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Key features of diagnosis, treatment and prevention of infections with transmissive mechanism

June 29, 2024

Key features of diagnosis, treatment and prevention of infections with transmissive mechanism. Diagnosis and treatment of complicated forms of tropical malaria. Problem of arbovirus infections and hemorrhagic fevers (dengue fever, pappatachi, Congo-Crimea with renal syndrome, Lassa, Marburg, Ebola). Differential diagnosis of riketsiosis (epidemic typhus, marsel fever, vesiculous rickettsiosis), preventive measures to reduce the incidence of rickettsial disease. Differential Diagnosis of Lyme disease. Tactic of physician in identifying patients with infectious diseases, regulated the International Health Regulations (plague, yellow fever, poliomyelitis, West Nile fever). The problem of sepsis in medical practice

MALARIA

http://health.nytimes.com/health/guides/disease/malaria/overview.html

Definition

Malaria (from the colloquial Italian “mala” – bad, and “aria” – air) is an infection characterized by certain febrile disturbances caused by protozoan parasites of the class Sporozoa and of the family Plasmodiidae. Man is the intermediate host of these parasites, which undergo an asexual stage of development in the red corpuscles. The Parasite undergoes a sexual phase of development in the Anopheles mosquito, which is hence the definitive host. Man acquires infection from the bite of such an infected mosquito. Clinically, malaria is characterized by periodic attacks of fever, associated with anemia and enlargement of the spleen, and if untreated, with cachexia and a deposit of black pigment in the various organs. The malady is amenable to treatment with quinine and several other synthetic compounds inimical to the life of the parasite.

History

Malaria was formerly supposed to be due to poisonous emanations from damp ground, hence the term “malaria,” introduced into English literature about 1829. Hippocrates, 460-370 B.C., in his book on epidemics, noted the existence of periodic fevers, divided them into quotidian, tertian, quartan, and subtertian, and referred to the enlarged spleen. Celsus recognized 2 types of tertian fever, one benign and similar to quartan fever, the other in which the attack is of longer duration and far more severe in character, the fever occupying 36 of the 48 hours and not entirely subsiding in the remissions, but being only mitigated.

Columella, about 116 B.C., suggested that the virus of malaria emanated from marshes and associated the disease with insects originating in them which attacked man in swarms. Also in the time of Caesar, views were expressed by Varro that swamp air might be the cause of malaria and furthermore that animals, so small that the eye could not follow them, might transmit diseases by way of the mouth or nose. In view of our present knowledge, it is remarkable that Lancisi. in 1718, should have associated marshes with the development of gnats, which insects he thought could not only introduce with their proboscides the putrefying organic matter of such swamps, but animalcules as well.

In 1638, Countess del Chinchon, wife of the Viceroy of Peru, was cured of an intermittent fever by treatment with the bark of a certain tree, which bark was introduced into Europe in 1640. Linne, who named the genus of quinine-producing about 100 years later, left out the first «h» in the name, hence the mistaken spelling Cinchona.

Discovery of the Parasite

The year 1880 was a most important one in the history of malaria, for on November 6, 1880, Laveran, at Constantine, first recognized the parasites of malaria while carrying on investigations as to the origin of the “pigmented bodies” and pigmented leukocytes. He observed not only spherical pigmented bodies, but also crescents, and in particular the flagellation of the male gamete, which demonstrated to him that these were living organisms. He proposed the name Oscillaria malarias on account of the movements of the flagellate body, but this had to be dropped as not valid, the generic name Oscillaria having been previously applied to another organism.

In 1894 Manson formulated the hypothesis of the mosquito transmission of malaria. He based this upon facts he observed in tracing the life-history of filaria and upon the fact that in malaria the flagellation of the male gametocyte does not take place for several minutes after the removal of the blood from the peripheral circulation. He also suggested that larvae might feed upon infected mosquitoes dying upon the water and thus acquire the disease.

Ross for 2 years caused mosquitoes to feed upon the blood of malarial patients which contained crescents, but as he used insects of the genera Culex and Aedes no development of the parasites in the tissues of the mosquitoes occurred, m 1897 he used eight dappled-wing mosquitoes (Anopheles Stephens) and in 2 of these, upon dissection, he noted the development of the pigmentary bodies to be different from anything he had observed in hundreds of dissections of other mosquitoes.

In 1886 Metschnikoff, from observation of sporulating parasites in the brain capillaries at the autopsy of a malarial case, considered them to be coccidial iature.

Four parasites, all of this genus, may give rise to malaria in man; the names of the species are Plasmodium vivax which produces benign tertian malaria, Plasmodium malarias of quartan malaria, Plasmodium ovate another tertian parasite, and Plasmodium falciparum, which causes malignant tertian malaria. Each of these species shows the following characters which are possessed by the genus, as it affects man.

Before proceeding to study the parasites there are certain terms which require definition.

Life history

This comprises two cycles or phases of development (Fig. 1):

a) schizogony in the tissues of man, which is succeeded by schizogony occurring in the blood stream of man ; these form the asexual cycle of the parasite ;

b) sporogony, the sexual cycle, which occurs in the body of an anopheline mosquito.

Cycles of Plasmodium development

Schizogony. When the sporozoite is introduced into man’s skin by the bite of an anopheline mosquito it passes into the blood stream from which it rapidly disappears to enter a parenchyma cell of the liver. Here a process of growth and multiplication occurs, known as preerythrocytic schizogony, which results in the development of a large schizont, measuring up to 60m in diameter and containing thousands of tiny merozoites less than 1m in size. The mature schizont ruptures about the seventh to the ninth day liberating the merozoites which enter the circulation and invade red blood corpuscles. This starts the phase of erythrocytic schizogony which, however, may not become demonstrable by the examination of blood films until one or two days later.

Erythrocytic schizogony occurs in the circulation and extends from the newly liberated merozoite which is ready to infect a fresh cell, to the rupture of the mature schizont with its contained daughter merozoites. This cycle occupies a period of forty-eight hours in P. vivax, ovale, falciparum and seventy-two in P. malaria, for its completion. The merozoites attack fresh cells, and in them develop into rings, after which the parasites grow through the large trophozoite stage, attain full size, and then proceed to reproduce by division. As soon as this has commenced, when there is evidence that the nucleus has divided and the cytoplasm begun to segment, the term “immature schizont” is applied. Later, when the parasite has reached the stage at which it is fully segmented, and when the merozoites are just about to be liberated by the disruption of the red cells, it is called a “mature schizont” The distended cell ruptures, and the merozoites are thus liberated into the plasma. The residual material is at the same time set free, and, with its contained pigment, is quickly ingested by fixed endothelial cells of the blood vessels, or by wandering phagocytes, usually large mononuclears. Such pigmented leukocytes may be found in stained films if the blood is examined soon after the schizonts have ruptured. The liberated merozoite contains no pigment, immediately enters a fresh red cell and starts the cycle again. As a result of repetition of the erythrocytic cycle and progressive invasion of fresh cells, the infected person in the course of ten days or so develops fever; the period of incubation may, however, be shorter or much longer than this.

There is strong indirect evidence to suggest that in the case of P. vivax, P. ovale and P. malaria the tissue phase of the parasite does not end with the rupture of the pre-erythrocytic schizont and the invasion of the circulation by its merozoites. It is believed that a cycle, known as exoerythrocytic schizogony, continues in the tissues, some of the liberated merozoites invading fresh liver cells and again proceeding to schizogony. According to this hypothesis, even when parasites are absent from the blood, schizogony is continuing repeatedly in the tissues, persisting often for years. On occasions merozoites are discharged into the circulation where they infect red blood corpuscles and thus recommence erythrocytic schizogony, causing parasitaemia. No such evidence exists in the case of P. falciparum, and it is thought that when the preerythrocytic schizonts of this species have discharged their merozoites into the blood stream the cycle of the parasite in the tissues ends.

Sporogony. The sexual or sporogony cycle occurs almost entirely in the Anophelis mosquito. In this method of reproduction there are, however, as we saw, preliminary, and also terminal, stages in the blood. Certain merozoites, instead of repeating the asexual cycle, become gametocytes, of which some are male and some are female. These are found in the peripheral blood. If they are taken up by the mosquito in biting, further development very quickly occurs, the remains of the infected red cell being discarded during the process. The asexual parasites ingested with the blood by the mosquito are destroyed in the gut; it is only the gametocytes which survive, and are able to infect the insect. In the case of P. falciparum, as we saw, the gametocytes are crescent-shaped, and the first step in the development is that they assume a rounded form like those of P. vivax and P. malarias. The next step is, that in the male, or microgametocyte, the pigment is suddenly observed to be in violent commotion and soon several filaments are extruded each of which contains a granule of the nuclear chromatin. These are extremely active, and it is they which caused the rapid movements of the pigment granules. They detach themselves and swim away; these are the male gametes or the microgametes, which correspond to spermatozoa. The female or macrogametocyte has meanwhile undergone a nuclear reduction process by which it is transformed into the female gamete or macrogamete. This is an unfertilized ovum, and it attracts the active microgametes, one of which penetrates and fertilizes it. After this, the ovum or zygote, as it is now called, is capable of slow movements and hence is known as an “ookinete”. This passes between the cells lining the insect’s gut, till it reaches the outer limiting membrane. It then ceases to move, becomes round and proceeds to grow, the membrane acting as a cyst wall. This stationary growing ookinete with its covering is called the oocyst, and it grows from about 6 to 60 nm in size. Since the zygote is simply the female malaria parasite after fertilization by the filamentous male gamete, there is still some pigment in it, and this can be detected inside the oocyst. The nucleus of the zygote divides repeatedly, and finally there are produced, inside the oocyst, thousands of minute thread-like structures called sporozoites. When the oocyst becomes mature it ruptures, and the contained sporozoites are set free in the insect’s haemocoele, the circulation of which carries them to all parts of the mosquito’s body.

