic”, “fatal infection”, “catarrhal fever”, “infectious fever”, “quick catarrh”, etc. Even the names show the essence of the disease. In spite of it, the authenticity of the information is not absolute.

It is impossible to determine the regularity of epidemics in the past. In some cases they were of local character affecting the population of few countries. In other cases influenza spread pandemically and affected the population of several continents.

 

Etiology

http://emedicine.medscape.com/article/219557-overview#aw2aab6b2b3aa

During the influenza pandemic of 1918 – 1919 filter-passing virus was more often considered to be influenza pathogen. This notion was confirmed by the classical experiments carried out by P. Zeiter who infected himself with washing off taken from the nasopharynx of an influenza patient and bacteriologically filtered.

In 1933 English scientists W. Smith, K. Andrews, P. Loudlow isolated influenza virus from a sick person, starting a new stage in the scientific study of the influenza etiological structure. In 1940 T. Frensis and T. Magil isolated a virus which was quite different from the ones isolated earlier. It was suggested to name the first virus – influenza type A virus, and the virus isolated by T. Frensis – type B. In 1947 R. Tailor isolated and described a new type of influenza virus which was later named type C.

The influenza pathogen belongs to the group of orthomyxoviruses. Virions have a ball form and a diameter of 100 – 120 nm, they have a core of a tightly turned spiral of ribonucleic acid in the case of protein molecules (Fig. 1).

On the external capsule there are glycoproteids in the form of a fence of pins: hemagglutinins (HA) and neuraminidase (NA) causing the development of a specific immunity after the disease.

The influenza virus quickly dies at drying, high temperature, it is resistant to low temperatures, extremely sensitive to ultraviolet rays and many disinfectants.

Influenza B virus has a more stable antigenic structure and doesn’t change so often. It has one neuraminidose but different hemagglutinins.

The most stable in relation to antigens is virus C. It causes only sporadic diseases and small outbreaks. It is spread mostly in Ukraine, Moldova and other southern regions.

Fig. 1. Influenza virions

 

 

 

http://emedicine.medscape.com/article/219557-overview#a0156

Epidemiology

 Influenza remains the most spread mass disease nowadays, which does not recognize any borders and affects great masses of the population (up to 50 % and more) at short periods of time. The influenza contagious character was noticed even in 1735 by Gexgame during the epidemic in Scotland, he called the disease «epidemicus».

A sick person is the only source of the disease. The epidemiological role of virus carriers has not been studied well. The virus quickly multiplies in the epithelial tissue of the respiratory tract mucous membrane of a sick person and in 24 – 48 hours there is an aerosol cloud with a great concentration of influenza virus around a patient at sneezing and coughing. As the immunity of a specific type forms very quickly, the virus disappears from the organism of a sick person on the fifth day of the disease.

Influenza infection is spread with the help of small particle aerosol dispersion. The mechanism of virus spreading is based on the condition that the virus is in the air for a long time, it has an ability to keep its infectious force under unfavorable conditions of the environment and the ability of virus particles to move with air at long distances and penetrate different parts of respiratory tracts infecting a person.

The influenza virus of full value can live and be infectious in the air for 2 -3 hours. It can live for 1 -2 days on the furniture and other surfaces. The ultraviolet rays, humidity decrease and temperature increase and other factors shorten the virus life time. The virus lives within the limits of 1 -3 meters. The speed of influenza spreading depends on the speed of people moving on the territory. The considerable increase of transportation, the movement of great numbers of people within separate countries, between countries and continents ensures a constant possibility of the virus spreading at considerable distances and the ability to infect people in any part of the globe.

There are small local epidemics and pandemics. The epidemics last 10-14 weeks.

The majority of people are naturally susceptible to influenza. The sick rate depends on many factors. First of all, on the level of the population specific immunity and on the circulation of the influenza virus serotypes.

The number of the influenza cases among adults has considerably decreased during the last years, as for the children aged 7 -14 the number of influenza cases is growing slowly but steadily.

The influenza B sick rate tends to grow in all the age groups.

http://emedicine.medscape.com/article/219557-overview#a0104

Pathogenesis

After penetrating the respiratory tracts, the virus sticks to the epithelial cells which have receptors – things of the lipid and carbohydratic nature. When the virus fixes on the cell surface receptors some complex enzymatic processes begin to occur, they ensure its penetration a cell in which it reproduces. This complex multistage process results in the cell death, and new virions born in the cells occupy new areas of the mucous membranes. The virus multiplication cycle lasts 7-10 hours. Every virion which penetrated a cell gives birth to 1000 virions and there will be 10²⁷ of them in a day. That’s why the influenza incubation period is so short.

If there were no obstacles for reproduction, the entire tissue of the respiratory tract would be affected in 1-2 days and it would result in a lethal outcome. It happens in rare cases – «quick influenza» develops and a patient dies in 2 days. But it doesn’t usually happen so, because a cell, in which virus reproduces, produces and secretes interferon. This interferon gets into the neighboring cells and after that they are not defenseless against the virus invasion. Interferon prevents virus protein from synthesis. The further development of virus infection depends on the struggle of these two forces -virus genome and cell interferon: either it stops at the very beginning or the disease lasts a short time and a patient gets well or the infection spreads in the lungs and fatal pneumonia develops.

The cells affected by a virus are rejected and the products of their decomposition are absorbed, causing a general feverish disease. At the same time in the submucous membrane there develop inflammatory processes with distinctive circulatory disorders, that clinically manifests by hemorrhage syndrome.

When the process spreads in the lung tissue, in severe cases with the development of influenza pneumonia, there are signs of general edema with scattered or confluent foci of hemorrhage.

Under these conditions the influenza virus easily penetrates the blood and virusemia develops. However, virusemia at influenza doesn’t last long, as the virus quickly dies under the influence of nonspecific immunity factors -interferon, complement, properdin, β-lysines, β-inhibitors, histones, leukins, etc.

It is quite possible that the affection of the internals at influenza is connected with virusemia. However, the great maiority of authors doubt the specificity of such affections, as there are no specific receptors in all the other organs, and they think that in the pathogenesis of affections the leading role doesn’t belong to the cytopathogenic phenomena, it belongs to the organism reaction to toxic products or other substances, which appear at the influenza virus reproduction process.

Besides, it is a fact that even in the mild cases of the disease there are signs of the organism hem poetic and immune system considerable depression. The number leukocytes in blood decreases and their functions are suppressed. Macrophages become less active. Due to it bacteria and viruses become more active and the accompanying diseases take an acute form. Influenza «opens» the gate for the enemy, that’s why it is called after Tarpeya, a legendary traitor, who opened the gate of Rome for the enemies. So influenza infection is mostly a combined virus-bacterial or virus-virus infection.

In conclusion it is necessary’ to note that interferon production is very important for the disease outcome in the struggle between viruses and the organism protective forces. Antibodies of class IgM appear only at the end of the first week of the disease when the organism wins the first main battle, and antibodies of class IgG in two weeks.

Pathologic Anatomy.

There are three main groups of pathoanatomic changes at influenza: the first one – primary changes, caused by the virus itself; the second ones – secondary changes, caused by influenza virus in combination with cocci and bacterial flora; the third ones – late changes in patients who had influenza and died of complications or worsening of other diseases.

The most important morphological signs of the first group are dystrophic changes of the respiratory epithelium and lungs with distinctive disorders of microcirculation; sharp plethora, edema and pericellular infiltration of submucous membrane and thickening of basal membrane.

The interalveolar septum of lung tissue are considerably thickened due to plethora and edema with leukocytic-lymphoid infiltration. The walls of small vessels and capillaries are thickened, in some vessels there are fibrous and leukocyte thromboses. The cells of alveolar epithelium became partially hyperplastic, in some places – died, there is a small microphagic exudate in the alveoli lumens.

In the second group there remain signs of pure influenza infection, but more or less they are prevailed by the purulent affections of the respiratory system and serious blood circulation disorders in the lungs. Pyo-hemorrhagic and pyo-necrotic tracheitis with a destruction of epithelium is developed in trachea. The lung tissue is low-pneumatic, the surface of the incision is motley, with alternation of large dark-red and gray foci. During microscopy massive foci of pyo-hemorrhagic pneumonia are found.

In the third group there are different kinds of pneumonia with various inflammatory exudate: purulent, pyo-hemorrhagic and abscess, plethora, edema and in some places hemorrhages into parenchymal organs, and also changes, which are characteristic of the accompanying chronic diseases.

http://emedicine.medscape.com/article/219557-clinical#showall

Clinical  manifestations

The incubation period at influenza is short – from several hours to 2 -3 days. Its duration depends on the dose and toxic characteristics of the virus. The incubation period is short if the dose is big and the virulence is considerable. Thus, its duration has a prognostic meaning for a doctor.

There have been different opinions about the preliminary symptoms of the disease. It should be admitted that there is a prodromal period, which is characterized by an elevated temperature for a short period of time (2-3 hours), slight malaise, chilliness, myalgias. These symptoms don’t last long and are usually ignored by both a patient and a doctor. The disease begins to develop on the next day. In some patients the disease develops so fast that a practically healthy person becomes seriously ill in several minutes or hours.

The first symptoms are chilliness (always more or less manifested), high temperature, headaches, dizziness, a syncope condition, fever, malaise, pains in different parts of the body i.e. the symptoms of general intoxication. The headache is located in the forehead, temples and over the brows, it can be of different intensity. There is an early distinctive symptom – pain in the eye pupils especially intense at the eye movement or pressing, hyperemia of conjunctivas and sometimes scleras. Dizziness and syncope conditions are characteristic of teenagers and old people. The fever which is one of the main symptoms of influenza does not last long – 1-4 days (in 86% patients). The ‘two-humped’ character of the temperature is connected with the condition when the chronic infection takes an acute form or a secondary flora joins. Such symptoms as unconsciousness, delirium, convulsions and meningeal manifestations are characteristic of children at intense toxicosis.

