Typhus Fever by Dr. Sookun Rajeev Kumar
- 1. Epidemic Typhus Dr. Sookun Rajeev K (MD) Dept of General Medicine Anna Medical College
- 2. Aetiology •The causative agent of epidemic typhus is Rickettsia prowazeki. •The microorganisms are unstable in the environment but in dry lice faeces they can live from one to several months. •The rickettsia can be found in the body of epidemic typhus patient, inside cells of intestinal epithelium of lice and in their faeces.
- 3. Epidemiology •The only source of infection is a human patient with epidemic typhus who becomes contagious during the last days of the incubation period (2-3 days), during the entire fever period, and till the 7-8th day of the disease after normalization of body temperature. •The overall length of the contagious period is 20- 21 day.
- 4. Epidemiology •The infection is transmitted by body lice, less frequently by head lice.
- 5. Epidemiology •Body lice deposit their eggs on hair, in pleats and folds of underwear and clothes, while head lice lay them only on hair.
- 6. Epidemiology •Eggs yield larvae which undergo triple sloughing before they grow to mature insects. This period lasts 7-10 days and should be taken into consideration when observing the focus and prescribing repeated sanitary treatment.
- 7. Epidemiology •When a louse sucks the blood of a typhus patient it becomes contagious in 4-5 days during which rickettsia multiply in the louse intestinal epithelium. •After destruction of the epithelial cells the rickettsia gain entrance to the intestinal lumen and are excreted in great amount with faeces.
- 8. Epidemiology •When a louse sucks blood, it excretes a substance that causes itching.
- 9. Epidemiology •As a person scratches the site of a louse bite he rubs the faecal mass with rickettsia into the puncture wound and the scratch site. •Contamination can occur when a crushed louse is rubbed into the skin.
- 10. Epidemiology •An infected louse lives 20-40 days instead of 45-60 days and dies of the ruptured intestine.
- 11. Epidemiology •The social factor is decisive in epidemiology of this disease. •Famine, inadequate housing and sanitary conditions, absence of baths and disinsectants, poor sanitation of population, its intensive migration in connection with war, or other disasters promote dissemination of the infection.
- 12. Pathogenesis •The pathogenic microorganisms enter the body through scratched or bitten skin. •Rickettsia invade the cells of vascular endothelium where they multiply and are carried by the blood stream to cause rickettsaemia. •Part of the microorganisms die to release toxin which causes toxaemia.
- 13. Pathogenesis •In fine vessels, rickettsia cause thrombi with subsequent proliferation of the vascular wall and around the vessel; thrombophlebitis and specific granuloma thus develop. •Vascular changes become manifest in 4-8 days of the disease in all organs and tissues, especially in the brain, skin, conjunctiva, adrenal glands, myocardium, spleen and the kidneys. •These lesions are manifested by specific symptoms on the part of the nervous, psychic, and cardiovascular systems, skin and other organs and tissues.
- 14. Pathogenesis •Organic changes develop in 18-20 days and their development terminates by the end of the 4th week and later. •Rickettsia are not completely eliminated from some patients, and the process becomes latent with persistence of the microorganisms in the reticuloendothelial cells.
- 15. Clinical Picture •The incubation period lasts from 6 to 25 days (usually 12-14 days). •The onset of the disease is acute. •The body temperature increases; headache, chills, malaise, and thirst develop; the patient loses appetite. •Headache intensifies and becomes debilitating; insomnia develops.
- 16. Clinical Picture •Irritability and anxiety of the first days are then followed by excitation. •Increasing symptoms, especially weakness and fever, force the patient into bed on the 2-3rd day of the disease. •Hyperaemic and swollen face, hyperaemic conjunctiva, injected and dilated scleral vessels (rabbit eyes) are seen during the first days of the disease. •Skin of the neck and the upper trunk is also hyperemic.
- 17. Clinical Picture •The tongue is dry and is difficult to protrude (Godelier's sign). •The skin is dry and hot to feel. •Dyspnoea , moderate tachycardia and hypotension are seen. •Petechial haemorrhages can develop in 3 days on the conjunctival fold; the haemorrhages also appear on the shoulder or the thigh, below the point where a tourniquet is applied.
- 18. Clinical Picture •Specific rash appears on the 4-5th day of the disease by which the initial period of the disease ends.
- 19. Clinical Picture •During the period of the disease in full swing the rash is first represented by roseoles which later change to petechia. •Rash develops on the flanks, chest, and the back, covers the whole body.