Some of them invade the cells of the salivary glands, pass through them and reach the lumen, which communicates with the salivary ducts. The mosquito is now infective. When next it bites man, the salivary fluid containing the sporozoites passes into the skin wound. A mosquito may acquire and be able to transmit a double infection. It is possible for a single infective mosquito to transmit malaria to several people in succession, and at considerable intervals. The supply of sporozoites in the salivary ducts is replenished by a further passage of those in the hemocoele, through the gland cells, into the lumen.

The sporozoite is a narrow, slightly curved organism, measuring about 12 nm in length; it tapers at both ends, has an elongated central nucleus and is devoid of pigment. It is capable of slight undulatory movement As already noted, when it is inoculated into man it is carried in the blood stream to the cells of the liver, which it enters; there it rounds up, starts to grow, and so commences the asexual cycle in man.

The sexual cycle in the mosquito requires about eight to eighteen days for completion, depending on conditions such as moisture and temperature. In the case of P. malarias the sexual cycle in the mosquito is commonly as long as four weeks.

The asexual cycle can be started in a person otherwise than by the bite of an infective mosquito, for example, by inoculating blood which contains asexual forms, into a fresh subject. If it happens that the only forms present in the infected person’s blood are gametocytes, such as the crescents of malignant tertian malaria, no infection will result, as these can only infect the mosquito, and do not infect man.

Epidemiology and endemiology

Conditions which favour the presence and breeding of anopheles mosquitoes tend to the increase of malaria, and vice versa, and, whatever favors access of those insects and the parasites they contain, also favours the acquisition of malaria.

In subtropical regions subtertian malaria is a primary infection in summer and early autumn, hence the popular term – cestio-autumnal fever. This peculiarity can be explained to some extent by the higher atmospheric temperature required for its development in the mosquito. Hence, though benign and subtertian forms are frequently associated, and the latter can be acquired at any time in the tropics, it is only in the summer and early autumn that subtertian can be acquired in more temperate zones. When the temperature falls below 15° C. development of the oocyst in the mosquito is arrested, but when once the sporozoites have entered the salivary glands, they are capable of infecting man, even during the winter season.

Malaria incidence is usually endemic, but hyperendemicity is a distinct form, demanding for its production such an intensity of transmission that a high degree of tolerance to the effects of reinfection is induced in those who experience its effects over a number of years, especially as a result of repeated infections in early childhood.

The World Health Organization has proposed the following classification:

I. Hypoendemic Malaria with spleen rate in children 2-10 years of age 0-10 %

II. Mesoendemic Malaria with spleen rate in children 2-10 years of age 11-50 %

III, Hyperendemic Malaria with spleen rate in children 2-10 years of age constantly over 75 %. Spleen rate in adults is also high.

IV. Holoendemic Malaria with spleen rate in children 2-10 years of age constantly over 75 5. Spleen rate in adults low; it is in this type of endemicity that the strongest adult tolerance is found.

Morbid anatomy and pathology of malaria

The pathology of malaria is based really upon subtertian infections (P. falciparum). Most of the lesions in the internal organs are due to infection of red blood corpuscles with consequent disturbance of the oxygen supply to the tissues. The vascular flow within the organs is disturbed by vascular collapse, obstruction of the smaller vessels by auto-agglutination, thrombosis, infarctions and similar effects brought about by the clumping together of parasitised cells. All these factors slow down the circulation and cause “ludging” (Knisely) which is thought to be mainly due to the production of a fibrin-like substance. Cardiac and vascular failure may ensue. In addition there are explosive discharges of protein from the liberated merozoites and the disintegration of disrupted red cells, defunct parasites and extrusion of pigment. The spleen, when grossly enlarged, used to be popularly known as the “ague cake”. Although it is apt to fluctuate in size it is most certainly always swollen during an acute attack. On section the surface is dark, at times almost black, dark-red, purple or chocolate color from congestion and melanin pigmentation. In severe subtertian infections, the parenchyma may be so softened as to be almost diffluent and so swollen that the capsule is tightly stretched. When the pulp is washed, the malpighian bodies stand out as gray particles.

In chronic cases perisplenitis develops from stretching or tearing of the capsule, so that rupture may occur spontaneously or as the result of violence. On microscopic examination the organ contains a large number of macrophage cells, the special cells of Billroth, fibrinous cords, and sinus-lining littoral cells. In the chronic stage there is replacement by fibrous tissue. The malpighian bodies shrink while the pigment becomes scattered. All erythrocytic stages of the parasites can be detected in the red cells (P. vivax or P. falciparum) as well as the merozoites set free in the pulp. Numerically they are more numerous than in any other organ.

Malaria pigment is readily recognized free within the tissue spaces and enclosed within the reticulo-endothelium, and especially in the mononuclear cells. In acute cases the reticulo-endothelial system becomes blocked with pigment and in the later stages this is also replaced by fibrous tissue. Areas of thrombosis and hemorrhagic necrosis also occur.

The liver is usually congested, enlarged, pigmented, and olive-brown in color, especially in the left lobe which receives the splenic blood. Glisson’s capsule which surrounds the portal system is thickened and stretched. In chronic malaria there is fibrosis and round-cell infiltration which originates, it is thought, from the cryptozoic or tissue stages of the parasites. In infancy and early childhood, the enlargement, is mainly due to sinusoidal dilatation; in later years, the congestion is

mainly confined to the center of the lobule, and so the appearance resembles that, of the “nutmeg” liver of heart failure. The slaty gray color frequently encountered is due to deposits of pigment. Parasitized erythrocytes and melanin (hemozoin) pigment are found within Kupffer cells.

It is probable that the slight periportal fibrosis which is commonly encountered in African livers has a dual pathology because, in addition to malaria, there is malnutrition which is responsible for diffuse, piecemeal necrosis of the hepatic cells. Parasites, in all erythrocytic stages, are found in the sinusoids and in the parasitized erythrocytes. The parenchyma, cells do not usually take up malaria pigment, but contain granules of hemosiderin. Lysis of the red cells leads to obstruction and over-distension of the bile canaliculi which become obstructed by bile pigment. The parenchyma cells show all stage of degeneration, and in severe P. falciparum infections there is widespread focal necrosis surrounding the central vein. Small hemorrhagic areas may also be present.

Malaria pigment is now termed hemozoin, and is a compound of hematin which contains non-ionizable iron; hemosiderin also does so but it does not give the Prussian blue reaction with potassium ferrocyanide, unless first acted upon by nitric acid and hydrogen peroxide. In the kidneys, it is to be noted that albuminuria is common in malaria and may adumbrate serious renal damage, and this is specially true in subtertian and quartan infections. Sometimes there is azotemia with hyperpiesia and cardiac hypertrophy. In severe cases the lumen of the tubules becomes filled with granular casts and the cells show fatty changes resembling parenchymatous degeneration. Signs of glomerulonephritis are also sometimes present. In quartaephrosis Surbek (1931) occasionally found the enlarged, pale, white kidneys typical of degenerative parenchymatous nephrosis.

The changes in the heart in subtertian malaria are edema due to cardiovascular failure. In the bone marrow the yellow and adipose tissues are very vascular. The red marrow is of a chocolate brown, especially at the periphery and this is due to deposits of pigment. Phagocytosis is evident with hemozoin, macrophages and parasitized cells in large numbers. In chronic cases the reticulo-endothelium is hypertrophied. In the marrow itself there is a normoblastic response. Occasionally megaloblasts may be seen and reticulocytes are increased in the peripheral blood.

In the pancreas there is often focal necrosis, affecting the nutrient vessels of the Islets of Langerhans. Rarely the pancreas is hemorrhagic. The suprarenals are attacked in subtertian malaria, resulting in partial or complete loss of lipoids in the cortex, with congestion and blockage of vessels with malaria parasites; this is probably responsible for algid symptoms in subterian malaria. In the placenta the . maternal sinuses are packed with parasites interfering with the nutrition of the fetus, which may become infected at birth, possibly through the umbilical cord, or through a tear in the placenta. In the intestinal tract achlorhydria is common in I acute stages. The blood capillaries are loaded with parasites and degeneration of the mucosa is encountered which may give rise to dysenteric symptoms in life.

The brain usually bears a leaden hue due to deposition of hemozoin and the presence of parasitized cells in the capillaries. The gray matter is smoky gray while the white matter is speckled with punctiform hemorrhages (cerebral purpura). The smaller capillaries become completely blocked with parasitized cells and the plugging is most common at the bifurcation of the blood vessels (Ariete).

Malarial granulomata are focal degenerations in the brain substance, the result of former hemorrhages. Granuloma is sometimes an inappropriate term, for these lesions somewhat resemble tubercles and are formed by an agglomeration of glial cells around a focus of degeneration.

In massive infection the capillaries are blocked and thrombosed. As Maegraith has pointed out, thrombosis takes place. There are numerous small hemorrhages with “granulomata” in the subcortical zones. Clinically this is associated with malarial coma. Generalized toxemia is characterized by fits and convulsions. There are small and scattered hemorrhages. Embolism produces punctiform hemorrhages, especially in the corpus callosum.

Clinical manifestations

An attack of malaria may either be a primary attack or a relapse. A primary attack normally develops after an incubation period of 10-14 days; by direct blood inoculation it is about 11 days. In insect transmitted subtertian malaria, where the number of infecting bites is high, the incubation period tends to be shorter and may only be five days. Iaturally transmitted benign tertian malaria, especially in Europe, there may be latent period of several months before symptoms appear; the latent period usually covers the winter months. P. ovale may also show very long latent periods (Trager and Most, 1963). This is known as latent malaria. The latent period preceding the primary attack is known as incubation latency; a period or periods following upon the primary attack are know as infection latency. In subtertian malaria there is no latency in the same sense as in benign tertian. The type of temperature curve, whether intermittent or remittent, is less significant than formerly considered to be the case. Thus primary benign tertian infections may produce a remittent temperature curve before assuming the classical intermittent character. Two or more generations of tertian parasites, maturing in the blood at different times, will produce quotidian fever and two or more generations of quartan will give a fever on two successive days—quartana duplex—or conversely on three successive days, a quotidian fever—quartana triplex.