Such symptoms as malaise, pains in the limbs and muscles, bones or in the whole body appear during the first hours of the disease and disappear when fever and other signs of toxicosis decrease. Adynamia, malaise can be considerable and are manifested from the first day of the disease. The skin on the face is hyperemic during the first 2-3 days, in severe cases they become pale with cyanotic shade. It is often a bad prognostic sign. Sweating is a characteristic feature. Intoxication is a characteristic feature of influenza, its degree and frequency vary in case of different microbes. In different epidemics there is hemorrhage syndrome, in 10 -20% cases, its symptoms are nasal bleeding, sometimes reciprocal, hemorrhage in the fauces, metrorrhagia, short hemoptysis and gum bleeding sickness. Cough appears during the first days of the disease, dry, excruciating, heart-rending which is accompanied by the feeling of tickling, scratching behind the breast bone. Almost all the patients have a catarrhal syndrome which has such symptoms as rhinitis, pharyngitis, tracheitis. There are often such combined affections of the mucous membrane as rhinopharyngitis, laryngotracheitis, tracheobronchitis, etc. They usually appear in the first days of the disease. Such symptoms as herpetic rash is quite frequent, but appears; on the  3^rd-4^th  day. Photophobia and lacrimation are finite rare.

There are no specific changes on the skin. Different kinds of rash which were described result from other reasons (taking drugs, accompanying diseases). As it has been mentioned before, quite often there is herpetic rash, theoretically there is a possibility of petechiae, hemorrhages, if we take into consideration the affection of vessels and their hyperpermeability. There can be random rash.

A natural manifestation of the influenza infection is the affection of the respiratory organs, as different pathological processes take place in them, they are located on a certain level, but sometimes affect the entire area. The affection of the upper respiratory tracks is accompanied with hyperemia and swelling of mucous membrane, sometimes with slight hemorrhages. There is nasal obstruction, rough breathing, and discharge of different nature and consistence: mucous, mucopurulent and sttaguinolent – in severe cases. During rhinoscopy swelling and hyperemia of mucous membrane can be seen, especially at the middle turbinated bone. At the same time accessory nasal sinus can be affected (maxillary sinusitis, frontal sinusitis, eustachitis with the development of otitis) with different nature of affection – from catarrhal to purulent.

During fauces examination the hyperemia of tonsils, uvula palatina and posterior wall of the throat could be found. Sometimes there are granules with vascular injection and hemorrhages on the soft palate. The development of influenza laryngitis and false croup is extremely dangerous, especially in children. Patients become pale, cyanosis develops, they often breathe with the help of additional musculature, the voice remains. Lethal outcomes are not rare, because not only larynx is affected, but trachea and bronchi as well, they are full with croupous superposition. The swelling of the mucous membrane of trachea and bronchi results in their permeability and leads to the deterioration of lung ventilation. Depending on the severity of the disease the degree of manifestations is different – from the hidden forms, which can be found with the help of pharmacological tests (aerosolic injection of eusporinum) to the severe forms accompanied with dyspnea and cyanosis. The most common and dangerous complication of influenza is pneumonia. It is necessary to mention, that even during the first days of the disease there are roentgenologic strengthening of the vessel picture in the inferiomedial parts, that looks like indistinct infiltrate, and hurried breathing, shortening of the percussion sound and appearance of so called «conductive» rhonchi, resemble pneumonia. But they often disappear without any traces in 2 – 3 days. It may not be pneumonia, but some circulatory disorders. Not everything is clear in the problem of pneumonia origin. After the detection of pathogen it was considered that during the first three days pneumonia is of virus etiology, on the 3 -5 day – virus-bacterial, later – bacterial etiology. There is a picture of the so called «big motley lung» on the section. Hemorrhage pneumonia foci of different sizes can be seen along the whole length, they are small and large and separated by some parts of unaffected tissue. The foci of festering appear quite early. The rough beginning with severe toxicosis, catarrhal syndrome, significant and diverse changes in the lungs, are characteristic of influenza infection, which is complicated with pneumonia.

Diverse changes in the cardiovascular system have been described. The vascular system is usually affected, and sometimes considerably, it is probably connected with a toxic action of influenza virus on capillary vessels. Dilation of capillaries, turbid background, sometimes formation of the arterial aneurysms, are seen at the capillaroscopy. Arterial and venous pressure decreases, especially in case of pneumonia, the speed of blood flow slows down. The pulse is very often corresponds the fever, there is sometimes tachycardia, especially at the beginning of the disease, in some cases there is bradycardia. The heart sounds are muffled, heart borders are widened, slight systolic murmur and sometimes extrasystoles appear. All these manifestations disappear when the general condition of the patient becomes better. There is elongation of the PQ interval, decreasing and notching, and sometimes inversion of the wave T at different abductions on the ECG. These disorders are interpreted as toxic and dystrophic. They are unstable and disappear in 1 – 2 weeks. The myocarditis described at influenza is disputed by other authors. More severe and diverse disorders are found in patients with chronic affections of the cardiovascular system (coronary atherosclerosis, rheumatic heart diseases, etc.). These disorders are not pathognomonic for influenza, and arise because of the aggravation of the main disease under the influence of influenza infection.

There are various affections of the nervous system during the influenzal infection. The functional disorders of the vegetative nervous system are distinctively manifested. We have already got acquainted with such symptoms as sweating, changes of the pulse rate, dizziness, etc. However, all these changes quickly disappear. At the same time serious affections of the central and peripheral nervous systems are observed, they are manifested as meningitis, meningoencephalitis, radiculitis, neuritis, etc. The rate of these complications is different in different epidemic outbreak. The pathogenesis of these diseases is still a difficult question. Side by side with the theories of the toxic and parainfectious factors in their development, it is possible, that the virus invasion plays a significant role.

The complications in the digestive system are less often, and there are evidently no specific disorders, although fur, dryness in the mouth, decreased appetite, and heaviness in the epigastrium are observed. These symptoms are characteristic not only of influenza, but of any disease with fever. And now such forms of influenza as gastrointestinal, intestinal and abdominal which were the results of diagnostic mistakes are mentioned in conversations but not in literature.

The changes in the urinary tracts are manifested as pyelitis, pyelocystitis and sometimes nephritis, which result from metabolic-dystrophic manifestations of fever and bacterial superinfection.

The described affections of the endocrine system (adrenal gland, thyroid and pancreas glands) are very rare and it is not possible to completely exclude the influence of influenza virus in these cases.

The changes in the hemogram are manifested as leukopenia or normocytosis. If there are no complications and accompanying diseases, there is absence or decrease of the eosinophils, neutropenia and relative lymphocytosis in the hemogram at influenza (the percentage of lymphocytes increases whereas their absolute number is the same). ESR is normal or insignificantly increased. The connection of the bacterial complications is accompanied with leukocytosis and neutrophilia. It is important to take into account the absolute number of elements of white blood in the dynamic of the disease.

http://emedicine.medscape.com/article/219557-differential

Differential diagnosis

Besides careful clinical and epidemiological findings, modern methods of lab diagnostics are used for influenza diagnosis and differential diagnosis of other diseases.

Diagnosis does not seem to be difficult during epidemic outbreaks. However, at the same time besides influenza there 30-60% patients with the respiratory tracts affection syndrome are registered, they are not of the influenza etiology, and clinical diagnosis is even more difficult during a non-epidemic period. As we see, influenza doesn’t have specific symptoms which are characteristic of it only, but there are 3 strongly pronounced symptoms: abrupt onset with chilliness, general intoxication and the affection of the upper respiratory tracts. But they also accompany other acute respiratory diseases, and that is why there are many cases when patients with the diagnosis «influenza» are taken to hospital, but they have different other infectious and non-infectious diseases. That is why it is always important first of all to take into account the epidemic situation in the region.

A short incubation period is characteristic of influenza that is why the contacts with sick people, especially in the foci 1-3 days before the disease should be taken into account. If it is possible it is advisable to make up a general conception of the disease clinical picture in the people the patient contacted.

A careful and detailed physical examination of the patients, analysis and a comparative evaluation of the reveled changes with the consideration of the time past from the disease onset is also of great importance. It is important to remember that the preceding therapy can have a considerable influence on the natural disease course, sometimes changing or allaying some symptoms, and in other cases, on the contrary, resulting in the development of the new symptoms with are not typical of influenza. These can be various manifestations of the medication disease: skin rash, lymphoadenopathy, the toxic affection of the liver, hemogenic system, development of asthmatic syndrome, etc. Only a careful analysis of all the clinical symptoms can reveal the main syndromes, the peculiar mosaic of which is characteristic of one or another nosological form.

There is not any typical temperature curve. A relatively short febrile temperature reaction (5-6) days with a quick rise and maximum values during the first 2-3 days and shortened lysis should be considered to be more or less typical if the fever lasts longer than this period, it is always necessary to think of a possibility of another disease or joining of a complication. The usage of antibiotics, analgetics, sulfanilamides and glucocorticoides can considerably change a natural course of the temperature curve.

An intoxication syndrome is the main in influenza, and various symptoms of the syndrome can be expressed in different ways and occur in different combinations. A headache and general malaise are the most frequent. But they are typical of many other diseases, mainly the infectious ones, and do not have a diagnostic value. In influenza there is no skin rash except a herpetic one. In acute meningitis of different etiology there is a complete or incomplete meningeal syndrome and typical changes of the spinal liquor. It is not meningitis but meningism that is typical of the severe hypertoxic form of influenza, meningism is characterized with incomplete meningeal syndrome, liquor hypertension without any inflammatory changes in the spinal liquor, the spinal puncture solves the diagnostic problem in these cases.

The development of edema swelling of brain – is accompanied by sopor, coma, convulsions, olygopnoe and bradycardia. These condition should be distinguished from coma and convulsion syndrome of another nature. A general malaise, dizziness, fainting, asthenisation, do not have a diagnostic value, but in combination with a headache and retroorbital pains as well as with catarrhal symptoms might help diagnose influenza. Nasal bleeding is the most frequent manifestation of the hemorrhagic syndrome in influenza, but they also occur in-other diseases and can help in diagnostics only in combination with other characteristic symptoms. The appearance of the blood admixture in sputum is almost always a bad symptom. Acute hemorrhagic toxic edema of the lungs is one of the variants of hypertoxic influenza, its clinical symptoms are asphyxia, cyanosis, bubbling breathing and liquid pink foamy sputum. It must be distinguished from poisoning connected with breathing in vapors of poisonous substances, acute left ventricular heart insufficiency. Taking into account the epidemic situation, high temperature, intoxication and tracheitis can help diagnose influenza.

