2. Aetiology
• Typhoid fever is caused by Enterobacteriaceae, genus
Salmonella.
• The microorganism is motile. Pathogenic only towards
human.
• It is stable in the environment:
in running water it persists for 5-10 days
in stagnant water for a few months.
It can survive over winter in ice.
3. Aetiology
In fruits and vegetables it lives for 5-10 days
In other foods from 2 to 8 weeks.
On some objects of the environment it persists from several
hours to a month and even longer.
• When dried in direct sun light the pathogenic microorganism is
rapidly destroyed.
• A 3 % solution of lysol and a 3 % chloramine solution kill the
bacteria within 2-3 minutes and Boiling kills it instantaneously.
4. Epidemiology
•The source of infection is a typhoid patient or a
carrier.
•Patients with typhoid fever are contagious for the
surrounding people beginning with the 1st week of the
disease.
•They are the greatest danger during the 2nd and 3rd
week of the disease as the maximum amount of
pathogenic microorganisms are excreted in the urine
and stools.
5. Epidemiology
• Beginning with the first week of the disease, specific immunity
develops in most patients. This helps the patient to free from
the pathogenic microorganisms and to terminate toxaemia.
• The leading role in the spread of infection belongs to chronic
carriers, especially if they are engaged occupationally in
handling of food that is not cooked before use.
• Chronic carriers are dangerous not only as the source of
infection, but also as depots of typhoid infection.
6. The Mechanism of Transmission
• Typhoid fever is characterized by the faecal-oral mechanism of
infection.
• The pathogenic microorganisms are released from the patient or carrier
with faeces and urine, and enter the body of a healthy person with
water or food.
• The transmission factors are:
Water
Food
Soiled hands
Environmental objects such as dishes, toys, linen, towels, flies,etc…
7. The Mechanism of Transmission
• If infection is transmitted with water, the morbidity rate depends on a
particular source of water: water supply system, river, well, pond.
• Water-borne epidemics of typhoid fever can be classed as:
1. Acute, that develop periodically and last over a comparatively short
period of time;
2. Chronic, that last for a few months and even years.
8. The Mechanism of Transmission
• Acute water-borne epidemics result from breakdown in the
water supply system or neglected rules of their maintenance.
• Chronic water-borne epidemics develop as a result of
systematic contamination of water with surface pollutants
through maintenance wells or some other routes.
• Food-borne transmission is characterized by ingestion of
contaminated milk and dairy products, and dishes not cooked
before consumption.
9. The Mechanism of Transmission
•During transmission of infection by person-to-person
contact, the microorganism is transmitted from the
patient or a carrier to a healthy person directly through
soiled hands or infected environmental objects. Spread
of infection is facilitated by suboptimal sanitation and
poor socio-economic conditions.
•If sanitation is inadequate and disposal of wastes is
below standards, flies promote the spread of typhoid
fever.
10. The Mechanism of Transmission
•Typhoid fever occurs in various countries but the
incidence is never pandemic, because typhoid fever is
characterized by a prolonged incubation period and the
maximum amount of pathogenic microorganisms are
released by the patient in 2-3 weeks after the onset of
the disease, that is, when the patient is already
hospitalized.
•The incidence is the highest during the warm season
(summer and autumn).
11. Pathogenesis
• The pathogenic microorganisms enter a human through the
mouth.
• If the defensive function of the stomach is adequate, the
microorganism is killed in the stomach and the person does not
develop the disease.
• If the defense function is impaired and the number of
microorganisms that enter the stomach is great, they can reach
the lower portions of the small intestine where they get into the
aggregations of lymphatic follicles (Peyer's plaques) and
solitary follicles, and into the nearest mesenteric lymph nodes,
where they multiply.
12. Pathogenesis
• At the end of the incubation period ,the pathogenic microorganisms
are released from the mesenteric nodes into the blood to cause
bacteraemia. The pathogenic microorganisms are thus carried
throughout the entire body and precipitate in the spleen, bone
marrow, lymph nodes and the liver.
• As the microbes die, they release endotoxin that poisons the body.
The endotoxin acts on the central nervous system to induce status
typhosus, which is characterized by dimmed consciousness,
inhibition, sleepiness alternated by insomnia, headache.
13. Pathogenesis
• The rate of bacteria removal from the patient depends largely
on the function of the excretory organs and systems (the liver,
the intestinal glands, the intestine, the kidneys) and formation of
specific antibodies.
14. Pathogenesis
• From the liver, the microbes are released with bile into the intestine and
are partly excreted from the patient. The remaining microbes precipitate
in aggregated and single lymphatic follicles in the lower portion of the
small intestine. The re-entrance of the microbes into the presensitized
aggregated and solitary lymphatic follicles causes an allergic
inflammation with ulceration and necrosis of tissues.