- 20. Clinical Picture •It is intensive and its elements are different in size: from the size of a pin-head to that of a lentil. •In moderate cases rash persists till the 12-14th day. •As rash develops, fever intensifies and becomes continuous or remitting, and remains so for 6-8 days. •The height of the fever period is characterized by moderate neutrophilic leucocytosis (to 9-11 x 109/1), thrombocytopenia and aneosinophilia; ESR is high (18- 25 mm/h).
- 21. Clinical Picture •The initial symptoms intensify with appearance of skin eruption, and new symptoms supervene. •Involvement of the nervous system increases. •Consciousness is dimmed, hallucination and delirium develop, the patient is restless. •This condition, in the presence of high fever, is known as status typhosus.
- 22. Clinical Picture •Symptoms of meningoencephalitis develop: stiff neck, Kernig and Brudzinski's symptoms, increased tendon reflex, tremor of the extremities, inarticulate speech, throat itching, and difficult swallowing. •The heart sounds are dull, heart rate is fast, arterial pressure is low, collapse is possible. •The liver and the spleen are enlarged. •Constipation develops. Severely ill patients can defaecate and urinate involuntarily, or the urine can be passed in small portions while the bladder is overfilled.
- 23. Clinical Picture •In 12-14 days of the disease, body temperature drops and the recovery phase begins. •The fever resolves within 2-3 days; less frequently the fall of temperature is critical. •Toxaemia decreases and all its symptoms (status typhosus in the first instance) subside gradually.
- 24. Clinical Picture •Rash resolves, consciousness clears, the patient shows interest in the surrounding, sleep and appetite improve, urination normalizes, pulse and arterial pressure normalize as well. •But despite the considerable improvement of the patient's general condition, weakness and pain in the legs and by the course of the nerve trunks persist for a long time. •The central nervous system remains easily excitable.
- 25. Clinical Picture •Mild, moderate and severe forms of epidemic typhus are distinguished. •The clinical picture of the disease has considerably changed in recent years (compared with the described classic symptoms).
- 26. Diagnosis •The diagnosis is based on clinical, epidemiologic and laboratory findings. •Serologic methods of examination are most important diagnostically. •Blood specimens (3-5 ml) are tested in the laboratory beginning with the 5-7th day of the disease.
- 27. Diagnosis 1. Rickettsia agglutination reaction. •The reaction of rickettsia agglutination with corpuscular rickettsia antigen is considered positive with titres of 1:160 and higher.
- 28. Diagnosis 2. Complement fixation test, •Complement fixation test is conducted with corpuscular or soluble rickettsial antigen. •The diagnostic titre is 1:160 and higher. •The maximum quantity of antibodies is found in 12-20 days of the disease (1:640-1:1280).
- 29. Diagnosis 3. Indirect haemagglutination •Indirect haemagglutination tests are most valuable diagnostically. •They are performed on the 3rd-5th day of the disease and the result is considered positive with the titres of 1:250 and higher. •The maximum antibody level is seen in 14-20 days of the disease (1:1000 and higher).
- 30. Diagnosis 4. Immunofluorescent and 5. Allergic tests are among the most sensitive methods.
- 31. Treatment •Modern treatment quickly decreases body temperature, eliminates toxaemia, promotes resolution of rash. •The following tetracyclines are used during the full swing of the disease, in accordance with the severity of the patient's condition:
- 32. Treatment •Tetracycline hydrochloride, Terramycin, Dioxycycline hydrochloride per os, 0.3 g qid until normal temperature persists for three days. •Chloramphenicol is inferior to the Tetracyclines with respect to its efficacy but whenever necessary it can be given per os in doses of 0.5 g qid until normal temperature persists for 3 days.
- 33. Treatment •In order to decrease toxaemia, a 5 % glucose solution or an isotonic sodium chloride solution (800-900 ml each) should be given intravenously. •Upset circulation of blood is managed by administration of a 10 % glucose solution, Ringer solution, mesaton (1 ml of a 1 % solution), Strophanthin (0.3-0.5 ml of a 0.5 % solution with glucose). The solutions are given intravenously at a low infusion rate.
- 34. Treatment •Barbiturates, bromides, aminazine are given to control excitation. •In order to prevent thrombosis, anticoagulants (heparin, phenylin) are given.
- 35. Thank You