The appearance of sputum containing blood (pus and blood) in influenza, which is complicated by pneumonia, often testifies about the latter’s staphylococcus nature. The pleura is often involved in the pathological process, severe respiratory and cardiovascular insufficiency develops. Hemorrhagic pneumonia and influenza should be distinguished from the croup pneumonia. In croup pneumonia there are no symptoms of the upper respiratory tract affection which are characteristic of influenza, the disease has a sudden onset with pains in the side and sudden temperature rise, there is “liver” dullness over the affected lobe and bronchial breathing with the following development of moist rale, the sputum is rusty though there can be admixture of crimson blood in it.

The fever and vomiting, which are observed in influenza may be diagnosed as alimentary toxic infection of salmonelesis or another etiology. But in influenza there are other symptoms of intoxication which are considerably expressed, they are combined with the nose stuffing, tickle in the throat, pain behind the sternum and dry cough. Sometimes even in influenza there are pains in the upper part of abdomen stipulated by mialgia. Diarrhea often occurs in this disease. That is why in case of moderate toxicosis, vomiting, pains in the abdomen and frequent watery stool with an admixture of slime and blood it is necessary to think of some acute alimentary disease, but not influenza.

The development of symptoms of the upper respiratory tract in influenza makes one distinguish this disease from other acute respiratory diseases caused by adenoviruses respiratory-syncytial viruses, paragrippal viruses, rhinoviruses, reoviruses, coronaviruses, ECHO-viruses, Koksaky viruses, mycoplasma pneumonia.

The catarrhal syndrome in influenza develops later and is less expressed than intoxication. Tracheitis, to be more exact laryngotracheitis is the main syndrome in influenza. Scattered dry rale together with hard breathing develop when the inflammatory process spreads along the bronchial tree. The symptoms of laryngotracheitis stay even in case of the development of pneumonia or other complications, this helps to suspect influenza as the main disease. Rhinitis and pharyngitis in influenza do not always occur and have peculiarities in the form of dryness and stagnant hyperemia of the nose and throat mucous membranes, absence of scanty discharge from the nose, spontaneous nasal bleeding.

Adenoviral infection is characterized by a more prolonged incubation period (7-14) days. The fact that there are simultaneous cases with various clinical picture in the foci of adenoviral infection is a characteristic feature; the clinical picture: acute rhinitis, rhinopharyngitis, pharyngoconjunctivatis, covering conjunctivitis, exhantema, hepatolienal syndrome, etc. A less acute than in influenza onset, moderate intoxication in spite of the high and sometimes prolonged temperature reaction is typical of the adenoviral infection. However the syndrome of intoxication is less important as compared with the expressed catarrhal changes on the part of upper respiratory tract and conjunctiva, which are of exudative character. The pathological process sort of “crawls over” from one zone to another, and the involvement of each new are of the respiratory tract is accompanied with a temperature rise which results in the two or three top character of the temperature curve. Together with this or some time later peculiar tonsillitis may develop together with exudative pharyngitis which manifests itself with edema and bright hyperemia of the back wall of the throat, on which one can see hypertrophic lymph follicles. If the disease starts with rhinitis (it can be limited by it), the discharge from the nose can be abundant, serouse. Laryngitis and tracheitis in contrast to influenza are not characteristic of adenoviral infection.

If the adenoviral infection is complicated by pneumonia, in adults it has approximately the same course as a moderate severe affection of the lungs in influenza and can be cured by usual antibacterial therapy. The adenoviral infection itself preserves its main clinical features, which allow to distinguish it from influenza. In case of the combination of influenza and adenoviral infection the disease has the symptoms characteristic of both nosological forms.

The respiratory-syncytial infection (RS) in adults is usually a sporadic disease, which equally effects all the age groups. In contrast to influenza the disease does not often have acute onset. The intoxication syndrome is expressed moderately or slightly. The temperature is subfebrile or moderately febrile. The changes of the upper parts of the respiratory tract are slightly expressed. The symptoms of acute bronchitis which are often accompanied with bronchial spastic component (continuous cough that is dry or has some scanty sputum, scattered dry rale and rare medium bubbling moist rale, prolonged inhaling, difficult exhalation, swelling of the lungs and others) dominate. The liver gets involved more often in the respiratory-syncytial viral infection in adults than in other acute respiratory diseases. At the high point of the disease it is enlarged and sensitive at pulpation, the Orthner symptom becomes positive (pain at beating on the costal arc).

Paragrippal diseases in adults like RS-infection have a more gradual onset the intoxication is slight or moderate as well as the temperature reaction, which in fact lasts longer than in influenza. Rhinitis and pharyngitis are moderately expressed, laryngitis is considered to be typical. There is no syndrome of false croup in adults as compared with children.

The rhinoviral infection occurs only in adults. The disease is characterized with subfebrile or normal temperature, slight intoxication symptoms or their complete absence and expressed exudative inflammation of the nose mucous membrane with abundant rhinorea, which is the main clinical symptom.

The coronaviral infection is also not severe disease, which is difficult to distinguish from a rhinoviral one and which affects not only adults but also children, and besides rhinitis the patients may have slight pharyngitis and even bronchitis.

ECHO- and Koksaky viruses can cause the diseases with affection of the upper respiratory tract. But the involvement of the brain meninx and spinal radices in the pathological process is more characteristic of the enteroviral infection.

Mycoplasma pneumonia can cause a respiratory disease in adults. It has a gradual onset and has a course with both low and febrile temperature, relatively slight symptoms of intoxication, slight affection of the upper parts of the respiratory tract, prolonged and persistent bronchitis.

The disease named “legionaries” disease is given to a new disease, which appeared in 1976 in the USA, its bacteriological nature was proved later. Now it is determined that this disease is widely spread in all the countries. The most cases are registered in the warm season. The elderly man suffering from different chronic diseases or alcoholics who use immunedepressors and smoke a lot fall ill more frequently. The disease takes a course of severe progressive abscedic pneumonia with parapneumonic pleuritis and affection of the parenchimal organs.

Ornitosis and Q-fever are diseases which must be no often differentiated from influenza complicated with pneumonia. Both diseases are not accompanied with affection of the upper respiratory tract but have an expressed intoxication and prolonged fever hepatolienal syndrome and atypical affection of the lungs. Well gathered epidemiological anamnesis (contact with birds or their discharge in ornitosis, contact with different animals usage of raw milk and other diary products, usage of cotton brought from endemic regions, etc. in Q-fever) helps to diagnose the disease.

It is necessary to say in conclusion that the differential diagnostics of influenza and its complications in spite of the seeming simplicity is actually quite difficult. The basis of diagnostics and differential diagnostics should be a careful analysis of clinical epidemiological data which can allow either to suspect influenza or doubt this diagnosis. The most simple clinical investigation of blood, urine and spinal liquor help in the diagnostics. The serological, bacteriological and immunefluorescent methods of investigation are of primary importance.

http://emedicine.medscape.com/article/219557-workup#showall

Diagnosis

The virusological methods of diagnostics are used to isolate and identify the influenza virus. As a rule these methods are used to find out the nature of the outbreaks but not the sporadic cases of the disease because they are very laborious and less sensitive as compared with the serologic methods.

The infection of the chicken embryos is universal method of the primary isolation and cultivation of influenza virus. This method is more accessible and sensitive than the infection of the laboratory animals. It is performed by insertion of the virus containing material in the amniotic or allantoic cavities and causes the infection of organs and tissues of the chicken embryo with the following accumulation of the influenza viruses in the embryos liquid. The presence of the influenza virus in the allantoic or amniotic liquid is stated by the hemagglutination reaction (GAR). The simultaneous erythrocytes of the chicken an guinea pig testifies in favor of the viruses A and B presence, various the agglutination of only chicken erythrocytes suggests the presence of virus type C. In case of the erythrocyte agglutination absence it is necessary to make 2-3 additional passages by the way of embryos infection with the mixture of allantoic and amniotic liquid from the previous passage. In case of the negative results of GAR after the passages the investigation of the material is finished.

The methods of the influenza virus isolation in the tissue culture are preliminary and demand the following pathogen cultivation on the chicken embryo. The trypsineted cultures from the kidneys of monkeys and human foetus are the most suitable for the influenza virus isolation.

The serological diagnostics of influenza ensures an accurate determination of etiology by the way of revealing the quantitative growth of specific antibodies in the disease dynamics in blood. The serological diagnostics is especially important in case of the atypical or symptomless course of the influenza infection. In such cases the discovery of antiinfluenza antibodies in the blood of the examined people in the dynamics of the increasing concentration independently of virusological investigation is the only truthful of the influenza virus participation in the development of the disease and its cooperation with the human organism. Among the methods of influenza serological diagnostic the reaction of hemagglutination inhibition (RHAI) and the reaction of complement banding (CB) is the most widely spread.

The immunefluorescent method is recommended by WHO as one of the reliable means of quick deciphering of the etiology of acute respiratory diseases. The sorting of patients with acute respiratory diseases is done on the bases of the immunefluorescent method data, it is especially important for the prevention of the cross infection of children of an early age. Being widely used this method is an important and reliable means of control of the etiological structure of the acute respiratory diseases in different periods according to the epidemic situation. The essence of the immunefluorescent method is in specific reaction of antigen-antibody which reveal the presence of viral antigens in the cells by the way of joining antibodies to them, the antibodies are connected with the fluorescent mark, which lights in the ultraviolet rays.

Treatment.

Among antiviral agents which are indicated at influenza type A, Remantadin is recommended in such doses: at 1-st day  0,1 gr. 3 times per day, at 2-nd and 3-rd day  0,1 gr. 2 times, at 4-th   0,1 gr after meal.

The positive effect at influenza of type A and B is at using Adampromin. Synthetic preparation Ribamidil (Ribavirin) has positive influence on viruses of grippe of types A and B which is indicated at a daily dose 0,3 – 0,6 gr. during 5 days, however in clinical conditions rather inconsistent data are received. Perspective combined indication of Ribavirin with Remantadin or Adampromin as medical aerosols is represented. Adampromin influences on viruses of an influenza A and B. Similar antiviral property have Midantan, Deitiforin, Arbidole.

