New hemorrhagic fevers (Marburg, Lassa, Ebola) - clinical features, diagnostics, treatment.
Hemorrhagic fevers are acute contagious virus infection characterized by serious course, intoxication, development of hemorrhagic syndrome, impairment of various organs and possible lethal outcome.
Pathogenesis includes: penetration of a virus through a skin and mucous => hematogenous dissemination with an impairment of many organs and systems => infringement of a permeability of blood vessels, increase of their fragility, disorder of a hemostasis (disseminated intravascular coagulation, thrombohemorrhagic syndrome) => decrease of volume of a circulating blood, fall of BP, renal insufficiency, sometimes toxic shock.
Febris Lassa is wide-spread in Western and Central Africa. The reservoir is multipapillary rat, rodents. A source of infection is a sick person. The ways of transmission are airborne, nutritional, direct contact, sexual, parenteral ones.
Clinics. Incubative period lasts 3-17 days.
1. Hyperpyrexial temperature.
2. The toxinfectious set of symptoms is expressed.
3. Ulceronecrotic pharyngitis (from the 3d day), conjunctivitis.
4. Diarrhea,pain in epigastrium, vomiting occur from the 5th-6th days of illness.
5. Dehydration.
6. Hemorrhagic eruption appears at the end of the 1st or beginning of the 2d week.
7. Hepatomegalia.
8. Renal insufficiency (oliguria, albuminuria).
9. Impairment of CNS.
The causes of death are renal insufficiency, toxic shock. A lethality is 37-67%.
Febris Marburg is wide-spread in a Sudan, Zaire, Kenya. The reservoir and source of infection are green marmosets and a sick person. The ways of transmission are same.
Clinics. Incubative period lasts for 2-16 days.
1. Hyperpyrexial temperature.
2. The toxinfectious set of symptoms is expressed.
3. Hyperemia of a mouth mucous, erosions on tongue (without a necrosis).
4. Diarrhea (fluid stool with slime and blood, cholemesis, hematemesis).
5. Dehydration.
6. The hemorrhagic syndrome is expressed on the 3th-5th day.
7. Rash appears on the 5 th-7th day: petechia, purpura, ecchymoses, vesicles, enanthema (vesicles and erosions).
Lethality is up to 90 %.
Febris Ebola is wide-spread in Sudan, Zaire. The reservoir is rodent, monkeys, bats. A source of infection is sick person. The ways of transmission are airborne, contact (blood of the patient!), parenteral.
Clinics. Incubative period lasts for 4-16 days.
1. Hyperpyrexial fever.
2. The toxinfectious syndrome is expressed.
3. The muscular pains are typical.
4. Cough, dryness in a throat, quinsy.
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5. Diarrhea with a blood, abdominal pain, vomiting occur on the 2th -3th day.
6. Hemorrhagic syndrome starts on the 5th -6th day.
7. Impairment of CNS.
The causes of death are toxic shock, bleeding.
Laboratory diagnostics:
1. Virologic research of a material from the patients (blood, urine, nasopharyngeal secretion).
2. Serological investigation determins increase of antibody titre in paired serums.
3. Detection of antibodies by an immunofluorescence.
4. Electron microscopy of the contagious material.
5. Express-diagnostics - chain polymerase reaction.
Treatment includes plasma of convalescents, immunoglobulin, antiviral drugs (Ribavirin in febris Lassa), pathogenetic therapy.
Malaria
13. Clinics of malaria according to a kind of causative organism.
Malaria (Intermittent fever) is an acute infectious disease caused by protozoa transmitted by malarial mosquitos (Anopheles genus) and characterized by cyclic course with change of the period of acute feverish attacks and interictal states, hepatosplenomegaly, anemia, sometimes - serious impairments of nervous system, kidneys and other inner organs.
There are 4 kinds of malarial plasmodiums - P.vivax - causative organism of tertian malaria (terziana), P.malariae - causative organism of quartan malaria (qartana), P.ovale – ovale-malaria, P.falciparum - causative organism of tropical malaria.
The life cycle passes with change of the hosts: sexual cycle or sporogony occurs in an organism of the final host - mosquito, asexual cycle or schizogony proceeds in an organism of the intermediate host – a man.