Relapses are defined as recurrences of malarious symptoms and the reappearance of malaria parasites in the peripheral blood, following recovery from the initial attack. Therefore relapses must be distinguished from reinfections.

Recrudescences of malaria are defined as relapses of the patient at the time he is removed from the endemic area. Relapses often follow the cessation of suppressive treatment, exposure to cold, exertion, parturition, or surgical operations.

The characteristic ague is divided into three stages : (1) cold stage, (2) hot stage and (3) sweating stage. One or even all these stages may be absent on occasions, especially when the infection is of long standing, whilst in subtertian fever many symptoms are so bizarre that they may be most misleading, so as to enforce the conviction that in many respects it is quite a different disease.

Herpes on lips and nose (fever sores), often extensive, frequently follow the rigors and are an accompaniment of all forms of malaria. Similar eruptions have beeoted on the ears.

Premonitory stage.—For several days before the actual attack the patient may be conscious of headache, lassitude, a desire to stretch or yawn, aching in the bones, anorexia, sometimes vomiting.

Cold stage.—This usually lasts one to two hours, and is the rigor, or “ague.” The feeling of cold is intense and universal. The teeth chatter; – the patient shivers from head to foot and wraps himself up in any garment he can lay his hands upon. Vomiting may be most distressing. The features are pinched, the fingers shrivelled and the skin blue like “goose-skin” (cutis anserina). The feeling of cold is purely subjective, because the temperature is rapidly rising. Children usually have convulsive fits.

Hot stage.—The hot stage may last from three to four hours. The shivering abates and gives place to, or alternates with, sensations of great heat. The clothes are thrown off. The face is flushed ; pulse full, bounding and usually dicrotic; headache intense ; vomiting usual; respiration hurried ; skin dry and burning; the temperature rising to 40° C, sometimes 41,1° C, rarely higher.

Sweating stage.—This usually lasts from two to four hours. The patient breaks out into profuse perspiration with sweat literally running off him in streams, saturating clothes and bedding. With sweating the fever rapidly declines. Headache, thirst and distress give place to a feeling of relief and tranquillity. When it has ceased the patient may feel exhausted, but quite well and able to go about. The body temperature is now subnormal and remains so until the approach of the next paroxysm, one or two days later. The total duration of the fever cycle may be from six to ten hours.

Urine and feces in ague.—During the cold stage the urine is abundant and limpid, and micturition frequent; during the hot sweating stages it is scanty, cloudy, sometimes albuminous. Urea excretion is increased during the rigor and hot stages, and so is that of the chlorides and sulphates. Phosphates, on the contrary, diminished during the rigor and hot stages, are increased during defervescence. Augmentation in urea excretion commences several hours before the attack, attains its maximum towards the end of the rigor, and decreases during the terminal stages, though still above the normal figure.

A fleeting glycosuria has also been observed from time to time. The urine usually contains urobilinogen and urobilin in excess during the attack, but they decline with the temperature and form a valuable diagnostic sign, especially in subtertian malaria. The corresponding pigment in the feces (hydrobilirubin) is increased twenty times the normal amount whilst parasites persist in the blood.

The spleen during ague.—The spleen is enlarged and painful during the rigor, but in early infections is not always palpable, a feature which became specially noticeable in the second World War in India, Burma, and New Guinea, in benign as well as in subtertian infections. At first, the enlargement recedes during remission, but later, when relapses and reinfections occur, it becomes permanent as in the “ague cake.” In primary infections the spleen is soft and spongy and therefore difficult to palpate, but in subsequent relapses it becomes harder and more fibrous. Spontaneous rupture of the spleen has been reported more frequently in P. vivax infections them with other species. Usually it is the result of violence, but Bearn (1961) has shown that in an adherent spleen it may be due to extensive subcapsular hematoma. Successful splenectomy does not necessarily extirpate the malarial infection.

Period of the day at which ague commences.—Quite a large proportion of agues ” come off” between midnight and noon or in the early afternoon. This time factor may constitute an important point in diagnosis, especially as pyrexial attacks somewhat simulating malarial agues may be caused by liver abscess, tuberculosis, Escherichia coli infections of the urinary tract and septic conditions, in all of which febrile recurrences are apt to take place during the afternoons or evenings.

Course of benign tertian and quartan fevers.—Benign tertian ague usually lasts ten hours or less and may be taken as the type of a malarial attack. In some cases the rise of fever is rapid and high, and the temperature may reach 40,6° to 41,1 °C within an hour or so; on the other hand, in some cases none of the clinical phenomena are present and the temperature does not rise above 37,2°-37,8 °C. Benign tertian, unless complicated, is not usually fatal; but the persistent and relapsing character makes it a tiresome disease and, if prolonged, it may produce severe anemia and debility. It may also produce thrombocytopenia.

In Central Russia, a fulminating type of benign tertian malaria, with hyperplasia of the spleen and cerebral edema, especially in children, has been described. Also two types (Nikolaev, 1935) are recognized: the Northern with an incubation period of 8-14 months; the Southern with an incubation period of 9-21 days. The length of this period does not depend upon the number of sporozoites introduced. Different incubation periods are actually produced by mosquito bites of the same batch after feeding on the same donor (Tiburskaya, 1961).

Certainly many strains of P. vivax seem to exist which differ in their virulence; some are mild, as in Holland; sometimes the fever is trivial and isolated attacks, without recurrence, are common enough. Various strains of P. vivax have been found to possess distinctive characters and vary in the number and frequency of the relapses they produce.

The presence of a rigor appears to be an index of severity. The mean maximum temperature for the paroxysms is 40,1 °C. As a general rule, the duration of a simple benign tertian infection before the parasites die out from the peripheral blood is nine months to one year after leaving the endemic area, but exceptions to this rule occur, as clinical relapses, with parasites in the blood, have been recorded as long as three years after the original infection. As it is seldom fatal, the pathology is not so well known as that of subtertian malaria, but it resembles it in a minor degree.

The fever in quartan malaria is generally smart while it lasts, and is well defined in its various stages, but it does not produce much systemic disturbance or cachexia or rigors. It has often been remarked that, whilst individual attacks of this infection are amenable to quinine and atebrin, the disease is more persistent than tertian or subtertian, so that attacks are apt to occur from time to time over a period of many years and may persist as long as 12-21 (Duggan and Shute, 1961). It is becoming increasingly realized that sometimes quartan parasites may be present in the blood without evoking any special symptoms. Parasites are usually scarce in the peripheral blood. They are more resistant to antimalarial drugs in the sense that they persist in the bloodstream for a week or more while the patient is taking the drug.

Quartan periodicity is the hall-mark of quartan malaria and is hardly ever found in any other disease. Double quartan and triple quartan fevers may be observed. In the latter the temperature course becomes quotidian. Occasionally, quartan fevers are encountered without splenomegaly and apparently when parasites can be found in the blood only after prolonged search: sometimes not at all, so that their true nature can be ascertained solely by the action of chloroquine by injection.

Relapses in quartan malaria may be of two forms: those occurring after a short interval are due to exacerbation of a low-grade parasitemia, but those in the longer interval of several months to release of exoerythrocyte parasites from the liver into the bloodstream.

Coma.—Sometimes the patient, without hyperpyrexia (the temperature perhaps not rising above, or even up to, 40°), may lapse into coma. The coma may pass away with a crisis of sweating ; on the other hand, an asthenic condition may set in and death supervene. There is often a paralytic squint, extensor plantar response and Cheyne-Stokes respiration. When subcortical hemorrhages are present, death usually ensues. There is a marked increasing of pressure in the cerebrospinal fluid, with increasing of lymphocytes up to 400 per mm, as well as of albumin and globulin. Occasionally, granules of malarial pigment may be found. It is important to note that parasites may be very scanty in the peripheral blood and not infrequently they may be absent altogether. The coma may persist for as long as 46 hours and then recovery ensue with quinine injections (chloroquine) as in the case reported by A. Cr. Tresidder in 1914.

Other cerebral manifestations are cerebral depression, excitation, cerebellar ataxia (Sawyer-Brown variety), behavior changes and character alterations, meningismus closely simulating meningitis. Rarely a focal spine lesion may cause paraplegia.

Algid forms. The algid forms of pernicious attack, as indicated by the name, are characterized by collapse, extreme coldness of the surface of the body or, in other words, by peripheral vascular failure. These symptoms usually co-exist with elevated axillary and rectal temperature. Flooding of the peripheral blood with vast numbers of parasites in all stages of development gametocytes as well as schizonts sometimes found. The prognosis is usually bad, but rarely this may be seen in an attack of average severity. It indicates a continuous fever of at least two weeks, or a relapse of short duration.

There are some misleading clinical forms of subtertian malaria which are important, for instance the gastric, choleraic, dysenteric, hemorrhagic, and edematous forms. The last with generalized anasarca were prevalent in war refugees from Givece (1945) and in the great Ceylon epidemic of 1934. Acute hemolitic anaemia, resembling pernicious anemia, may be a prominent of subtertian malarial cachexia. More rarely seen are the edematous forms with anasarca and ascites and also with nephritic signs with blood cells and albumin in the urine.

Diagnosis from clinical signs. The most important clinical sign is periodicity of the fever, which occurs in its most typical form in the tertian and quartan infections; in the subtertian, however, fever may be most irregular, or there may be no pyrexia at all.