As agent of a choice can be a human leukocytic interferon:  3 – 5 drops in each nasal meatus through 1 – 2 hours not less than 5 times per day during 2 – 3 days or as aerosole with the same frequency.  Treatment of virus rhinitis includes:– Unguent of Oxolini, grease a mucosa of nose 2 – 3 times per day 3 – 4 days. The preparation is indicated at herpetic superinfection, however its efficiency is low. The specified antiviral agents should be applied in the first days of disease, later they are not effective.

To decrease a body temperature, and to reduce a headache and muscular pain   Analgin, Ascofen, Upsarin with vitamin C, Eferalgan, Paracetamol are indicated. As a preparation of a choice you can use noarcotic analgetic Amison, rendering analgetic, anti-inflammatory, antipyretic and inferonogenic action.  The fever is the major adaptive and protective reaction of organism, induces synthesis of an endogenic interferon. Antipyretic preparations are indicated only at a hyperpyrexia and expressed cerebral and cardiovascular disorders in adegnote dose to lower a body temperature on 1 – 1,5 C.

As the stimulation of endogenic interferonotransformation apply Amixin  0,125 – 0,25 gr. per day for 2 days, then on 0,125 gr. in 48 hours for one week or in the first 2 – 3 days prescribe Mefanam acid 0,5 gr. 2 times per day. For patients Polyvitamines, Ascorutin are indicated. At excruciating tussis indicate Codein phosphat, Codterpin, tablets against tussis, at labored nasal respiration – Halazolin, Farmasolin or Naphthyzin, Efedrin hydrochloride, Pinosol, at exaltation and disorders of sleeping – mixture of Behterev, Fenobarbitalum for the night.

In serious cases of influenza and the weakened patient, with  indicated specified agents, infuse antiinfluenza  donor immunoglobulin 3 ml. (I.M.) unitary, sometimes repeatedly in 6 – 12 hours.

In connection with the expressed toxicosis infuse Reopolyglucin,  solution of Albumin,  isotonic solution of  Sodium chloride, 5 % a solution of glucose (I.V.). For prevention of hypertension in a small circle of a circulation and a fluid lungs, it is necessary to infuse no more than 500 – 800 ml of liquids slowly and simultaneously to use diuretic preparations – Furosemid, Diacarb, Etacrinic acid. Appoint Corglykon, Sulfocamphocain,  Euphyllin, inhalations of Oxygen or Carbogen.

Patients with especially serious (hypertoxical) form of influenza should be treated in departament of intensive treatment.  Antiinfluenza gamma-globulin or a serumal polyglobulin indicate  3 – 6 ml. in 4 – 6 hours (in  muscle or even in  vein). Infuse (I.V.) admixture of the following structure: blood plasma –150- 200ml; solution of glucose  40 %  – 20 ml, Mesaton 1 % or Noradrenalin 0,2 %  1 ml.; strophanthin 0,05 %  or Corglykon 0,06 %  0,5- 1 ml.; Furosemid (Lasix) 40 -80 mg; Hydrocortizon  250- 400 mg; Euphyllin 2,4 %  1 ml; ascorbic acid solution 5 %  5- 10 ml; calcy chlorid solution 10 %   10 ml; polyglobulin-3 ml. At disorders of cardiac activity use- Corglykon or  Strophanthin. At increase of hypoxia and  fluid of lungs prescribe to inhale Oxygen-alcohol mixture on extremity impose venous garrots, apply diuretic preparations.

In case of development of acute edema and  brain swelling in a vein infuse Mannit (or. Mannitole, Furosemid (or. Lasix), preparations of a potassium, glucocorticoids.

Widely use tinctura of the herbs, with sudorific, anti-inflammatory, soothing, spasmolytic, expectorating and antimicrobial properties.

The collecting  №1 consists of- root of Altea medicinal (2 parts), buds of a birch white (1 part), flowers of elder black (1 part), a rhizome with roots of Inula (1 part), a grass of St.-John’s wort (7 parts), berries and leaves of a raspberry ordinary (2 parts), a leaves of mint peppery (2 parts),  buds of a pine ordinary (2 parts), a grass of a sage medicinal (2 parts), leaves of Eucaliptus (2 parts);

the collecting №2 consists of- root sweetflag (1 part),  buds of a birch white (2 parts), herbs of Origana ordinary (3 parts), a root of Valeriana medicinal (1 part), a herb of St.-John’s wort  (3 parts),  leaves of Viburn ordinary (2 parts), a seed of flax sowing (2 parts), a herb of a yarrow ordinary (2 parts), fetuses of fennel garden (2 parts). It is necessary to fill 4 or 6 dining spoons of the collecting in a thermos (0,7 – 1 l.) to fill up to top with abrupt boiled water, to sustain 3- 4 houres and to drink all within day in 3 – 4 receptions. Course of treatment by such shock doses lusts 3 – 5 days.  The next days use usual doses- making 2 – 3 dining  spoons of an admixture 0,5 l. of boiled water. Among other medicinal herbs for preparation tinctures it is possible to use leaves of Fragarias wood, Tussilagoes farfara, flowers of Camomily Calendulaes, an elder black, lindens. For inhalations use broths of leaves of sage, Eucalyptus, grasses of thyme, pine buds, buds and young branches currants, birches, raspberries, a root of willow-leaf inula, better acidified- then rinse a mouth, a throat and wash out a nose. Revaitl Garlick Pearls  indicate to rise immunity . The heating of a thorax with the help of Sinapismuses, mustard wrappings or pepper Emplastr is prescribed. The same agents put to a plantar surface of the feet and shins.

Antibiotics at an influenza are indicated in following cases: 1) at serious current of disease (the hypertoxical form with encephalitis if disease begins with a pneumonia); 2) to children of the first 2 years of the life, the pregnant,to weaken patients, to persons of elderly and senile age; 3) at bacterial complications; 4) at accompanying chronic diseases of inflammatory character which may become aggravated at influenza. In other cases antibiotics contrindicative, as they strengthen allergization of organism and enlarge frequency of various complications.

Treatment of bacterial complications is necessary to start, before getting results of bacterial inoculation and definitions of sensitivity on antibiotics of the allocated microflora. At the pneumonia indicate benzylpenicillin or one of semisynthetic Penicillins. At a hypersensibility of organism to these preparations use Erythromicin, Oleandomycin or Doxycyclin. At ambulatory treatment also frequently indicate one of the combined preparations – Oletetrin, Tetraolen, and at more serious current of pneumonia – Vancomycin, Tienam and antiinfluenza a gamma-globulin or a polyglobulin. The expressed effect is spotted at a combination of preparations of Tetracyclines or Cefalosporines with semisynthetic Penicillins and Gentamicin, infused parenterally. At unsuccessful treatment after 5 – 7 days choose antibiotic in view of sensitivity of microflora of sputum. Alternative preparations may be a Fusidin – Natry, Bactrim, Nitroxolin.

    At serious bacterial complications of influenza apply Macrolides of II – III generations: Sumamed, Claritromicin, Cefalosporines of III -IV generations – Cefotaxim, Cefoperason, Cedex, Cefpirom, combinations of Cefalosporines and Penicillins with inhibitors of β-lactamazes ( acid Clavulanic, Sulbactam, Tasobactam) and Aminoglicosides. Preparations of a choice may be Ftorhinolones – Ofloxacin, Ciprofloxacin, Pefloxacin and others, which have high antibacterial activity and wide spectrum of action, including influence on polyresistant of Gram-negative and Gram-positive bacteries.

 Use  antitussive (Glaucini hydrochloride, Libexin, Tusuprex), expectorating ( terpin hydrate, Natrii benzoic, broth of a herb of Termopsis, a root of althaea, mucolytic (Acetylcystein, Bronchoclar, Bromhexin, Ambroxole, Lasolvan, Fluditec) agents, physical methods of treatment.

http://emedicine.medscape.com/article/219557-treatment#showall

http://emedicine.medscape.com/article/219557-medication#showall

ADENOVIRAL INFECTION

Definition

Adenoviral infection is a disease developing mainly in children and having the symptoms of the mucus affection of the respiratory tract, eyes. intestines as well as lymphoid tissue.

Historic Reference

The pathogens of the adenoviral diseases were first isolated in 1953 by W. Rowe and his staff from the tissues of the surgically extracted glands and adenoids. The belonging of the isolated viruses to the respiratory infection pathogens was established in 1954 when M. R. Hilleman and J. H. Werner discovered the increase of the neutralizing complement binding to them antibodies in the blood serum. In April of 1954 F. Neva and J. F. Enders isolated a similar virus from the excrement of a two-year-old child who had a fever accompanied by conjunctivitis, pharyngitis and the increase of the neck and groin lymph nodes. A year later R. J. Huebner and W. P. Rowe reported on the isolation of more than 100 cultures of viruses from the nasopharynx, conjunctiva and excrement of the patients who had different forms of the acute febrile diseases of the respiratory tract.

In 1956 the commission at the International committee of the nomenclatures that studied viruses named the isolated viruses “Adenoviruses” as they had first been isolated from the adenoids and the diseases caused by them got the name “adenoviral diseases”.

http://www.cdc.gov/adenovirus/about/overview.html

In 1962 J. Trentin and his co-author R. Huebner together with their co-authors made some experiments on the newbom hamsters that showed that the adenoviruses were oncologically active.

The adenoviruses constitute a family of Adenoviridae including two clans: Mastadenovirus (M) (mammal) of more than 90 kinds and Aviadenovirus (A) (birds) – 18 kinds. The gene of the adenoviruses is a lineal double spiral DNA. They are thermolabile, get destroyed at 56° C in 30 minutes, stable to pH 5-9. They can be preserved in the frozen form. They can be lyophilized without losing the infectious titer (Fig. 2).