Sporogony: male and female gametocytes => zygote => ookinete => oocyst => sporozoits in salivary glands of mosquito. This cycle depends on the temperature of the air (minimum - 16оC, for tropical malaria - more than 20oC).
In an organism of a man:
1) exoerythrocytic or tissue (or paraerythrocytic) schizogony in a liver (10 000-50 000 tissue merozoites are formed from sporozoit);
2) erythrocytic schizogony in erythrocytes (stages: ring => juvenile trophozoit => semi-adult => adult trophozoit => immature schizont => mature schizont (morula) => going out into a blood from 8 up to 32 schizonts. Duration is 48 hours (vivax, ovale, falciparum) or 72 hours (malariae). There are bradysporozoits (or hypnozoits, somnolent) in a liver in vivax and ovale malaria, which begin development in 6-8 months - 1,5-2 years and cause late relapses. The male and female gametocytes are formed from a part of merozoites (in tropical malaria they are formed in 8-10 days from the beginning of illness and live about 6 weeks).
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The ways of transmission are:
1. Transmissible (bite of a mosquito)
2. In hemotransfusions
3. Transplacental (vertical)
Clinics: primary latent period is for P.vivax 10-21 days (for taxisporozoits, till 9-11 months for bradysporozoits), 11-16 days for P.ovale , 30-40 days for P.malariae, for P.falciparum - 8-16 days).
Primary attack (fresh, acute malaria):
1. Prodrome (malaise, headache, muscular pain, dyspeptic syndrome, subfebrile condition) is typical for vivax, ovale malaria and for tropical malaria in the nonimmune persons.
2. There is remittent or daily fever for some days (initial fever) (it is not typical for P. ovale and P. malariae).
3. The malarial paroxysm consists of three phases:
- tremendous chill (15 min. - 2-3 hours) is manifested by pale and cold skin, cyanosis, headache;
- fever heat (temperature 39-40оC, intoxication, hyperemia of the face, delirium, tachycardia, hypotonia, breathlessness) lasts for 6-12 hours;
- profuse sweat (critical fall of temperature, weakness).
In tertian and ovale-malaria the attacks arise every other day (in 48 hours), in quartan malaria in 2 days (72 hours) and tropical malaria has constant or remittant fever.
In tertian malaria an attack occurs in the afternoon, all phases are expressed.
In ovale malaria the attack begins in evening, chill is not expressed, temperature is lower, number of attacks is small.
In quartan malaria all phases are expressed, duration of primary attack is several months.
In tropical malaria an attack arises at any time of a day, chill and sweat are not expressed (they may be absent), the phase of fever heat lasts up to 24-36 hours and proceeds very hardly (frequently with unconsciousnesses and abdominal syndrome), duration of primary attack is about 2 weeks.
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4. Enlargement of the spleen and the liver (the spleen enlarges faster and more than the liver).
In ovale- and quartan malaria the spleen enlarges slowly, the function of the liver is not impaired.
In tertian malaria the spleen is enlarged by the end of the first week of the illness, the function of the the liver is impaired a little.
In tropical malaria the spleen is enlarged by the 10th day of the illness, the function of a liver can be impaired considerably.
5. Anemia:
In tertial malaria it is moderate during the 2d-3d week of illness.
In ovale-malaria it may be observed only in considerable duration of illness.
In quartan malaria it develops slowly, its level is low (mature erythrocytes are involved only).
In tropical malaria it occurs early and progresses quickly.
The afebrill period is replaced by early relapses in 2-3 months (it arises in all kinds of malaria, it is erythrocytic). The beginning has not a prodrome, the type of a temperature curve is regular at once, gametocytes appear at once, a course is benign.
The secondary latent period is replaced by late relapses (it is tissue) only in tertial ovale-malaria in 6-18 months. Course is the same as at early relapses.
Complications in tertial and ovale-malaria are rare. In quartan malaria nephrotic syndrome may be observed. Tropical malaria has serious complications frequently (especialy in the nonimmune persons) such as cerebral malaria (coma), acute kidney insufficiency, algid (toxinfectious shock), collapse, acute hemolysis, hemoglobinuric fever.
Duration of tropical malaria is till 1,5 years, of tertial and ovale-malaria is 3,5-5 years, of quartan malaria is tens of years.