Enlargement of the spleen is a common clinical sign in all forms of malaria. In old-standing infections it may be very large indeed, and occupy the greater part of the abdominal cavity, but in early, and it may be very severe, cases it may not be sensibly enlarged at all, and therefore fails entirely as a clinical guide; usually, however, in the absence of splenic enlargement, splenic pain is present during the attack. Moreover, the patient may be suffering from some totally different disease, and the palpable spleen may be the result of a long-standing malaria infection, quite unconnected with the attack in question.

To the clinician accustomed to many cases, the general appearance of malaria patients, the bright glistening eye, set in rather a dusky orbit, contrasted with the pale and ochreous complexion, combine to create an almost diagnostic appearance. Amber colored urine due to excessive urobilinuria. especially in subtertian malaria, and even in the absence of parasites in the peripheral blood, may be suggestive.

Sudden fever in a previously healthy person who has recently arrived from a malarious country usually turns out to be malaria. The patient will generally give a history of similar attacks while resident abroad, but there are exceptions to this rule, for, occasionally, residents of tropical countries may develop their first attack of malaria shortly after arriving in a cold climate, and this attack, aggravated by the conditions, may run a very severe course; this is especially the case with recent arrivals from the west coast of Africa, and it is true for both benign tertian and subtertian infections, the parasite lying dormant in the blood-stream perhaps as long as eight months; in the benign form a year or more. It should be borne in mind that, in the case of P. vivax, P. malarias and P. ovale all “prophylactic” drugs are in reality only suppressive. A possible diagnosis of malaria should therefore not be discounted on the grounds that drugs were continued for the advised 14 days after return to a non-malarious country.

An actual description of the febrile attack itself may be suggestive. The rapid rise of temperature, the history of the cold, the hot, and the sweating stages, the rapid defervescence of the fever, and the subsequent sense of well-being, are more characteristic of a malarial attack than of any other febrile disease. At times periodicity is a trustworthy enough clinical test. Tertian and quartan periodicity usually occur only in malarial disease, but have been seen in meningococcal septicaemia.

Differential diagnosis of malaria

The differential diagnosis of malaria entails a knowledge of all fevers, both tropical and non-tropical.

The following are often mistaken for malarial fever cerebrospinal meningitis; fever of urinary origin (sometimes renal calculus); the fever attending the passage of gall-stones, or inflammation of the gall-bladder; that associated with pyelitis and surgical kidney; perirenal abscess; amoebic hepatitis and amoebic abscess of liver; lymphangitis, particularly that form associated with elephantiasis and other filarial diseases; undulant fever, relapsing fever; trypanosomiasis; kala-azar; “short-term fevers” of which dengue and sandfly fever are the most typical; the fever associated with tuberculous disease, with ulcerative endocarditis, with some types of pernicious anemia, with splenic leucocythemia, with visceral syphilis, with pulmonary carcinoma, with rapidly growing sarcoma, with forms of hysteria, and with many obscure and ill-defined conditions.

Treatment

http://www.malariasite.com/malaria/Treatment1.htm

At cupping of fever attacks at any kind of a malaria use preparations with shizotropic action: Chingamin (or.: Delagil, Hlorohin, Nivachin, Resochin, Trochin), and also quinine sulfas, quinine Dichlorid, Hydroxyhlorin (Plaquenil), Chloridin (Pyrimethamin, Tindurin), Sulfanilamid preparations, Meflohin, Tetracyclin, Doxycyclin. These preparations are active against bloody shizontes. The greatest action has Chingamin. Concerning tissue forms of plasmodiums the most active is Primachin.

At acute disorders of disease use Chingamin diphosfat during 3 days more often: in 1 day 1,5 gm (at once 1 gm and in 6 hours the others 0,5 gm), in 2 nd and 3-rd day – unitary 0,5gm. The serious form of a tropical malaria demands prolongation of treatment course by Chingamin 2 days 0,5 gm 1 time in days If plasmodiums are refractory to Chingamin, indicate quinine Dichlorid 2 ml 50 % of solution 2 times in 6 – 8 hours or in a vein very slowly 1 ml in 20 ml. 40 % solution of glucose, and then two injections under skin 1 ml. 50 % of solution. Chloridin in combination with Sulfanilamides preparations of prolonged action or the combined preparation Fansidar, which contains 0,5 gm of Sulfadoxin and 0,025 gm of Chloridin: 3 tablets unitary. Fansidar may be given also for prophylaxis of relapse of tropical malaria.

The mentioned preparations provide complete convalescence at tropical malaria. In case of tetrian fever and oval malaria indicate Primachin which have action upon tissue shizontes and prevent appearance of recedives. Similar activity have also Tetracyclin. Primachin is indicated simultaneously with Chingamin or right after terminations of treatment by it.

Treatment of specific complications is carried out in the urgent order. At development of malarial coma use a solution of quinine Dihydrochlorid. The next days indicate the preparations per os. Simultaneously carry out desintoxication therapy with Reopolyglycin, Polyglucin, Albumin, Rheogluman, Polyionic solutions. The total quantity of infused liquid should not exceed 1500 ml. Infuse up to 150 mg of Prednisolon in vein. Among other agents Diprazin, Suprastin, Furosemid are indicated.

At hemohlobinurine fever treatment starts with an immediate cancellation of Quinine, Primachin, Sulfanilamide preparations which might cause this complication. Infuse Cordiamin, Corglykon or Strophanthin, Phenylephin hydrochlorid, Prednisolon, and also Reopolyglycin, Quartasol or another polyionic solutions. In case of development of serious anemia transfuse the blood of the same group, blood plasma.

Individual chemioprofilaxis is carried out for the persons leaving in the endemic regions. For this purpose use Chingamin 0,5 gm once a week, and in hyperendemic regions – 2 times per one week. Preparation is indicated during 5 days before arrival, all period of stay and during 8 weeks after departure. Among local population chemioprofilaxis begin 1 – 2 weeks before occurrence of mosquitoes. Occurrence of the tropical malaria is caused by drug resistant plasmodiums, prevent by reception of Fansidar once a week. To the persons who have arrived from endemic center of a tetrian fever, seasonal prophylaxis of relapses by Primachin in tablets 0,027 gm per day during 2 weeks is carried out.

HEMORRHAGIC FEVERS

(FEBRES HAEMORRHAGICAE)

http://www.nlm.nih.gov/medlineplus/hemorrhagicfevers.html

Group of acute natural foci diseases characterized by a general intoxication, fever, systemic lesion of small-sized veins with development of a hemorrhagic syndrome.

There are hemorrhagic fevers with a renal set of symptoms hemorrhagic fever with renal syndrome, Lassa, Ebоlа and Маrburg fevers, Yellow fever, caused by viruses of miscellaneous sets and labors.

Etiology

The diseases are caused by RNA-containing viruses of Bunyaviridae family: from Hantaan kind (HFRS), Togaviridae – Flavivirus (Yellow fever), Filoviridae – (Ebola fever, Marburg fever), Arenaviridae (Lassa fever). They are inactivated at the temperature of 50 °C during the 30 minutes, at 0-4 °C they preserve stability till 12 hours.

Epidemiology

Source of hemorrhagic fever with a renal syndrome are mice-like (about 16 kinds), which are excreting the virus with urine, stool and saliva. Among the gnawers the transmissible way of causative agent is possible. The contamination of the person descends by air – dust, nutritional and contact pathes (routes). The transplacental transmission of a virus from the pregnant woman is possible. The probability transmission from the ill person is not fixed.

In the natural foci the source of an infection – multipapillary rat, and ill in the main (basic) visitants. For Ebola fever and Мarburg the source of contamination in the nature is not known yet, probably, it is primacy. The relevant feature contagious hemorrhagic fever Lass, Ebola and Мarburg – capability of transmission of a virus from the person. It results in originating intrahospital flashes, including among employees of hospitals and secondary diseases in monogynopaediums. The transfer (transmission) of the hospital causative agent from the person descends by an aerogenic way, and also at common use by subjects of household activities, at sexual contacts, is more often – at maintenance for ill, usage of not sterile medical instruments. The contamination is possible both in height of illness and in the period of a reconvalescence.

There are two forms of a yellow fever: a yellow fever of jungle (natural foci – monkey, hedgehogs) and urban yellow fever (source – ill person). Both are diffused by mosquitoes Haemagogus and Aedes. The contamination those at a puncture of the ill person are possible at the end of an incubation interval or per the maiden 3 days of illness. A sensibility of the people overall.

Yellow fever mosquitoes

Contagious hemorrhagic fevers Lassa, Ebola and Маrburg are usual for definite terrains of Africa. The cases of their delivery in countries of America and Europe by ill primacy and people are described, which one have caught and were in an incubation interval of illness. Yellow fever Peru is recorded in countries of Africa, and also in Bolivia, Brazil, and Columbiums. She falls into to conventional illnesses, the strife with which one is regulated by (with) international medico sanitary rules.

As the majority of causative agents hemorrhagic fever can be diffused with the help of the air drop, they are also potential agents of biological weapons.

Pathogenesis

After inoculation of organism of the person through an injured skin and mucous of respiratory tract or digestive tract the virus propagates lymphatic system, falls in a blood with the subsequent virusemia. The antipathy, histic destruction, and responses of an organism by the way immunopathologic processes, changes of a curtailing system of a blood, endocrine disturbance, development of acute renal failure develops. The virus causes a serious capillary toxicosis, multiple hemorrhages, hemorrhagic eruption, rising of a permeability of capillary tubes with an output for limits of a vascular bed of a fluid part of a blood, severe edema of tissues, violation of microcirculation, and dystrophic changes of internal organs of an internals.

Clinic

Hemorrhagic fever with a renal syndrome. An incubation interval on the average 10-15 day (duration from 8 about 35 day).