• Involvement of the sympathetic nervous system induces meteorism
(inflation of the intestine), diarrhoea, bradycardia, and hypotension.
• Endotoxin affects also bone marrow and induces leucopenia.
15. Clinical picture
• The incubation period lasts from 7 to 25 days (usually 14 days).
• The disease begins with a prodromal period. The patient
gradually develops:
• Weakness
• Malaise
• Chills
• Headache
• Impaired Appetite
16. Clinical picture
• The period lasts from a few hours to 2 days. The symptoms
then gradually intensify. The subjective condition impairs. The
patient develops
• Lack of Strength,
• Lack of Interest,
• Headache,
• Suffers from insomnia.
• Weakness makes the patient keep his bed.
17. Clinical picture
•The body temperature rises in steps, and by the 4th or
5th day it is 39-40 °C. For a period of time it remains
constantly high and then undulant fever develops.
•In the absence of specific treatment high fever can
persist for 2-3 weeks and then body temperature
decreases to normal in 4-5 weeks.
19. Clinical picture
• Visible mucosa and Skin pallor
• The tongue is thick, with imprints of the teeth by its edge; the tongue is
white, while the margins and the tip are free from the coat and are
crimson. If the disease runs a severe course, the tongue becomes dry,
its surface is cracked, the coat is stained with blood and turns brownish.
• The abdomen is inflated due to accumulation of a great amount of gas.
Constipation develops (diarrhoea is less common). The spleen becomes
enlarged by the end of the 1st week; the liver is enlarged later. The
pulse rate does not agree with the body temperature (relative
bradycardia); arterial pressure falls.
20. Clinical picture
• Rose spots occur on the abdomen, less frequently on the chest in 8-9
days of illness. The rash persists for 4-5 days and then regresses. Fresh
spots develop on new sites of the skin. In severe cases the rash can
bleed.
21. Clinical picture
• At the height of the disease, beginning with the 5th or 7th day, as
the fever intensifies, the nervous system is involved and the
status typhosus develops. The patient becomes indifferent,
delirium develops, headache intensifies along with increasing
meteorism and insomnia. In severe cases stupor develops
which can transform into sopor.
• A transient moderate leucocytosis is followed by leucopenia
with a relative lymphocytosis (40-60 %), aneosinophilia and
thrombocytopenia; ESR is moderately accelerated.
22. Clinical picture
• Bronchopneumonia and pharyngitis ulcerosa can develop at the
height of the disease; protein and casts can be found in the urine.
• Oliguria develops.
• Bacteriuria is associated with lesions of the urinary tract (pyelitis,
cystitis).
• As the clinical manifestations abate, toxaemia lessens, body
temperature gradually drops, sleep is normalized, appetite improved, the
tongue clears of the coat, and the amount of urine excreted increases.
After normalization of body temperature, the patient begins recovering.
23. Diagnosis
• The diagnosis of typhoid fever is based on the:
• Clinical picture of the disease
• Epidemiologic anamnesis
• Laboratory findings.
• The main method of laboratory diagnosis is bacteriologic study.
• The blood
• Urine
• Faeces
• Bile (duodenal contents) are examined in the laboratory.
24. Diagnosis
• The blood culture method is rapid and accurate for early diagnosis.
Blood cultures are mostly positive during the first days of the disease,
before antibiotic therapy is started.
• The immunofluorescence method is also used for early diagnosis of
typhoid fever. It reveals the typhoid bacillus in 10-12 hours after
inoculation.
• Stool and urine cultures are less important because they are positive
only beginning with the second week of the disease. Cultures are
inoculated from the first day of the disease.
25. Diagnosis
• In order to reveal carriers, the duodenal contents should be :
• Examined not earlier than 5-10 days following the fall of
temperature. Bile is taken from a fasting patient using a
duodenal tube.
• Serologic studies are used to confirm the diagnosis.
• In order to differentiate acute carriers from chronic ones, and
also vaccinated persons from carriers, indirect
haemagglutination tests with cysteine are used.
26. Treatment
• Chloramphenicol is used to treat typhoid fever. It is given in doses from 0.5 to 0.75 g four times
a day until the body temperature normalizes, and then for another 8-10 days (0.5 g three times a
day). Chloramphenicol is given per os, 20-30 minutes before meals. If vomiting develops,
chloramphenicol sodium succinate should be given intramuscularly or intravenously, 1.0 g three
times a day.
• Ampicillin in doses of 1 g four times a day (for 14 days) is also effective.
• Bactrim (biseptol), 2-3 tablets two times a day (for 3-4 weeks), or nitrofurane preparations in
doses of 0.15-0.2 g four times a day are given to patients with antibiotic-resistant bacilli.
• Antibiotics combined with vaccines decrease the incidence of relapses and prevent carrier state.
• An immediate surgical operation is necessary in intestinal perforation.
