Typhus Fever

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