The illness starts is acute with extremely strong chills. Temperature of a body is increased till 39-40 °С. The visual disturbances, decrease of visual acuity, “mist” before eyes) complain on a sharp headache, backache, muscles of extremities, photophobia. Arise nausea and vomiting. At inspection ill mark paleness nasolabial triangle, hyperemia of a face, necks, upper half of trunk. The palpebral fissures are narrowed down, scleratis. A mucosa of an oral cavity and pharynx are bright red with haemorrhages. The Kerning’s signs, Brudzinsky sign can be determined and stiff neck. Fever 7-9 days is prolonged. Ill at first is provoked, then flaccid, apathetic, sometimes delirium.

On 3-5th day of illness on a neck, lateral areas of a thoracic cell, in axillaries fossas, above clavicles occurs petechial eruption. It is sporadic the members small-sized, have the shape of sprockets and are assorted by the way of red or violet strias the eruption present during all feverish season (Fig. 3). Then there are nasal, intestinal, pulmonary bleedings.

Petechial eruption

Cardiac sounds are dull; the initial tachycardia is replaced by a bradycardia, hypotonia. The phenomena of bronchitis are possible. Almost for all ill the signs of a lesion of the alimentary canal are watched: dryness of tongue, nausea, vomiting, inflation and abdominal pain without definite localization. For 25 % of patients enlarged a liver and spleen and the icterus are possible.

Leading is the renal syndrome patient shows the sharp back pain, positive sign Pasternatsky from both sides, development of an oliguria, and in sever cases – anuria and uremia. In height of illness find a proteinuria reaching 40 gm/l and higher, hematuria, hyaline and fibrinous barrels, augmentation of number of cells of a renal epithelium. In a blood is sharply raised the level of a filtrate nitrogen, urea, creatinine. In a hemogram: the moderate hypochromia anemia, leukocytosis with a neutrocytosis, thrombocytopenia, increased ESR.

Flow of illness is predominantly severe, lethality up to 6-8 %. There are also moderate, mild and deleted forms .

Congo-Crimean hemorrhagic fever. The incubation interval lasts 3-7 day. The illness starts with chills, hyperthermia till 39-40 °С. There are pains in a head, joints and muscles, extremities and spin, gaste, repeated vomiting. Vessels of scleras and conjunctivas injected are provoked, their face, and neck, top of a chest hyperemic (Fig. 4, 5). The mucosa of an oral cavity bloodshots with punctulate exanthema, the soft palate is hydropic.

The fever stays 7-8 days, for the majority an ill temperature curve double-peak, the decrease of temperature of a body with occurrence (appearance) of a hemorrhagic set of symptoms is characteristic.

Skleritis

Conjunctivitis

On 2-4th the day of illness on a skin of a lateral area of a trunk, inguinal and axillary areas, on a gaste and extremities petechias and eruption occurs. The eruptions are of the round or oval shape with legible contours of dark – cherry colour, peter on 5-8th day. Simultaneously with an eruption there are odontorrhagias, nose, mild, alimentary canal, and icterus. The condition ill is sharply degraded. The hyperemia of a face is replaced by paleness and одутловатостью. It is marked sleepiness, adynamia, sometimes stiff neck, and Kernig’s sign. The liver enlarged, the icterus is possible (probable). The Pasternatsky sign is positive. Develop an oliguria, microhematuria, and proteinuria. In a peripheral blood: a leukopenia with a neutrocytosis, thrombocytopenia, augmentation ESR, on 2nd week of illness – relative lymphocytosis.

The illness can be mild, moderate and sever degree. The lethality reaches 40 %, predominantly owing to an infectious-toxic shock, massive bleedings, and hepatonephric failure.

Lassa fever. Incubation period lasts 3-17 day. The disease starts with a minor fever, malaise, muscle aches, and conjunctivitis. Step-by-step temperature reaches 39-40 °С and develops representative pharingitis, more often ulcerative-necrotic. The ulcers have yellowish center with bright erythematic borders, are localized on a soft palate, tonsils and mucosa of a pharynx. In height of illness the meningeal signs is marked a strong headache, giddiness, sleepiness, at a normal structure of liquor, violation (disturbance) of consciousness. Are watched nausea, a vomiting, diarrhea, deaquation, abdominal pain and chests, tussis, the dysuric phenomena generalized lymphadenopathy, specially enlarged cervical lymphonoduses. It are marked a relative bradycardia, sometimes dicrotism of sphygmus. The liver enlarged. In the analysis of a blood – leukopenia with shift of the formula to the left, the thrombocytopenia, ESR is step-by-step increased till 40-80 mm/hour. In moderate and severe cases – moderate bleedings of miscellaneous localization and petechias an eruption on a skin and mucosa, less often – roseola, papule, and spot. In very sever cases develops an edema of a face and neck, exudates (pleural, pericardial, peritoneal). Considerably complicate flow of illness pneumonia, fluid lungs, uremia, and infectious-toxic shock. Lethality is up to 30-67 of %. In the period of a reconvalescence the palindromias, deterioration of hearing, baldness are seen an asthenia, sometimes.

Incubation period of Ebola fever 7-14 day, Marburg fever – 4-9 days a beginning is acute, precursory symptoms serve conjunctivitis and exanthemas. Per the maiden days of illness there are a strong pain of a head, chills, fever till 39-40 °С, dorsodynias, muscles, joints, the nausea, vomiting, often watery chair, that can result in a considerable deaquation of an organism. The маculo-papular eruption distributing to a neck and a face, upper extremities, breech is representative, further there is an eruption on palms and base surfaces. Is watched enantema on a mucosa of a mild and firm palate, ulcer. Dermatitis of a scrotum quite often develops. Enough often on the maiden week of illness the lymphadenitis in occipital, cervical, axillary areas is marked. The lymph nodules enlarged up to the pea size, mild, are a little morbid. From the 5-7-th of day of illness the hemorrhagic set of symptoms more expressed is affixed than at Lassa fever; for the women – parent bleedings, spontaneous abortions. The psychics, hyperesthesia, cramp is sometimes upset. Complications – bronchopneumonia, orchitis, panreatitis, uveitis. After petering fevers is long the external tags of illness – deeply sunk down of an eye, cachexia labored gait are saved. In a blood at first leukopenia, then leukocytosis with a left-shift, thrombocytopenia. Immediate causes of death – infectous-toxic shock, heart failure, cerebral distresses. Lethality – 30-90 %.

Yellow fever. An incubation period is 3-6 days. Distinguish two stages of illness. First stage is characterized by the sudden beginning with strong chills, fever repeated vomiting. Ill has pains in a head, back, lower back, bones. It are marked a sharp hyperemia and edema of a face and neck, eye injected by a blood. A mucosa of a or pharynx and tongue of bright red colour. The photophobia develops. Patients are irritable and are provoked. Pulse is fast. From the 3-rd day of illness there are yellow colouring of a skin and sclera, dot hemorrhages on a skin, are enlarged a liver and spleen. Then there comes a remission continuing 1-2 days. Temperature of a body is reduced up to the norm, the state of health is improved.

From the 5-th day of illness the condition of patient is sharply degraded (stage of venous stasis). Temperature of a body up to 40 °С and above is again increased, there can be a delirium. The icterus rises. The face becomes pale yellow with cyanotic tint. Strengtheausea and vomiting. Emesis masses are of dark brown or black colour. A feces are dark (melena). On a skin of a trunk both extremities there are petechias and ecchymomas. The copious nasal and parent bleedings, bleeding gums are observed. The nephroses – oliguria or anuria, blood and barrels in urine, azotamia are struck.

The tachycardia is replaced by a bradycardia (Faget’s sign). The arterial pressure is reduced. In the analysis of a blood a leukopenia – up to 1,5-2,0-10 /l, neutropenia. Encreased ESR. Are characteristic a hyperbilirubinemia (at the expense of both fractions of a pigment), enhancement of activity aminotransferase, in urine – bilirubin, urobilin, it is a lot of albumin, erythrocytes, leucocytes, barrels.

The fever stage lasts 8-9 days. The death can occure due to bleedings, shock, hepato–renal failure. The lethality makes 5-10 %, in the season of epidemics – up to 60 % and higher.

The abortive forms of illness without an icterus and hemorrhagic set of symptoms are possible mild, deleted.

Diagnosis

The diagnostic hemorrhagic fever is carried out with allowance for of epidemiological anamnesis (seasonal prevalence, connection with the causative agent, contact with ticks, rodens and exotic animal) and representative clinical developments acute onset, fever, hemorrhagic syndromes. The diagnosis confirms virology and serological methods of research. Causative agent of Lassa fever, Ebola and Маrburg – on culture of cells Vero or on guinea pigs epidemic parotitises. “The Gold standard” – detection of RNA of the originator. For serodiagnosis will use RCC, RN, RIA, RIIF, IFA with double serums of patients, immunosorbent methods. With material of sick persons work only in the specially equipped labs, adhering to strick safety measures (Fig. 6).

Specially equipped department for treatment

The differential diagnosis

As against hemorrhagic fever, for an ill flu the hemorrhagic developments are very seldom. The high contagiousness, more short feverish season(term), availability катарального of a set of symptoms, Morozkin sign is characteristic for him(it). In outwashes with a slimy nasopharynx by a method find antigens of a virus of a flu.

The virus hepatitises often start step-by-step, with preicteric of the period, the flow which one is accompanied catarrhal,dyspeptic, asteno-vegetative syndromes. In height of illness are not watched a hyperemia and одутловатость of a face, горячка, озноб, lesion of nephroses. The hemorrhagic set of symptoms arises only at a very serious degree of illness.