 

Fig. 2. Adenovirus

Epidemiology

The adenoviral diseases are registered everywhere all the year round, more often in the cold seasons. The natural reservoir of the adenoviruses for humans is a human. The infection is spread by both the people with the clinically expressed disease and virus carriers. The adenoviruses are excreted from the respiratory tract till the 25^th day of the disease, and from excrement for two months. Though the main way of the infection transmission is an airborne one, an alimentary way cannot be excluded. In the period of the epidemic spread the adenoviruses can also be isolated from the sewage. The diseases can be observed both in the form of the epidemic outbreaks and sporadic cases. The epidemic process during the outbreaks develops slowly. At first the single cases of the disease and then a more rapid growth. Taking into account the meaning of the separate serotypes in the pathology and the peculiarities of the epidemic process the adenoviruses are divided into epidemic, latent and a group which role in the pathology is unclear. The adenoviruses of the latent group also cause acute diseases but in this case there is a less intensive coverage of people at outbreaks, a higher per cent of the latent infection and a mild course are observed.

http://virus.stanford.edu/adeno/adeno.html

Pathogenesis

The adenoviruses usually affect different organs and tissues: the respiratory tract – eyes, lymphoid tissues, intestines and urinary bladder.

The upper parts of the respiratory tract and conjunctivas are the most frequent entrance gates. The virus penetrates the lower parts from the upper part through the bronchial paths and causes atypical pneumonia in adults and children. The virus intensively reproduced in the parenchyma of the lungy and in the cells of the upper respiratory tract. Virusemia is one of the stages of the adenoviral infection. Because of virusemia the virus can penetrate not only the lower respiratory tract but also other organs and tissues by a hematogenic way. In the diseases connected with the adenoviruses of the academic type, virusemia is observed in the acute period from the 1^st to the 8th day. In the latent type cases the period of virusemia lasts up to 2-3 weeks.

The viruses are supposed to affect the endothelium of the vessels and thus cause the exudative type of affection, inclination towards the prolapse of fibrin, necrotic changes in the mucus membrane (exudative pharyngitis, tonsillitis. film conjunctivitis).

Irrespective of the fact that an adenoviral disease has only respiratory or respiratory and intestines symptoms the reproduction of the adenoviruses is observed in the small intestine for longer periods of time (10 days and longer) than in the respiratory tract.

An association of the adenoviruses with the immune deficiency conditions has been described. They were isolated from the urine and excrements of the AIDS patients as well as from the urine of the patients who were ill with other immune deficiency illnesses.

Lymphadenopathy has such symptoms as the increase of the tonsils, periphery lymph nodes, liver, spleen, tracheobronchial. bronchopulmonal and mesenteric nodes.

http://emedicine.medscape.com/article/211738-overview#showall

Clinical manifestations

The disease caused by the adenoviruses is characterized by the polymorphism of the clinical manifestations, that do not develop simultaneously. There are symptoms of the affection of the respiratory tract, eyes, intestines mucous membrane, the disease is accompanied by a prolonged fever and a moderately expressed intoxication. The incubation period lasts 5-7 days with the fluctuations from 4 to 12 days. The adenoviral infection is mainly characterized by a gradual development of the disease with the accumulation of the clinical symptoms, the replacement of some symptoms by others and the prevalence of the local symptoms over the general ones. Besides, an acute onset of the disease is also possible. As a rule the expressed catarrhal symptoms with a labored nasal breathing come to the foreground. The intoxication is expressed by flabbiness, adynamia, the appetite worsening, moderate and inconstant headaches, sometimes vomiting. The rise of the temperature is usually gradual, in the beginning 37.2°C. on the following days – 38° C and sometimes higher. The duration of the fever is 5-7 days less often – up to 12 days.

The acute respiratory disease is the most frequent clinical manifestation. There are usually no pathognomonic symptoms. In the beginning its diagnostics is considerably difficult, especially, in the first cases because they do not practically differ from catarrh caused by different other pathogens. The onset can be acute or gradual. Already on the first day there is a labored nasal breathing, and on the second-third day an abundant serous or serous-mucous discharge. There develops hyperemia of the nasopharynx mucous membrane, edema of the uvula, hyperplasia of the lymphoid tissue, especially, on the back wall of the throat. There is sometimes a vesicular rash on the mucous membrane of the mouth cavity. The submandibular lymph nodes and the ones on the back of the neck are enlarged. The cough is usually dry, it becomes rough, barking when laryngitis develops. sometimes the voice becomes hoarse, but there is no aphonia. In contrast to influenza croup develops in the first hours of the disease. The physical manifestations in the lungs are absent or they are poorly expressed.

Acute Pharyngitis. It is usually in the cold season of the year that the disease is observed, the general condition often remains satisfactory. The main complaint is a pain in the throat at swallowing. Moderate hyperemia of the airfoils, back wall of the throat with hyperplasia of the lyinphoid tissue can be noticed during the throat examination. The mucous membrane of the throat, airfoils, uvula, tonsils is loosened, edematic. On the surface of the tonsils there is a thin whitish patch in the form of dots which covers the tonsils. The exudate often spreads beyond the borders of the airfoils to the soft palate, back wall of the throat. The patches disappear during 5-6 days, but the edema of the mucous membranes of the throat and rhinitis usually remain longer. At the same time the peripheral lymph nodes are often enlarged. The cough is frequent, but not constant, it is moist, less often dry.

Pharyngoconjunctival  fever is the most typical clinical variant of the adenoviral infection. The term “pharyngoconjunctival fever” (FCF) was proposed by J. A. Bell and his co-authors (1965) while describing an outburst in the children’s summer camp. They also most fully described the clinical form characterized by the triad: fever, pharyngitis with the enlargement of the lymph nodes and conjunctivitis. As a rule the disease starts with the increase of the temperature which often increases up to 39-40°C and remains for 2-10 days (5-6 days on the average). There is a lytic temperature decrease. The main complaints of the patients are redness and uncomfortable sensation in the eyes, watery eyes. affection of the throat, headache. Somnolence and malaise often develop at the end of the feverish condition. Nausea, vomiting, diarrhea and nasal bleeding are observed very rarely. The bone-muscle aches and weakness are often observed in adults. During the throat examination the hyperemia of the back wall of the throat and lymphatic toll ides on it is observed. The submaxillary lymph nodes are often enlarged even it there is no pain in the throat. The disease is accompanied by the one-side nonpuruleiit follicular conjunctivitis, which remains from several days to three weeks and is manifested by the injection of the eye and eyelid vessels. The enlargement of the parotid lymph nodes is sometimes observed. There is no photophobia and pain in the eyes. The iris of the eye and cornea are usually not involved in the process. The exudale is almost always serous. The clinical symptoms (fever, pharyngitis and conjunctivitis) are manifested in different combinations. The pharyngoconjunctival fever in the form of sporadic cases or outbursts is registered in different countries.

Eye Affection. The intensely expressed inflammation of the conjunctiva with bright hyperemia and scarce discharge is a peculiarity of adenoviral conjunctivitis. The inflamed mucous membrane of the conjunctiva looks like a “conflagration without a fire”. Unlike in conjunctivitis of another etiology only the lower eyelid is usually affected. In the beginning the inflammatory process in the eye develops only on one side and only later the second eye gets involved in the process, but the changes in it are less expressed. There are such forms of the eye affection as catarrhal follicular. membranous conjunctivitis and keratoconjunctivitis. The last ones usually develop in adults; a long recurring course is typical of them.

In case of the catarrhal form hyperemia. tissue infiltration, edema of the eyelids and conjunctiva are observed. The edema and the infiltration of the tissues usually disappear in 2-5 days. but the hyperemia of the conjunctiva remains up to three weeks, sometimes – up to a month.

In case of the follicular form of conjunctivitis along with conjunctiva infiltration and edema of the eyelids there is abundant eruption of the large follicles on the conjunctiva. There is no discharge or it is scarce. One third of the patients have a hemorrhage into the sclera of the eyeball. The hemorrhage dissolves slowly, during 7-9 days. and then during 3-4 days a vessels’ netting “sclera injection'” can be observed. Sometimes the hemorrhages are so large that the eye looks like a rabbit’s one (Fig.3).

Fig.3. Conjunctivitis

In case of membranous conjunctivitis the tissue infiltration, eyelid edema are much more expressed (often a patient cannot even open the eye) than in catarrhal or follicular forms, and the edema of the eyelids is soft in contrast to the diphtheritic one. The hemorrhages into the conjunctiva and sclera of the eye are more massive. The gray dense films appear on the 4-6 day of the disease. The bleeding surface remains after their removal. The discharge is scanty, very often there is sanioserous discharge. Parents say that “the child cries with bloody tears”.

In case of keratoconjunctivitis the disease has an acute onset and is manifested by hyperemia and the conjunctiva edema. On the 2-3 rd day together with the eyelid edema, redness of the eyeball conjunctiva, lachrymal muscle and semilunar fold. Hemorrhages appear on the eyelid conjunctiva and the hypodermic fold. In some cases the films appear on the eyelid conjunctiva. The abundant eruption on the eyelid conjunctiva and transitional folds of the superficial follicles is very typical. The discharge is usually scanty. The enlargement and tenderness of the parotid and sometimes submandibular lymph nodes are important diagnostic symptoms (Fig.4).

 

Fig.4. Keratoconjunctivitis

The typical changes in the cornea appear on the 7-14th day of the disease. Their appearance often coincides with the disappearing of the inflammatory processes in the conjunctiva. On the cornea, usually in the center, in the pupil zone. there are delicate subepithelial round infiltrates, which do not tend to ulceration. The disease is sometimes accompanied by the temperature increase. Quite often the patients complain of a headache and general malaise. A patient considers the dimness of the cornea to be a foreign body. photophobia. and vision disorder. In half of the patients only one eye is affected, but in some time (7-10 days) the second eye can get involved in the process. The disease lasts from 8-10 days to 6-7 weeks. The foci of dimness on the cornea dissolve slowly, during 3 months. In some cases the dimness remains for a long time and causes the vision worsening.