14. Severe forms of malaria, first aid.
Severe forms occur in tropical malaria. Causes of particular malignancy of tropical malaria are:
1. The greatest number of tissue merozoites (up to 50000) in tissue schizogony.
2. The greatest number of schizonts during erythrocytic schizogony (up to 32).
3. Impairment of erythrocytes of all ages.
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4. Erythrocytic schizogony takes place in the capillaries of internal organs, that promotes to deep distresses of microcirculation in them => damaged erythrocytes become capable to adhere to a wall of vessels (sequestration) => «parasitic clots», infringement of microcirculation, disseminated introvascular coagulation.
5. Ability to bind undamaged erythrocytes by ponticuluses ("formation of rosulae") leads to their hemolysis.
6. The change of parasite’s antigenic structure prevents the development of immunity.
The criteria of the severity of the course are:
1. Disturbance of consciousness or coma.
2. Severe normocytic anemia (Hb 50 g/l).
3. Renal failure (diuresis 400 ml/day)
4. Pulmonary edema.
5. Hypoglycemia (2,2 mmol/l).
6. Hypotonia, shock.
7. Spontaneous bleedings, disseminated intravascular coagulation.
8. Generalized convulsions.
9. Acidosis.
10. Hemoglobinuria.
11. Impairment of more than 5 % of erythrocytes by plasmodiums.
Cerebral malaria (malarial coma) is most dangerous, it can lead to lethal outcome for 1-2 days.
Causes are: parasitogenic thrombuses in capillars of the brain, increasing of a permeability of capillaries => inflammatory congestion => autoimmune processes.
Malarial coma has three stages: 1) a somnolence (headache, giddiness, vomiting, retrobulbar pain, apathy or exaltation, sleepiness, mental exhaustion); 2) a sopor - confused consciousness, cramps, increase of reflexes, pathological reflexes, meningism, flaccid reaction of pupils; 3) a coma - areflexia, collapse, breathlessness, paresis of sphincters, absence of a reaction of pupils on a light, amimia, intermittent fever, arrhythmical superficial breathing.
Treatment includes being in cubicle of an intensive care, measuring of the temperature, pulse, blood pressure, respiration rate, diuresis, hemoglobin, erythrocytes, thrombocytes, hematocrit, residual nitrogen, biochemical parameters, acid-base equilibrium, level of a parasitemia.
1. Qininum glyuconat 50 % 15 mg/kg i.v. in 250 ml salt solution slowly for 4 hours, further - 7,5 mg/kg i.v. for 4 hours q8h. (not more than 2g/day). It is possible to combine i.v. and hypodermic injection. At the first opportunity substitution for the use of quinine sulfas po is necessary without delay. A course of treatment is 7-10 days. The dose must be decreased on 1/3 at signs of renal or liver failure.
2. Disintoxication (1500 ml/day) - 5 % glucose, saline solution, neohaemodesum, reopolyglucinum.
3. Prednisolonum (or Dexamethazonum) - 90-120 mg (dose depends on a blood pressure - up to 20 mg/kg/day)
4. Antihistaminic drugs, inhibitors of COG-2.
5. Treatment by the oxygen (during a coma intubation must be executed).
6. Therapy by vitamins.
7. Cardiac drugs.
8. Antipyretic medicines.
9. Anticonvulsive therapy.
10. Diuretics.
11. Catheterization of bladder.
Hemoglobinuri с fever (massive intravascular hemolysis of erythrocytes).
The causes are: the prescription of quinine, quinacrine, primaqinum, sulfanilamides on a background of a deficiency of the enzyme G-6-PDG.
In clinic there is sudden worsening of a general condition, chill, hyperthermia, pain in the muscles and loin, bilious vomiting, anemia, jaundice, urine like a black beer or red wine, hepatolienal syndrome, blockage of kidneys => anuria => renal failure (azotemia, hyperkalemia, albuminuria, hematuria, cylindruria).
Treatment includes:
1. Interruption of using antimalarial medicines.
2. Antishock therapy (phenylephine hydrochloride, morphine, cardiovascular remedies).
3. Hormonal preparations (prednisolone or dexamethazone, hydrocortisone).
4. Transfusion of fresh blood or packed red cells.
5. Disintoxication (5 % glucose, saline solution, haemodesum, “Trisolum”)
6. Perinephric novocaine blockade
7. Haemodialysis
8. Treatment of malaria after recovery of a state (except quinine and primaqinum).
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