The тyphoid-paratyphoid diseases have a gradual beginning, stepwise temperature rise, reference predominantly roseola eruption. Easy diagnostic confirming epidemiological anamnesis, research of a hemoculture, serological tests.

At a canicola fever the strong muscle pains, specially in икроножных muscles are characteristic; a liver, often icteric forms(shapes) of illness with the sharply expressed hyperbilirubinemia practically always enlarged; in a blood on all stretch(extent) of illness – hyperleukocytosis with a neutrocytosis, shift of the formula to the left, very high ESR. The diagnosis confirms by the laboratory data – detection of the originator at a dark field method of a blood and urine, serological tests RMA with leptospira.

For a hemorrhagic vasculitis are characteristic long-lived recurrent flow, lesion of joints, and localization of an eruption on extensor surfaces of top and bottom extremities.

At Q fever are struck mild with development of a pneumonia, are enlarged a liver and lien.

For a malaria pathognomic representative attacks of a fever with definite periodicity. At examination find a splenomegaly, in a blood – malarial plasmodium.

The meningococcal infection contamination starts is acute, but in a clinical picture of the generalized form (shape) on the foreground more often the meningitis or sepsis with a copious hemorrhagic eruption acts, it is a lot of members of the star-shaped form (shape) with a necrosis of an epithelium. In the analysis of a blood a hyperleukocytosis with shift of the formula to the left, enlarged ESR. The diagnosis confirms by detection менингококка in sowings from a nasopharynx, blood and liquor.

Treatment

All sick are subject to mandatory hospitalization. The basis of treatment make desintoxication (i.v. 5-10 % glucose, polyionic solutions, 5 % donor Albuminum), glucocorticoids, strife with a hemorrhagic set of symptoms (Ascorutinum, Vicasolum, Dicynonum, Etamsylatum, calcium Dobesilat, Adroxonum, Acidum aminocapronicum; blood). In case of renal failure (for decreasing of remic intoxication a gastric lavage and intestine with 2 % sodium of Sodium hydrogenum solutions; at increasing of acute renal failure and infectious-toxic shock – extra corporal haemodialysis). Antiviral drugs per the maiden days of illness assign virolex, ribavirin, inducers of endogenic interferonogenesis (cycloferon, groprinosin), specific immunoglobulin or plasma. The antibiotics in case of bedding of a bacterial infection contamination.

Prophylaxis and measures in the locus

At hemorrhagic fever with a renal syndrome the preventive measures are directed on strife with the gnawers. Are offered inactivated cultural and cerebral vaccines (China, Russia, Japan), recombinant of a vaccine (USA, China), which one have appeared effective in endemial terrains. With this purpose carry out a disinfestation in the natural locuses, puttings, and also collect of tongs with animal and poultries. For a disinfestation will use gexachloran. In a burn-time in a field and on timber loggings it is recommended to use a special protective clothing and repellents.

Medical observation in the focus for 10 days. Conduct mandatory final disinfection with 3 % Chloraminum solution and chlorofos. For contact persons or one who was bitten by tongs in endemial districts enter a specific immunoglobulin i.m. in doses 5-7.5 ml for adult, 2.5-3.5 ml – for children. Apply a vaccine, inactivated by formalinum for specific prophylaxis of Congo-Crimean hemorrhagic fever.

Primary antiepidemic measures after detection of sick with contagious hemorrhagic fevers Lassa, Ebola and Marburg, and also yellow fever same, as well as at other quarantine infection contaminations. Patient will hospitalize in hermetic isolation ward with independent life support, monitor behind absence of an air inflow from a zone of isolation ward, paste vent holes. The staff should work in a protective clothing, including a mask or respiratory supplied with a special inhaler. Conduct careful current and final disinfection.

The specific prophylaxis contagious hemorrhagic fever. The quarantine for arriving from epidemic areas lasts 17 day. In endemial districts of yellow fever vaccination of the population by an alive “Dakar” vaccine or 17-D is carried out. The immunodefence is saved 10 years, and then make a revaccination.

EPIDEMIC TYPHUS FEVER

http://www.vdh.state.va.us/epidemiology/factsheets/pdf/Typhus_louse.pdf

Treatment

The treatment of the patient is complex: etiotropic, pathogenetic and symptomatic.

Etiotropic therapy. Chloramphenicol and tetracycline are more effective in epidemic typhus. The recommended dose for tetracycline is 0.3-0.4g, chloramphenicol – 0.5g four times per day. Usually antibiotics are abolished from the third day of the normal temperature.

Pathogenetic therapy includes heart (corglycon, strophantin) and vascular (cordiamin, ephedrine, mezaton) remedies. During the serious course the disintoxicative and dehydrative therapy is performed. Sometime during the case of expressive exciting bromides, aminaszin, barbiturates, seduxen are prescribe. The patients may walk from 7-8 day of the normal temperature. The discharge of the patients from the hospital may be realized at 12 day of the normal temperature.

MALARIA

Definition

Treatment

PLAGUE

http://www.nlm.nih.gov/medlineplus/plague.html

Plague is an acute infectious disease caused by Yersinia pestis with an severe intoxication, fever, affection of lymphatic system and lungs. It belongs to the group of the extremely dangerous infections (quarantines).

Pathogenesis

Penetration of Yersinia pestis through skin (respiratory or gastrointestinal tract).

Involving of the lymph node (primary bubo).

Penetration into blood (bacteremia, generalization of the process, formation of methastases) also spreading through lymphatic system (secondary buboes).

Destructive effect of the toxin (general congestion of all organs of the body).

Morbid pathology

The main points noted in a plague autopsy are:

1) The marked involvement of the lymphatic system as shown by intense congestion and hemorrhagic edema of the lymphatic glands. Not only are the glands involved tributary to the site of inoculation, thus forming the primary bubo, but there is secondarily more or less inflammatory change in many of the lymphatic glands of body. There is also a marked periglandular edema, with hemorrhagic extravasations of the connective tissue surrounding the primary bubo, this mass being made up of a group of glands matted together by this periglandular exudate.

2) The marked destructive effect of the toxin of the plague bacillus, upon the endothelial cell lining of blood vessels as well as of lymphatic ones. This causes the extensive blood extravasations are characteristic of plague and shown by petechial spots, not only of the skin, but of the serous and mucous membranes as well throughout the body.

Microscopically there is a distension of the alveoli and bronchial passages with a hemorrhagic exudate. There is practically no fibrin in the alveolar exudate. The process seems to extend by continuity along the bronchi and bronchioles. Plague bacilli pack the exudate found in the bronchi and bronchioles. In a report on the autopsy findings of septicemic plague in Ceylon in cases where plague bacilli were demonstrated in smears and cultures from spleen and blood, Castellani noted especially meningeal congestion and some splenic enlargement.

Clinical manifestations

Incubation period of human plague varies usually from 2 to 10 days, but is generally from 3 to 4 days. In primary pneumonic plague it may not be over 2 or 3 days.

In bubonic plague premonitory symptoms are not usually observed, though occasionally there may be 1 or 2 days of malaise and headache. The onset, except in mild cases, is usually abrupt, with fever commonly accompanied by a moderate rigor or repeated shivering. The temperature rises rapidly to 39,4 °C or 40 ˚C. sometimes even reaching 41,7 °C. The pulse becomes rapid and the respirations increased. There is headache which is usually severe and mental dullness, and this condition is generally followed by mental anxiety or excitement. The patient may become maniacal. The skin is hot and dry, the face bloated, the eyes injected, and the hearing dulled. The tongue is usually swollen and coated with a creamv fur, or later with a brown or black layer. The symptoms usually complained of within the first 24 hours are very severe headache and backache. Burning in the throat or stomach, and nausea and vomiting may occur. Constipation is present as a rule. The pulse is either very small and thread-like or full and bounding. At times there may be acute delirium; at others, lethargy and coma. In children, convulsions usually occur. The urine is scanty and generally does not contain more than a trace of albumin and no casts. Later in the disease the albumin may increase somewhat, The high febrile stage lasts from 2 to 5 days or longer. The decline in temperature may be sudden or gradual. Cases that do well usually show a gradual fall of temperature, and after 14 days the temperature may be subnormal. Buboes, inflammatory enlargements of the lymph glands are sometimes the first sign to attract attention by their pain. They more often make their appearance from the second to the fifth day after the onset of the fever. The temperature frequently shows a decline when they appear.

The affected gland is often hard and painful to the touch. In fatal cases, it may retain these characteristics; in others it suppurates. The average size of the bubo is from a walnut to an egg. Generally the plague bubo at the onset is hard to the touch and very painful. Often at the time of onset of the bubo, pain in it is the symptom of all others of the disease most complained of. In rare instances, however, the pain may not be marked. Usually if the bubo is in the groin the pain is sufficient so that the patient lies in bed with the thigh flexed and the leg drawn up to relieve any pressure on the inflamed glands while if the bubo is in me axillary region the affected arm is held away from the side. The bubo may terminate by resolution, suppuration, or induration.

If the bubo suppurates, the gland becomes at first more swollen and the overlying skin gradually more inflamed and tense during the first week. Later the gland begins to soften and necrosis then occurs more quickly. Frequently the whole center of the gland breaks down into an abscess cavity and perforation then occurs, revealing a cavity with dark scarlet or bright red walls. Later the walls become reddish yellow in appearance and emit whitish-yellow pus. On microscopical examination of the pus normal and degenerating plague bacilli are found and many polymorphonuclear leucocytes and degenerating endothelial cells. The bacilli are often seen engulfed in phagocytic cells. In the later stages the buboes often become secondarily infected with other microorganisms, particularly the pus cocci. Rarely the bubo does not perforate for several weeks. Sometimes its suppuration is accompanied by much sloughing of the skin in the vicinity when fairly large ulcers result with indurated infiltrated margins. In some instances the lesions may heal in from a week to ten days, but with larger buboes sometimes complete cicatrization does not occur for a month or two. In many other cases the bubo terminates by resolution. The tenderness, and periglandular infiltration then gradually decrease, the overlying and adjacent skin becomes softer, and the glands may eventually return almost to their normal size with but moderate induration about them. In other instances an enlarged cicatricial node remains at the site of the bubo.