 Pneumonia. Among different forms of the adenoviral diseases pneumonia causes the greatest alarm, especially, in the children of the young age. Clinically the symptoms of the pneumonia in case of the adenoviral infection are expressed quite distinctly. The disease has an acute onset with the temperature increase up to 38-39°C; the temperature curve is usually irregular, with oscillations, quite often the fever period has a lingering character up to 20 days and longer. The temperature reaction is not expressed or absent in the children of the first months. Pneumonia is accompanied by the expressed catarrhal manifeslations in the upper respiratory tract. The fauces mucous membrane is hyperemi, edematic, the tonsils are enlarged and in some cases they are covered with whitish fur. The nasal discharge is abundant. The discharge is mucous or mucopurulent. The cough is painful, often excruciating, dry or with the discharge of the mucopurulent sputum. During the first days of the disease the physical changes in the lungs may not be found, they usually develop later. From the 3-4th day of the disease along with the shortening of the resonance with the tympanic inflection there is a big amount of dry and mixed moist rale. The rale can disappear, and then come back again. Sometimes an asthmatic component joins these manifestations. The massive affection of the lung tissues is revealed during the X-ray examination. The inflammatory foci flow together. they dissolve slowly. A tendency to relapses, exacerbation and a slow reparation of the inflammatory process in the lungs are characteristic of adenoviral pneumonia. A severe course of pneumonia with an unfavorable outcome is usually observed in the children of the early age, and in other patients who are weakened by previous diseases or accompanied diseases. Pleuritis and abscesses can complicate pneumonia, but it occurs comparatively rarely.

The changes of some inner organs and systems, which are typical of the adenoviral disease (lymphadenopathy, hepalosplenic syndrome, changes in the cardiovascular, nervous system, hematological changes, etc.). are more expressed in case of pneumonia and occur more often comparing with the uncomplicated course of the disease. Sometimes pneumonia is accompanied by conjunctivitis which is characteristic of the adenoviral disease, that helps in the etiologic diagnostics.

 

 

 

Diagnosis and Differential Diagnosis

 The problems in the differential diagnostics of the diseases which form this group are due to the fact that different viruses can cause similar clinical syndromes and first of all the syndrome of the acute disease of the respirator, tract.

The differential diagnostics is possible only in case of the typical course of the disease during the clinical recognition of the nosologic forms taking into consideration the peculiarities of the location of the pathological process, the degree of the toxicosis, the presence and expressiveness of the catarrhal manifestations as well as changes in other organs and systems.

Times, in contrast to influenza in the adenoviral diseases the local limited outbreaks are registered, the incubation period in the infected patients is longer, the catarrhal manifestations with an abundant discharge are considerably expressed, there are typical changes in the fauces, the lymph nodes, liver and spleen are enlarged, relapses occur later.

In contrast to paragrippe the onset of the adenoviral diseases is often acute. the exudative component is more expressed, there is lymphoadenopathy. one-side conjunctivitis.

The clinical diagnostics of the RS infection is based on the primary affection of the lower parts of the respiratory tract, quite often with an asthmatic component and respiratory insufficiency. The changes in the upper parts are less expressed.

The confirmation of the diagnosis is based on the laboratory investigations. The collection of the material and the investigation methods are the same as in case of other viral infections of the respirators tract.

Treatment.

Treatment will carry out in view of gravity of current and the clinical form of disease. Localy use the etiotropic  preparation Desoxyribonucleasa which is instilated into  conjunctival bag and nasal courses as the solution. Apply also a solution of Oxolin, Oxolin Unguent, or Florenal for pawning edges of blepharons and for greasing mucosa of nose. As agent of a choice use solution of  human interferon as inhalations, dispersion or drops in a nose through every 1 – 2 houres during 2 – 3 days. Efficiency of treatment above, than earlier it is begun. Among inductores of interferon and imunomodulatores indicate amixin, amizin, cycloferon, proteflazid, erbisol. At serious forms of disease use human placental or serumal immunoglobulin (3 – 6 ml. unitary), at absence of effect give repeatedly in 6 – 8 houres or oext day. According to the indications apply infusions of 5 % of  solution of a glucose with ascorbic acid. Reopolyglucin,  sault solutions, humidified Oxygen are used through a nasal catheter.

    Recommend a hot drinks of tinctura of Raspberries, Lime color, flowers of a black Elder, tea with lemon, sudorific collectings. For inhalations use warm broths of leaves of eucalypt,  sage, pine buds, grasses of thyme, buds of a birch (separately or in admixture), for a gargle of pharynx and an oral cavity give broths of flowers Chamomiles, Calendula, grasses of a Yarrow, Sage. Indicated also sinapismuses on thorax cell and soles of stop.

In case of rhinitis  we instill into nose vasoconstrictive preparations,such as: naphthyzin ,  ephedrin hydrochloride, pharmasolin. For cupping of inflammatory process apply into nasopharynx Faringosept or Falimint. Among others agents recommend Pectusin or Terpin hydrate, Ascorutin,Calci of gluconate, Methyluracil, and also Diazolinum, Suprastin, Tavegil, Gismanal, Zestra, Loratidin, Alegra, Telfast.

In case of bacterial complications antibiotics and others chemotherapeutic agents are indicated in view of kind of the originator and its medicinal sensitivity. Use benzylpenicillin sodic salt, Ampicillin sodic salt, Carbapenicilin dinatri salt, Ampiox, Erythromycin, Oleandomycin phosphas or Doxycyclin hydrochloride, Cefalosporines (Cefazolin, Cefotaxim, Ceftriaxon).http://emedicine.medscape.com/article/211738-medication#showall

http://intranet.tdmu.edu.ua/data/books/And-INF.pdf 

 

CHILDRED DISEASES

http://intranet.tdmu.edu.ua/data/books/And-INF.pdf

Rubella

Fig.1. Rubella

 

Rubella, commonly known as German measles, is a disease caused by the rubella virus. The name “rubella” is derived from the Latin, meaning little red. Rubella is also known as German measles because the disease was first described by German physicians in the mid-eighteenth century. This disease is often mild and attacks often pass unnoticed. The disease can last one to three days. Children recover more quickly than adults. Infection of the mother by Rubella virus during pregnancy can be serious; if the mother is infected within the first 20 weeks of pregnancy, the child may be born with congenital rubella syndrome (CRS), which entails a range of serious incurable illnesses. Spontaneous abortion occurs in up to 20% of cases.

Rubella is a common childhood infection usually with minimal systemic upset although transient arthropathy may occur in adults. Serious complications are very rare. Apart from the effects of transplacental infection on the developing fetus, rubella is a relatively trivial infection.

Acquired (i.e. not congenital) rubella is transmitted via airborne droplet emission from the upper respiratory tract of active cases. The virus may also be present in the urine, feces and on the skin. There is no carrier state: the reservoir exists entirely in active human cases. The disease has an incubation period of 2 to 3 weeks.^’

In most people the virus is rapidly eliminated. However, it may persist for some months post partum in infants surviving the CRS. These children are a significant source of infection to other infants and, more importantly, to pregnant female contacts.

http://www.cdc.gov/Features/Rubella/

http://www.cdc.gov/Features/Rubella/

It should not be confused with rubeola, which was a historical name for measles.

Signs and symptoms

After an incubation period of 14–21 days, the primary symptom of rubella virus infection is the appearance of a rash (exanthem) on the face which spreads to the trunk and limbs and usually fades after three days. Other symptoms include low grade fever, swollen glands (post cervical lymphadenopathy), joint pains, headache and conjunctivitis. The swollen glands or lymph nodes can persist for up to a week and the fever rarely rises above 38 ^oC (100.4 ^oF). The rash disappears after a few days with no staining or peeling of the skin. Forchheimer’s sign occurs in 20% of cases, and is characterized by small, red papules on the area of the soft palate.

Rubella can affect anyone of any age and is generally a mild disease, rare in infants or those over the age of 40. The older the person is the more severe the symptoms are likely to be. Up to one-third of older girls or women experience joint pain or arthritic type symptoms with rubella. The virus is contracted through the respiratory tract and has an incubation period of 2 to 3 weeks. During this incubation period, the carrier is contagious but may show no symptoms.

Congenital rubella syndrome

Main article: Congenital rubella syndrome

Rubella can cause congenital rubella syndrome in the newly born. The syndrome (CRS) follows intrauterine infection by Rubella virus and comprises cardiac, cerebral, ophthalmic and auditory defects. It may also cause prematurity, low birth weight, and neonatal thrombocytopenia, anaemia and hepatitis. The risk of major defects or organogenesis is highest for infection in the first trimester. CRS is the main reason a vaccine for rubella was developed. Many mothers who contract rubella within the first critical trimester either have a miscarriage or a still born baby. If the baby survives the infection, it can be born with severe heart disorders (PDA being the most common), blindness, deafness, or other life threatening organ disorders. The skin manifestations are called “blueberry muffin lesions.”

http://emedicine.medscape.com/article/968523-clinical#showall

 

Cause

Main article: Rubella virus

The disease is caused by Rubella virus, a togavirus that is enveloped and has a single-stranded RNA genome. The virus is transmitted by the respiratory route and replicates in the nasopharynx and lymph nodes. The virus is found in the blood 5 to 7 days after infection and spreads throughout the body. It is capable of crossing the placenta and infecting the fetus where it stops cells from developing or destroys them.

Increased susceptibility to infection might be inherited as there is some indication that HLA-A1 or factors surrounding A1 on extended haplotypes are be involved in virus infection or non-resolution of the disease.

Diagnosis of acquired rubella

Rubella virus specific IgM antibodies are present in people recently infected by Rubella virus but these antibodies can persist for over a year and a positive test result needs to be interpreted with caution. The presence of these antibodies along with, or a short time after, the characteristic rash confirms the diagnosis.

Prevention

Main article: MMR vaccine

Rubella infections are prevented by active immunisation programs using live, disabled virus vaccines. Two live attenuated virus vaccines, RA 27/3 and Cendehill strains, were effective in the prevention of adult disease. However their use in prepubertile females did not produce a significant fall in the overall incidence rate of CRS in the UK. Reductions were only achieved by immunisation of all children.

The vaccine is now given as part of the MMR vaccine. The WHO recommends the first dose is given at 12 to 18 months of age with a second dose at 36 months. Pregnant women are usually tested for immunity to rubella early on. Women found to be susceptible are not vaccinated until after the baby is born because the vaccine contains live virus.

The immunization program has been quite successful. Cuba declared the disease eliminated in the 1990s, and in 2004 the Centers for Disease Control and Prevention announced that both the congenital and acquired forms of rubella had been eliminated from the United States.

Treatment

There is no specific treatment for Rubella; management is a matter of responding to symptoms to diminish discomfort. Treatment of newly born babies is focused on management of the complications. Congenital heart defects and cataracts can be corrected by surgery. Management for ocular CRS is similar to that for age-related macular degeneration, including counseling, regular monitoring, and the provision of low vision devices, if required.

