develops in most patients. It 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, which cause disease in other persons and epidemic outbreaks, but also as depots of typhoid infection.
The epidemiologic importance of healthy (transitory) carriers, compared with chronic carriers, is not great because they release the microbes only for a short period of time and in small amount.
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, and the like. 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.
Acute water-borne epidemics result from breakdown in the water supply system or neglected rules of their maintenance. Epidemics are characterized by a sudden onset and a relatively rapid termination after eradication of the cause that has promoted the spread of infection with drinking water.
Chronic water-borne epidemics develop as a result of systematic contamination of water with surface pollutants through maintenance wells or some other routes. The morbidity rate remains high over a prolonged period of time in such cases.
Food-borne transmission is characterized by ingestion of contaminated milk and dairy products, and dishes, not cooked before serving. Besides, the pathogenic microorganisms find a beneficial nutrient medium for their multiplication. The character of food epidemics depends on the scale of use of a particular food. Usually they are short-lasting.
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 e mental objects. Spread of infection is facilitated by s sanitation and poor socio-economic conditions.
If sanitation is inadequate and disposal of wastes in towns is below standards, flies promote the spread of typhoid fever.
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. Besides, the absence of conditions for microbe spreading with water and food are sometimes absent.
The incidence is the highest during the warm season (summer and autumn). During recent years the incidence of typhoid fever is mostly sporadic; local outbreaks are not significant.
It is believed that susceptibility to typhoid fever is universal but many people are not afflicted by the disease in the focus of infection. Immunity that is induced in persons who sustained typhoid fever is rather durable but it weakens with years.
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. 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 human 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.
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. 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, primarily sensitized by the microbes, 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 inflam-
^ii 'ai mation with ulceration and necrosis of tissues (Plate I).
Involvement of the sympathetic nervous system induces meteor-ism (inflation of the intestine), diarrhoea, bradycardia, and hypotension.
Endotoxin affects also bone marrow and induces leucopenia.
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; his appetite is impaired. The period lasts from a few hours to 2 days. The symptoms then gradually intensify. The subjective condition impairs. The patient develops adynamia, indifference, headache, and suffers from insomnia. Weakness makes the patient keep his bed. 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 (Botkin's type of the disease). 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.
Examination of the patient reveals pallor of the skin and visible mucosa, 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 first week; the liver is enlarged later. The pulse rate does not agree with the body temperature (relative bradycardia); arterial pressure falls.
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.
Rose spots occur on the abdomen, less frequently on the chest in 8-9 days of illness (Plate II). 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.
A transient moderate leucocytosis is followed by leucope relative lymphocytosis (40-60 per cent), aneosinophilia ai bocytopenia; ESR is moderately accelerated.
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.
Typhoid fever can recur. After several fever-free days, the body temperature can rise again; characteristic rash develops along with other clinical signs of the disease, but a new attack is usually milder and lasts shorter.
Uncomplicated typhoid fever can be mild, moderate, and severe.
Deviations from the normal course of the disease are possible. The disease can begin acutely with hyperpyrexia, intestinal disorders, and other symptoms; mild, obliterated and abortive forms of the disease are also possible.
An abortive form of typhoid fever runs a typical course with all specific symptoms, but ends by a sudden critical fall of body temperature and rapid recovery. Fever lasts 5-7 days.
Atypical cases are characterized by a short-lasting fever (6-9 days) superimposed upon meagre clinical symptoms. The patient may remain out of bed.
Complications. Severe complications can develop following even a mild form of the disease, and the patient must therefore always remain in his bed during illness, regardless of the subjective condition.
Intestinal haemorrhage and perforation are the most dangerous complications. They usually occur during the 2nd or 3rd week of the disease and are associated with ulceration of the small intestine. A septic shock is another possible complication.
Intestinal haemorrhage can be mild. If bleeding is severe, pallor develops, the body temperature falls, the pulse accelerates, arterial pressure falls abruptly, the face becomes pointed. Collapse develops in severe cases.
Ulcer is usually perforated in 3-4 weeks; it is a danger to the patient's life. Meteorism, increased peristalsis, rough food and heavy exercise can provoke perforation of the intestine. Abrupt abdominal pain is not obligatory, and even mild abdominal discomfort must therefore be considered by the physician. The abdomen is first retracted and later becomes inflated; the anterior abdominal wall is
\fSj>oh - <■ t s.vdf strained, the pulse is fast, the leucocyte count in the peripheral blood increases. Vomiting and persistent hiccup develop. Only a surgical operation performed within 6 hours following perforation can save the patient.
If septic shock develops, the body temperature abruptly falls, the patient perspires, his arterial pressure drops, tachycardia develops, oliguria transforms into anuria.
Other complications are also possible: pneumonia, parotitis, cholecystitis, myocarditis, pyelocystitis, thrombophlebitis, involvement of the nervous system (meningoencephalitis, etc.)
Diagnosis. The diagnosis of typhoid fever is based on the clinical picture of the disease, epidemiologic anamnesis, and the laboratory findings. The main method of laboratory diagnosis is bacteriologic study. The blood, urine, faeces and bile (duodenal contents) are examined in the laboratory.
The blood culture method is rapid and accurate for early diagnosis. A sterile syringe is used to take 10-15 ml of blood from the patient's ulnar vein. The blood specimen is placed into a vial containing Rappoport medium or 10-20 per cent bile culture medium (1:10). The flask is kept in a thermostat at 37 °C and then Endo agar and Ploskirev medium are inoculated in 1, 2 and 7 days. 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, but this does not exclude confirmation of the diagnosis by the classical blood culture method.
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.
In order to take a specimen of faeces, a disinfected pan is used; 3-5 g specimen is transferred into a test tube containing a 30 per cent glycerol mixture. The test tube is handled to the laboratory where the taken material is used to inoculate Endo or Ploskirev medium and an enriched culture medium.
A urine specimen shtmld be better taken by a sterile catheter. If a catheter is not available, the outer orifice of the urethra should be washed with an isotonic sodium chloride solution, the first portion of the urine discarded, and then a 20-50 ml specimen taken into a sterile flask. In the laboratory, the urine is centrifuged or settled, and the sediment is used to inoculate the medium.
In order to reveal carriers, the duodenal contents should be
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