Buboes appear in 75 % of the cases. In the cases in which buboes are present, they occur in the inguinal glands in approximately 65 to 70 %, in the axillary. 15 to 20 %, and the cervical, 5 to 10 %. Carbuncles appear in about 2 %, in which there are reddened indurated patches of skin, which subsequently necrose. The spleen is frequently moderately enlarged, but often cannot be palpated. Hemorrhages from the stomach and intestine are not uncommon, and when the disease is complicated with the pneumonic form they may occur from the lung. Epistaxis is also not infrequent. The blood usually shows a leucocytosis of forty thousand or more the increase being in the polymorphonuclear leucocytes. The plague organism can be isolated front the blood in about forty-five per cent of the bubonic cases.

The attack of high fever lasts generally three to five days or longer, but the patient may die earlier. If however, he lives for five days there is greater chance of recovery. If the bubo suppurates recovery may be delayed from two or three weeks to a month.

The onset of pneumonic plague is usually somewhat abrupt; prodromal symptoms are rare. The disease usually begins with chilly sensations, but a distinct rigor is unusual. Epistaxis is also rare. There is headache, loss of appetite, an increase in the pulse rate, and fever. Within from twenty-four to thirty-six hour after the onset, the temperature usually has reached 39,4 °C or 40 °C, and the pulse 110 to 130 or more beats per minute. Cough and dyspnoe appear within twenty-four hours after the onset of the first symptoms. The cough is usually not painful. The expectoration is at first scanty, but soon becomes more abundant. The sputum at first consists of mucus which shortly becomes blood-tinged. Later the sputum becomes much thinner and of a bright red color; it then contains enormous numbers of plague bacilli in almost pure culture. The typical rusty sputum of croupous pneumonia was not observed. The conjunctiva become injected, and the tongue coated with either a white or brownish layer. The expression is usually anxious, and the face frequently assumes a dusky hue. Labial herpes is very uncommon. The patients sometimes complain of pain in the chest, but usually this is not severe. Apart from the disturbances due to the dyspnoe and their anxiety for their condition, they usually appear to suffer but little and usually do not complain of pain. In the later stages of the disease, the respirations become greatly increased and the dyspnoe usually very marked, the patients frequently gasping for air for several hours before death. Cyanosis is then common.

The signs of cardiac involvement are always marked in the advanced cases, the pulse becoming gradually more rapid, feeble, and running; finally it caot be felt.

Septicemic plague occur during the course of bubonic plague, always occurs in pneumonic plague, and may occur as a form of primary infection. When primary septicemic plague results, the infection has usually occurred through the mucous membrane of the mouth and throat, death resulting from septicemia before macroscopic lesions are visible in the lymphatic glands or lungs. Nevertheless, at autopsy, at least some of the lymphatics are usually found to be enlarged, congested, and even hemorrhagic, and in a few instances early buboes may develop shortly before death.

In this form, the nervous and cerebral symptoms often develop with great rapidity and intensity, and the course of the disease is very rapid, the bacilli appearing in the blood almost at the onset of severe symptoms. The attack usually begins with trembling and rigors, intense headache, vomiting, and high fever. The countenance usually depicts intense anxiety. Extreme nervous prostration, restlessness, rapid shallow respirations, and delirium are common symptoms. In some cases the cardiac symptoms are the most prominent. The patients soon pass into a comatose condition, and die sometimes within 24 hours of the onset of the attack, but sometimes not until the third day.

Cases of primary septicemic plague are always fatal. Hemorrhages from the intestine sometimes occur in this form of plague as well as in bubonic plague. There is no distinct evidence that such cases are of primary intestinal origin. Hemorrhages from the nose and kidneys are also not uncommon.

The plague bacillus produces a powerful endotoxin which often causes a dilatation of the arteries, lowering of the blood pressure, and alterations in the functional activity of the heart, as well as degenerative changes in the heart muscle. It also acts particularly upon the endothelial cells of the blood vessels and lymphatics, the inflammatory reaction frequently causing circulatory obstruction. One of the most characteristic features of the pathology of plague is the tendency to produce general dilatation and engorgement of the vessels, with cutaneous, subserous, submucous, parenchymatous, and interstitial hemorrhages. In patients who have died of plague, the most common of the latter are in the epicardium, the pleura, peritoneal surfaces, the stomach and intestines, and the mucosa of the stomach and small intestine. Sometimes extensive hemorrhages are found in the peritoneal, mediastinal or pleura cavities. In the kidneys there are frequently subcapsular and renal hemorrhages, and blood extravasation into the pelves of the kidneys and ureters, as well as in the bladder and generative organs.

Sometimes there are considerable extravasations of blood into the substance of the brain. In bubonic plague, numerous hemorrhages are almost always present in the bubo. The tissues are characterized by vascular dilatation and engorgement. followed by edematous infiltration, the effect of the toxin being evident on the vessel walls. The endothelial cells become swollen, proliferated, and degenerated. Later hyaline degeneration of the walls may occur.

During the clinical course of the disease, hemorrhages are frequent. The bleeding may take place from the nose, mouth, lungs, stomach, or kidney, and sometimes from the uterus and bladder. These hemorrhages generally occur in severe cases of the disease. On examining the skin small punctifonn hemorrhages from about 1 to 2 millimeters in diameter are sometimes observed scattered over the skin in greater or less profusion. The petechie may occur on the face, neck. chest, abdomen or extremities. Sometimes larger patches of ecchymosis, in the neighborhood of 1 centimeter in diameter, are observed in the skin. Larger cutaneous effusions of blood are rarely seen, except at autopsy. The purpuric hemorrhages in bubonic plague usually do not appear before the third day of the disease. However, in septicemic plague they may be seen earlier.

At autopsy, the right side of the heart and the great veins are usually distended with fluid or only partially coagulated blood. During the disease, the patient frequently experiences a feeling of oppression over the precardial region. The heart sounds at first are clear, and the second pulmonic sound may be accentuated, but as the disease progresses they become feebler, or embryocardiac, in character and die first sound may be no longer heard. Sometimes heart failure may occur without any other sign of collapse. It may occur following exertion. such as sitting up. but it sometimes takes place while the patient is lying in bed. In primary septicemic plague, the course of which is very rapid, the cardiac symptoms are frequently the most prominent ones. In pneumonic plague, the limits of dullness of the heart are sometimes increased to the right of the sternum. At onset, the second pulmonic may be accentuated, but it soon becomes indistinct. As the disease progresses, gallop rhythm may occur. Death takes place usually from cardiac paralysis and exhaustion.

Diagnosis

After penetration into the organism plague bacillus fill up the lymphatic nodes, blood and sputum. Their presence in the urine is very inconstant, but their detection during the bacteriological examination is very valuable for diagnostic. All the materials from the patients are to be received before the antibiotic treatment.

The materials for the bacteriological diagnostics are taken from the inflamed lymphatic node or bubo with the help of the sterile syringe. After the skin. which is over it, is cleansed, the node is fixed by the left hand and the needle attached to the syringe is slicked into it. It is better to take the punctate from the peripheral dense part of the bubo. With the slight movement of the needle several times up and down in the node the aspiration is made. The received liquid is poured into a small test-tube and when with all the required precautions it is to be send to the special laboratory, where one drop is used for the inoculation into of ligue agar, and another one for the smears, and the rest is injected under the skin of the guinea-pig.

Treatment

http://sprojects.mmi.mcgill.ca/tropmed/disease/plague/treatment.htm

Patients, who suffer from plague necessarily, hospitalize in appropriate hospitals where they are transported by ambulance.

Treatment should be started already on place of revealing of the patient. Early prescription of antibiotics (during the beginning of disease), as a rule, salvages it life. Efficiency of therapy by antibiotics in later terms is considerably lowest.

The most effective is Streptomycinum. At the bubonic form immediately infuse 1 gm of preparation into muscle, and then in hospital indicate 0.5-1.0 gm 3 times per day during one week. At a pulmonary and septic plague a dose of Streptomycinum enlarge to 5-6 gm. Antibiotics of tetracyclines (oxytetracycline, chlortetracycline), 0.25-1.0 gm 4-6 times are recommended. From other antibiotics it is possible to indicate monomicin, morphocyclin, ampicilin. After clinical indications it will be carried out pathogenic and symptomatic treatment.

After normalization of a body temperature and reception of negative datas of bacteriological researching from nasopharynx, sputum, punctate of bubones- patients leave hospital after 4-6 week.

Dispensary observation during 3 months it’s necessary for reconvalescense with obligatory bacteriological researching from mucosa of pharynx and sputum.

It is necessary to protect people from expansion of plague diseases. This work is carried out by workers of sanitation center, ambulatory – polyclinic network and antiplague establishments. Plague is the quarantine diseases, so on it the international medico-sanitary rules (WHO, 1969) are distributed on it.

Workers of the general medical network observe health of the population with the purpose of early revealing the patients on plague. Each medical worker should know the basic attributes of disease, the rules of personal prophylaxis, be able to carry out initial antiepidemic actions.

At presence of epizootia among rats and diseases of camels vaccination of the population by local services under the control of antiplague establishment will be carried out. As active immunization use living plague vaccine (dose for epicutaneous indication for children till 7 years 1 billion, 7-10 years – 2 billion, adults 3 billion microbes bodies, at a hypodermic immunization 1/10 of epicutaneous doses). Immunity is kept during 6 months, then if it necessary will spend revaccination in one year.