Prognosis

Rubella infection of children and adults is usually mild, self-limiting and often asymptomatic. The prognosis in children born with CRS is poor.

Epidemiology

Rubella is a disease that occurs worldwide. The virus tends to peak during the spring in countries with temperate climates. Before the vaccine to rubella was introduced in 1969, widespread outbreaks usually occurred every 6–9 years in the United States and 3–5 years in Europe, mostly affecting children in the 5-9 year old age group. Since the introduction of vaccine, occurrences have become rare in those countries with high uptake rates. However, in the UK there remains a large population of men susceptible to rubella who have not been vaccinated. Outbreaks of rubella occurred amongst many young men in the UK in 1993 and in 1996 the infection was transmitted to pregnant women, many of whom were immigrants and were susceptible. Outbreaks still arise, usually in developing countries where the vaccine is not as accessible.

During the epidemic in the US between 1962-1965, Rubella virus infections during pregnancy were estimated to have caused 30,000 still births and 20,000 children to be born impaired or disabled as a result of CRS. Universal immunisation producing a high level of herd immunity is important in the control of epidemics of rubella.

 

Measles

Fig.2. Measles

 

Fig.3.  Measles virus

 

Measles (IPA: /mizəlz/) is an infection of the respiratory system caused by a virus, specifically a paramyxovirus of the genus Morbillivirus. Morbilliviruses, like other paramyxoviruses, are enveloped, single-stranded, negative-sense RNA viruses. Symptoms include fever, cough, runny nose, red eyes and a generalized, maculopapular, erythematous rash.

Measles is spread through respiration (contact with fluids from an infected person’s nose and mouth, either directly or through aerosol transmission), and is highly contagious—90% of people without immunity sharing a house with an infected person will catch it. The infection has an average incubation period of 14 days (range 6–19 days) and infectivity lasts from 2–4 days prior to 2–5 days following the onset of the rash.

Measles was historically called rubeola. In contrast, German measles is an unrelated condition caused by the rubella virus.

Signs and symptoms

Fig.4. This patient presented on the third pre-eruptive day with “Koplik spots” indicative of the beginning onset of measles.

The classical symptoms of measles include four day fevers, the three Cs—cough, coryza (runny nose) and conjunctivitis (red eyes). The fever may reach up to 40° Celsius (104° Fahrenheit). Koplik’s spots seen inside the mouth are pathognomonic (diagnostic) for measles but are not often seen, even in real cases of measles, because they are transient and may disappear within a day of arising.

The characteristic measles rash is classically described as a generalized, maculopapular, erythematous rash that begins several days after the fever starts. It starts on the head before spreading to cover most of the body, often causing itching. The rash is said to “stain”, changing colour from red to dark brown, before disappearing.

Complications

Complications with measles are relatively common, ranging from relatively mild and less serious diarrhea, to pneumonia and encephalitis (subacute sclerosing panencephalitis), corneal ulceration leading to corneal scarring. Complications are usually more severe amongst adults who catch the virus.

The fatality rate from measles for otherwise healthy people in developed countries is 3 deaths per thousand cases. In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates have been as high as 28%. In immunocompromised patients (e.g. people with AIDS) the fatality rate is approximately 30 percent.

Cause

The measles virus is a highly contagious airborne pathogen which spreads primarily via the respiratory system. The virus is transmitted in respiratory secretions, and can be passed from person to person via aerosol droplets containing virus particles, such as those produced by a coughing patient. Once transmission occurs, the virus infects and replicates in the lymphatic system, urinary tract, conjunctivae, blood vessels and central nervous system of its new host. The role of epithelial cells is uncertain, but the virus must infect them to spread to a new individual.

Patients with the measles should be placed on droplet precautions.

Humans are the only knowatural hosts of measles, although the virus can infect some non-human primate species.

Diagnosis

Clinical diagnosis of measles requires a history of fever of at least three days together with at least one of the three C’s (cough, coryza, conjunctivitis). Observation of Koplik’s spots is also diagnostic of measles.

Alternatively, laboratory diagnosis of measles can be done with confirmation of positive measles IgM antibodies or isolation of measles virus RNA from respiratory specimens. In cases of measles infection following secondary vaccine failure IgM antibody may not be present. However, in the rare case of a secondary vaccine failure, other external symptoms may be present, including nausea, headaches, or a feeling of slight dizziness when turning one’s head to the left. In these cases serological confirmation may be made by showing IgG antibody rises by enzyme immunoassay or complement fixation. In children, where phlebotomy is inappropriate, saliva can be collected for salivary measles specific IgA test. Adults ommended to seek medical help right away.

Positive contact with other patients known to have measles adds strong epidemiological evidence to the diagnosis. The contact with any infected person in any way, including semen through sex, saliva, or mucus can cause infection.

Histologically, a unique cell can be found in the paracortical region of hyperplastic lymph nodes in patients affected with this condition. This cell, known as the Warthin-Finkeldey cell, is a multinucleated giant with eosinophilic cytoplasmic and nuclear inclusions.^]

Prevention

In developed countries, most children are immunized against measles by the age of 18 months, generally as part of a three-part MMR vaccine (measles, mumps, and rubella). The vaccination is generally not given earlier than this because children younger than 18 months usually retain anti-measles immunoglobulins (antibodies) transmitted from the mother during pregnancy. A second dose is usually given to children between the ages of four and five, in order to increase rates of immunity. Vaccination rates have been high enough to make measles relatively uncommon. Even a single case in a college dormitory or similar setting is often met with a local vaccination program, in case any of the people exposed are not already immune.

In developing countries where measles is highly endemic, the WHO recommend that two doses of vaccine be given at six months and at nine months of age. The vaccine should be given whether the child is HIV-infected or not. The vaccine is less effective in HIV-infected infants, but the risk of adverse reactions is low.

Unvaccinated populations are at risk for the disease. After vaccination rates dropped in northern Nigeria in the early 2000s due to religious and political objections, the number of cases rose significantly, and hundreds of children died. A 2005 measles outbreak in Indiana was attributed to children whose parents refused vaccination.^[10] In the early 2000s the MMR vaccine controversy in the United Kingdom regarding a potential link between the combined MMR vaccine (vaccinating children from mumps, measles and rubella) and autism prompted a reemergence of the “measles party”, where parents deliberately expose their child to measles in the hope of building up the child’s immunity without an injection. This practice poses many health risks to the child, and has been discouraged by the public health authorities. Scientific evidence provides no support for the hypothesis that MMR plays a role in causing autism. However, the MMR scare in Britain caused uptake of the vaccine to plunge, and measles cases came back: 2007 saw 971 cases in England and Wales, the biggest rise in occurrence in measles cases since records began in 1995.

The joint press release by members of the Measles Initiative brings to light another benefit of the fight against measles: “Measles vaccination campaigns are contributing to the reduction of child deaths from other causes. They have become a channel for the delivery of other life-saving interventions, such as bed nets to protect against malaria, de-worming medicine and vitamin A supplements. Combining measles immunization with other health interventions is a contribution to the achievement of Millennium Development Goal Number 4: a two-thirds reduction in child deaths between 1990 and 2015.”

Treatment

There is no cure for measles. Most patients with uncomplicated measles will recover with rest and supportive treatment.

Some patients will develop pneumonia as a sequela to the measles.

Epidemiology

According to the World Health Organization (WHO), measles is a leading cause of vaccine-preventable childhood mortality. Worldwide, the fatality rate has been significantly reduced by partners in the Measles Initiative: the American Red Cross, the United States Centers for Disease Control and Prevention (CDC), the United Nations Foundation, UNICEF and the World Health Organization (WHO). Globally, measles deaths are down 60 percent, from an estimated 873,000 deaths in 1999 to 345,000 in 2005. Africa has seen the most success, with annual measles deaths falling by 75 percent in just 5 years, from an estimated 506,000 to 126,000.

History and culture

The Antonine Plague, 165-180 AD, also known as the Plague of Galen, who described it, was probably smallpox or measles. Disease killed as much as one-third of the population in some areas, and decimated the Roman army. The first scientific description of measles and its distinction from smallpox and chickenpox is credited to the Persian physician, Muhammad ibn Zakariya ar-Razi (860-932), known to the West as “Rhazes”, who published a book entitled The Book of Smallpox and Measles (in Arabic: Kitab fi al-jadari wa-al-hasbah).

Measles is an endemic disease, meaning that it has been continually present in a community, and many people develop resistance. In populations that have not been exposed to measles, exposure to a new disease can be devastating. In 1529, a measles outbreak in Cuba killed two-thirds of the natives who had previously survived smallpox. Two years later measles was responsible for the deaths of half the population of Honduras, and had ravaged Mexico, Central America, and the Inca civilization.

In roughly the last 150 years, measles has been estimated to have killed about 200 million people worldwide. During the 1850s, measles killed a fifth of Hawaii‘s people. In 1875, measles killed over 40,000 Fijians, approximately one-third of the population. In the 19th century, the disease decimated the Andamanese population. In 1954, the virus causing the disease was isolated from an 11-year old boy from the United States, David Edmonston, and adapted and propagated on chick embryo tissue culture.^[22] To date, 21 strains of the measles virus have been identified. Licensed vaccines to prevent the disease became available in 1963.

Fig.6. Intra oral rash of measles

Fig.7. Measles in African Child

 

Fig.8. Measles. This child shows a day-4 rash with measles

Fig.9. Histopathology of measles pneumonia. Giant cell

 

Mumps

 

Fig.10. Mumps

Mumps or epidemic parotitis is a viral disease of the human species, caused by the mumps virus. Prior to the development of vaccination and the introduction of a vaccine, it was a common childhood disease worldwide, and is still a significant threat to health in the third world.

Painful swelling of the salivary glands (classically the parotid gland) is the most typical presentation. Painful testicular swelling (orchitis) and rash may also occur. The symptoms are generally not severe in children. In teenage males and men, complications such as infertility or subfertility are more common, although still rare in absolute terms. The disease is generally self-limited, running its course before receding, with no specific treatment apart from controlling the symptoms with painkillers.