At occurrence of a plague among the population the antiepidemic actions carry out wich is directed on localization and liquidation of epidemic pesthole. They include: revealing of patients and their hospitalization in special hospitals in isolation wards with severe antiepidemic regime; and establishment of territorial quarantine: revealing and isolation of all persons which was in contact with patients they must be isolated for 6 days and will carry out emergency prophylaxis by antibiotics – Streptomycinum 0.5 gm 2 times per day in muscle or Tetracyclinum on 0,5 gm 3 times per day inside during 6 days); revealing the patients with fever and their hospitalization in special departaments; final disinfection, and also disinfestation and deratization at territory of settlement and around it. Invaluable things are liable to destruction. The personnel should be work in antiplague costumes. For persons who need to leave zone of quarantine, will carry out an observation.

SEPSIS

http://www.nlm.nih.gov/medlineplus/ency/article/000666.htm

The term sepsis has been used for a clinical situation in which there is evidence of infection plus a systemic response as manifested by an elevated temperature, tachycardia,increased respiration, leukocytosis or an impaired peripheral leukocyte response, and/or the presence of immature band forms of peripheral circulation.

Sepsis has some differences from the other infectious diseases:

1. Sepsis is polyetiological disease. The agents of sepsis may be different microorganisms –aerobic and anaerobic.

2. There is no united entrance gates.

3. There is no cyclicy of the course.

4. Immunity don’t form in sepsis.

Treatment

http://www.medicinenet.com/sepsis/page4.htm

Therapy of a sepsis should include at least two obligatory components – suppression of the originator and restoration of immunity.

Principles of a etiotropic treatment of sepsis:

Basis of sepsis therapy – is oppression and liquidation of the agent. There should not be ignored means of syndromes treatment which restore immunity, all others if in them there is a necessity, but all of them caot cure the patient on with sepsis without appropriate ethiotropic therapy.

Antibiotic therapy of sepsis may be successful, if:

1) It is carried out by address, that is after revealing the agent definition of its antibiotic sensivity;

2) It will be carried out (spent) by bactericidal drugs bacteriostatic drugs are used only as address;

3) It is applied at early septicemia (at this stage of illness recovery is achieved in 100 % with one antibiotic without all other means of treatment);

4) Dozes of antibiotics maximum high, and β-lactamic antibiotics (penicillines, cephalosporines) are used in megadozes;

5) Empirical antibiotic therapy (if the agent is unknown) is carried out on the basis of the clinical supposition about a nature of the agent (empirical antibiotic therapy is should not be carried out by random);

6) Combination of antibiotics is carried out by a rule: bactericidal drugs with the various mechanism of action;

7) Usage of more than two preparations in one combination is not expedient, as with increase of number of drugs harmful actions grow faster, than therapeutic effect;

8) It is not necessary to start antibiotic therapy from reserve antibiotics (carbopenems, cephalosporines of 4-th generation).

If treatment is successful, antibiotic therapy is cancelled last, after liquidation of all infection foci, but not earlier 5-th day of a normal body temperature. Sepsis is a general clinical problem. Comprehension of sepsis should become the common medical property because such patients are in all medical establishments without exception.

Among various combinations of antibiotics the greatest recognition has received combination of 3-rd generation cephalosporines (Ceftriaxoni, Cefotaximi, Ceftazidimi) with Aminoglicosides (Gentamicini, Amikacinum). All these combinations are effective enough at patients with sepsis without a neutropenia. Appreciable interest to Ceftriaxoni is caused by duration of its period of semiconclusion, that allows to apply preparation once per day. Other preparations have shorter period of semiconclusion and demand repeated injection during day. At sepsis caused by Pseudomonas aeruginoza, high efficiency of combination of Penicillinums with antipyocyanic activity (Ticarcilini, Clavulanati, Aztreonami) and Aminoglicosides is marked.

At sepsis caused by Gram-positive flora (Meticilini-resistant staphylococcus, coagulasenegative staphylococcuses, enterococus), using of Vancomycinum, Rifampicinum is effective.

Carbapenemes (Tienamicines) – Special group of β–lactames antibiotics (Imipenicemi, Tienami, Meropenemi, Biapenemi), the infections created for empirical therapy with serious current, including leukopenia. Very wide spectrum of action, high bactericides, that is not accompanied by superfluous remission of endotoxins at destruction of bacteria, allow to use with success Carbapenemes as monotherapy at the most serious infections, including sepsis.

After allocation and identification of the originator, definition of antibioticogram the choice of effective antibacterial therapy is considerably facilitated. In such cases monotherapy is frequently used. Nevertheless, the question of indication of monotherapy or a combination of antibacterial preparations remains debatable and, apparently, should be discussed in each concrete case. Determining arguments, probably, will be estimation of gravity of infectious process and condition of reactivity of organism, danger of occurrence of hospital infections in connection with invasive methods of diagnostics and treatment, transplantation of extraneous bodies. Nevertheless, at Gram-negative infections, in opinion of many scientists, the combined therapy is more expedient.

Antibiotics, as a rule, do not suppress immunity. It is proved, that Lincosamides and Macrolides have immunomodulative properties and are capable to stimulate the certain parts of the immune answer.

Duration of antibiotic therapy is determined by course of inflammatory process. As a rule, preparations cancel at proof normalization of temperature (absence of attributes of generalized process), absence of the clinical and laboratory data on presence of the localized center of an infection or joining of nosocomial infections. At average therapy lasts 2-3 weeks. At revealing clinical efficiency of empirical or purposeful therapy by antibiotics change of a combination or separate preparation is inexpedient during all period of treatment.

The immunotherapy should be directed on blocking of effects of endotoxin and citocines. Application of Pentoxifilini is perspective, that brakes the formation of FNO, has protictive influence on lungs, systemic hemodynamics, improves microcirculation and oxygenation of tissues, stabilizes electrolytic balance, preventing occurrence of hyponatremia.

Citoprotective antioxidantes (vitamin E, Acetylcysteinum) oppress activity of free radicals and may improve the forecast at sepsis. Hyperproduction of free radicals which are metabolites of an arachidonic acid is lowered also by Ibufrofenum.

Efficiency of polyclonal antibodies to bacteria E. coli and Salmonella which at septic shock caused by Gram-negative bacteria’s, reduce a lethality almost on 50 % was proved. Now polymyxin B or neutrophile bactericidal penetrating protein is used.

Efficiency of application for prophylaxis of the systemic answer on inflammation of vactination of patients by derivative of endotoxin – monophosphorolipides A is now studied. Monoclonal antibodies to interleucines, phospholipase, to adhesive molecules and contact factors are received and pass clinical approbation of antibody to lipid A, to endotoxin and PNO. It is possible, that in future by identification of mediators it will be possible to create “ cocktail “ from antibodies which block receptors and enable to stop progresive process at the systemic inflammatory answer.

Interferons – native and genoinginering preparations which concern mainly to IFN (Roferoni A, Introni A, Realdironi, Laferoni etc.) – natural ways of imunocorection and protection against infections, with success are applied at present of acute and chronic infectious diseases.

Combined using of Carbapenemes, Roncoleucines- or interferons is advanced achievement of modern therapy of septic diseases.

At serious course of a sepsis stabilization of hemodynamics has crucial importance . First of all it is necessary to restore volume of circulating blood. For this purpose infuse cristaloides and colloid solutions in the ratio 2-4:1 under the control of parameters of hemodynamics, including the central venous pressure.

The proof hypotension, even after fast restoration of blood volume circulation, may be connected with disorders of regulation of vascular tone. Application of inotropic preparations – Dopaminum, Dobutaminum, Dobutrexi in this case is expedient. The clinical effect from Dopaminum will increase the cardiac emission (B adrenergic effect), rising of peripheric vessels tone (A-adrenergetic effect), improvement of circulation in parenchymatous bodies, first of all in kidneys (dopamineergetic effect). Using of A-adrenomimetics (epinephrine) may be necessary only in case of inefficiency of high doses of Dopaminum.

Respiratory support is necessary for significant amount of patients with sepsis, however application of different methods of artificial ventilation of lungs is limited to cases of disease with development of acute respiratory insufficiency. In a combination of inotropic therapy ventilating support promotes decrease of work of muscles, improvement of oxygenation of blood and function of systemic circulation.

In support of appropriate level of metabolic and immune processes the important value has a feed of patients. The early high-caloric enteroalimentation with the enlarged contents of fibers and amino acids (an arginine, an ornithine) reduces frequency of complications and duration of treatment. It is necessary to use enteral alimentary admixtures (enpites), balanced under the contents of fibers, Adepses and carbohydrates.

It is expedient to use solutions of amino acids for parenteral feeding (Alvesini, Aminosoli-600, Aminosoli-800, Aminosoli KE, Infesoli 40 and etc.), Dextrosum, lipide emulsions (Intralipid).

DVS demands correction only in stage of a decompensation.

Prophylaxis

http://www.malp-research.de/malp_applications_sepsis_prophylaxis.html

It is necessary to perform reatment of primary foci. The measures, directing on increase of resistance of the organism have an important meaning. These measures are rational diet, regime of work and rest, physical tempering.

Staphylococci are more frequent etiological factor of sepsis, that’s why the prophylaxis of intrahospital staphylococcal infection is necessary. The early revealing and prohibition of work of medical personnel with purulent inflammatory diseases (sore throat, pyodermia) and opportune hospitalization of the patients with staphylococcal infection in special departments or wards. It is necessary the revealing of prolonged bacteriocarriers of hospital strains of staphylococces and its sanation for patients with immunodeficiency and operating-room.

The maintenance of sanitary-hygienic regime has leading meaning in the hospitals of different profile.

It is necessary to use remedies, increasing nonspecific resistance of the organism of the patients in the groups of risk (infants, patients with immunodeficiency and other).