Symptoms

Fig.11. Comparison of a person before and after contracting the mumps

The more common symptoms of mumps are:

·  Parotid inflammation (or parotitis) in 60–70% of infections and 95% of patients with symptoms. Parotitis causes swelling and local pain, particularly when chewing. It can occur on one side (unilateral) but is more common on both sides (bilateral) in about 90% of cases.

·  Fever

·  Headache

·  Orchitis, referring to painful inflammation of the testicle. Males past puberty who develop mumps have a 30 percent risk of orchitis.

Other symptoms of mumps can include dry mouth, sore face and/or ears and occasionally in more serious cases, loss of voice. In addition, up to 20% of persons infected with the mumps virus do not show symptoms, so it is possible to be infected and spread the virus without knowing it.

Prodrome

Fever and headache are prodromal symptoms of mumps, together with malaise and anorexia.

Signs and tests

A physical examination confirms the presence of the swollen glands. Usually the disease is diagnosed on clinical grounds and no confirmatory laboratory testing is needed. If there is uncertainty about the diagnosis, a test of saliva, or blood

 may be carried out; a newer diagnostic confirmation, using real-time nested polymerase chain reaction (PCR) technology, has also been developed. An estimated 20%-30% of cases are asymptomatic. As with any inflammation of the salivary glands, serum amylase is often elevated.

Transmission

Mumps is a contagious disease that is spread from person-to-person through contact with respiratory secretions such as saliva from an infected person. When an infected person coughs or sneezes, the droplets aerosolize and can enter the eyes, nose, or mouth of another person. Mumps can also be spread by sharing food, sharing drinks, and kissing. The virus can also survive on surfaces and then be spread after contact in a similar manner.

A person infected with mumps is contagious from approximately 6 days before the onset of symptoms until about 9 days after symptoms start. The incubation period (time until symptoms begin) can be from 14–25 days but is more typically 16–18 days.

Treatment

There is no specific treatment for mumps. Symptoms may be relieved by the application of intermittent ice or heat to the affected neck area and by acetaminophen/paracetamol (Tylenol) for pain relief. Aspirin use is not used due to a hypothetical link with Reye’s syndrome. Warm salt water gargles, soft foods, and extra fluids may also help relieve symptoms.

Patients are advised to avoid fruit juice or any acidic foods, since these stimulate the salivary glands, which can be painful.

Prognosis

Death is very unusual. The disease is self-limiting, and general outcome is good, even if other organs are involved.

Known complications of mumps include:

·  Infection of other organ systems

·  Mumps viral infections in adolescent and adult males carry an up to 30% risk that the testes may become infected (orchitis or epididymitis), which can be quite painful; about half of these infections result in testicular atrophy, and in rare cases sterility can follow.

·  Spontaneous abortion in about 27% of cases during the first trimester of pregnancy.

·  Mild forms of meningitis in up to 10% of cases (40% of cases occur without parotid swelling)

·  Oophoritis (inflammation of ovaries) in about 5% of adolescent and adult females, but fertility is rarely affected.

·  Pancreatitis in about 4% of cases, manifesting as abdominal pain and vomiting

·  Encephalitis (very rare, and fatal in about 1% of the cases when it occurs)

·  Profound (91 dB or more) but rare sensorineural hearing loss, uni- or bilateral. Acute unilateral deafness occurs in about 0.005% of cases.

After the illness, life-long immunity to mumps generally occurs; reinfection is possible but tends to be mild and atypical.

Prevention

The most common preventative measure against mumps is immunization with a mumps vaccine. The vaccine may be given separately or as part of the MMR immunization vaccine which also protects against measles and rubella. In the US, MMR is now being supplanted by MMRV, which adds protection against chickenpox. The WHO (World Health Organization) recommends the use of mumps vaccines in all countries with well-functioning childhood vaccination programmes. In the United Kingdom it is routinely given to children at age 15 months. The American Academy of Pediatrics recommends the routine administration of MMR vaccine at ages 12–15 months and at 4–6 years. In some locations, the vaccine is given again between 4 to 6 years of age, or between 11 and 12 years of age if not previously given. The efficacy of the vaccine depends on the strain of the vaccine, but is usually around 80%. The Jeryl Lynn strain is most commonly used in developed countries but has been shown to have reduced efficacy in epidemic situations. The Leningrad-Zagreb strain commonly used in developing countries appears to have superior efficacy in epidemic situations.

Due to the outbreaks within college and university settings, many governments have established vaccination programs to prevent large-scale outbreaks. In Canada, provincial governments and the Public Health Agency of Canada have all participated in awareness campaigns to encourage students ranging from grade 1 to college and university to get vaccinated.

Some anti-vaccine activists protest against the administration of a vaccine against mumps, claiming that the attenuated vaccine strain is harmful, and/or that the wild disease is beneficial. Disagreeing, the WHO, the American Academy of Pediatrics, the Advisory Committee on Immunization Practices of the Centers for Disease Control and Prevention, the American Academy of Family Physicians, the British Medical Association and the Royal Pharmaceutical Society of Great Britain currently recommend routine vaccination of children against mumps. The British Medical Association and Royal Pharmaceutical Society of Great Britain had previously recommended against general mumps vaccination, changing that recommendation in 1987. In 1988 it became United Kingdom government policy to introduce mass child mumps vaccination programmes with the MMR vaccine, and MMR vaccine is now routinely administered in the UK.

Before the introduction of the mumps vaccine, the mumps virus was the leading cause of viral meningoencephalitis in the United States. However, encephalitis occurs rarely (less than 2 per 100,000). In one of the largest studies in the literature, the most common symptoms of mumps meningoencephalitis were found to be fever (97%), vomiting (94%) and headache (88.8%). The mumps vaccine was introduced into the United States in December 1967: since its introduction there has been a steady decrease in the incidence of mumps and mumps virus infection. There were 151,209 cases of mumps reported in 1968. Since 2001, the case average was only 265 per year, excluding an outbreak of >6000 cases in 2006 attributed largely to university contagion in young adults.

Scarlet fever

 

Fig.12. Scarlet fever

 

Scarlet fever is a disease caused by an erythrogenic exotoxin released by Streptococcus pyogenes. The term Scarlatina may be used interchangeably with Scarlet Fever, though it is commonly used to indicate the less acute form of Scarlet Fever that is often seen since the beginning of the twentieth century.

It is characterized by:

·  Sore throat

·  Fever

·  Bright red tongue with a “strawberry” appearance

·  Characteristic rash, which:

·  is fine, red, and rough-textured; it blanches upon pressure

·  appears 12–48 hours after the fever

·  generally starts on the chest, armpits, and behind the ears

·  spares the face (although some circumoral pallor is characteristic)

·  is worse in the skin folds. These are called Pastia lines (where the rash runs together in the arm pits and groins) appear and can persist after the rash is gone

·  may spread to cover the uvula.

·  The rash begins to fade three to four days after onset and desquamation (peeling) begins. “This phase begins with flakes peeling from the face. Peeling from the palms and around the fingers occurs about a week later.”^[2] Peeling also occurs in axilla, groin, and tips of the fingers and toes.

Diagnosis of scarlet fever is clinical. The blood test shows marked leukocytosis with neutrophilia and conservated or increased eosinophils, high erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and elevation of antistreptolysin O titer. Blood culture is rarely positive, but the streptococci can usually be demonstrated in throat culture. The complications of scarlet fever include septic complications due to spread of streptococcus in blood and immune-mediated complications due to an aberrant immune response. Septic complications, today rare, include ear and sinus infection, streptococcal pneumonia, empyema thoracis, meningitis and full-blown sepsis, upon which the condition may be called malignant scarlet fever.

Immune complications include acute glomerulonephritis, rheumatic fever and erythema nodosum. The secondary scarlatinous disease, or secondary malignant syndrome of scarlet fever, includes renewed fever, renewed angina, septic ear, nose, and throat complications and kidney infection or rheumatic fever and is seen around the eighteenth day of untreated scarlet fever.

Fig.13. Scarlet Fever’s pebbly, dry rash.

Symptoms

The rash is the most striking sign of scarlet fever. It usually begins looking like a bad sunburn with tiny bumps, and it may itch. The rash usually appears first on the neck and face, often leaving a clear unaffected area around the mouth. It spreads to the chest and back, then to the rest of the body. In body creases, especially around the underarms and elbows, the rash forms classic red streaks (on very dark skin, the streaks may appear darker than the rest of the skin). Areas of rash usually turn white (or paler brown, with dark complected skin) when you press on them. By the sixth day of the infection the rash usually fades, but the affected skin may begin to peel.

Aside from the rash, there are usually other symptoms that help to confirm a diagnosis of scarlet fever, including a reddened sore throat, a fever at or above 101 °F (38.3 C), and swollen glands in the neck. Scarlet fever can also occur with a low fever. The tonsils and back of the throat may be covered with a whitish coating, or appear red, swollen, and dotted with whitish or yellowish specks of pus. Early in the infection, the tongue may have a whitish or yellowish coating. A person with scarlet fever also may have chills, body aches, nausea, vomiting, and loss of appetite.

When scarlet fever occurs because of a throat infection, the fever typically stops within 3 to 5 days, and the sore throat passes soon afterward. The scarlet fever rash usually fades on the sixth day after sore throat symptoms began, but skin that was covered by rash may begin to peel. This peeling may last 10 days. The infection itself is usually cured with a 10-day course of antibiotics, but it may take a few weeks for tonsils and swollen glands to return to normal.

In rare cases, scarlet fever may develop from a streptococcal skin infection like impetigo. In these cases, the person may not get a sore throat.

Treatment

Husband and wife Gladys Henry Dick and George Frederick Dick developed a vaccine in the 1920s that was later eclipsed by penicillin in the 1940s. Other than the occurrence of the diarrhea, the treatment and course of scarlet fever are no different from those of any strep throat. In case of penicillin allergy, clindamycin or erythromycin can be used with success. Patients should no longer be infectious after taking antibiotics for 24 hours. Persons who have been exposed to scarlet fever should watch carefully for a full week for symptoms, especially if aged 3 to young adult. It’s very important to be tested (throat culture) and if positive, seek treatment. For reasons unknown, toddlers rarely contract scarlet fever.