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Friday, December 17, 2021

Typhoid Fever: Causative agent, Mode of Transmission, Complications, Treatment, Prevention by Nurses Note

Typhoid Fever

It is an acute infectious disease of the small intestine, caused by Salmonella typhi, transmitted through fecal contaminated water, food, and vegetables, usually affecting the school children. Clinically, it is characterized by continuous fever for a prolonged period, severe prodromal symptoms, and involvement of lymphoid tissues. With the availability of antibiotics, the case fatality rate is reduced to 10 percent. 

The term ‘Enteric fever’ includes both typhoid and paratyphoid fevers. Para-typhoid fever is caused by Salm para typhi A and B. Unless otherwise specified, enteric fever always means typhoid fever. Para-typhoid is less severe. 


• In 1829, Louis distinguished typhoid from typhus fever. 

• In 1839, Schonlein showed by post-mortem studies that the lesions in the Peyer’s patches and mesenteric lymph nodes were specific in typhoid fever and not in typhus fever. 

• In 1856, Budd pointed out that the disease is transmitted through the excreta of the patients. 

• In 1880, Eberth saw the organisms in the lymphoid tissues. 

• In 1884, Gaffky successfully grew it in pure culture. 

• In 1890, Pfeiffer, Kolle and Wright independently performed the vaccination experiments. 

• In 1975, Germanier and Furer developed live, oral vaccine against typhoid.

Agent Factors of Typhoid Fever

Causative Agent of Typhoid Fever

The etiological agent is Salmonella typhi. It is a gram-negative bacilli, capsulated, flagellated, actively motile organism. (Exception: S. gallinarum and S. pullorum are non-flagellated and hence non-motile organisms). The organisms possess three types of antigens, namely somatic or ‘O’ antigen, (specific for the group), Flagellar or ‘H’ antigen (specific for the type), and capsular or ‘Vi’ antigen, related to the virulence of the organism. Antibodies to ‘O’ antigen is usually higher in cases of typhoid, antibodies to ‘Vi’ antigen among carriers and antibodies to ‘H’ antigen among immunized persons. 

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There are about 80 types of phage types. Phage typing has proved a useful epidemiological tool in tracing the source of epidemics. 

The organisms are sensitive to heat and chemicals. They are readily killed by heat at 60°C for 15 minutes and also by routine disinfectants like chlorine, bleaching powder, KMnO4, cresol, and formalin. S. Typhi mainly live in the intestine of human beings, which is the natural habitat, they also survive intracellularly in the tissues of various organs like spleen, heart, kidney, bone marrow, etc. They can also survive in the environment like food, water, sewage, ice-cream, soil, etc. for quite a long period of 15 to 20 days. 

On autolysis, inside the body, these pathogens release an endotoxin, which plays an important role in the development of the disease process. The nonhuman strains of Salmonellae, such as S. Typhimurium (from rats), S. gallinarum, S. pullorum, S. enteritidis result in Salmonellosis and not typhoid. Thus Salmonellosis is a zoonotic disease.

Reservoir of Infection

Human being is the only known reservoir of typhoid. Such a reservoir may be a case or a carrier. 

 A case may be an active clinical case or a subclinical case. For every clinical case, there are about 10 subclinical cases. A carrier may be, according to the type, an incubatory, convalescent or a contact carrier and depending upon the duration may be temporary or chronic and depending upon the portal of exit, maybe intestinal, urinary, or biliary carrier. They may shed the organisms continuously or intermittently. Thus, all types of carrier state occur in typhoid. These carriers constitute the submerged portion of the ice in iceberg phenomenon and are responsible for the endemicity of typhoid in the community. Thus, they are more dangerous than cases. 

Mary was a chronic carrier of typhoid, working in the food establishment. She was responsible for 25 deaths due to typhoid and 1250 cases of typhoid. Thus, she was named as ‘Typhoid Mary’. 

Such a carrier state occurs in typhoid following a clinical or a subclinical infection or incomplete treatment. Nearly 2 to 5 percent of the cases and majority of subclinical cases become carriers. The incidence of the carrier state is more among women than among men in the ratio of 5:1.

Thus, these carriers constitute a challenge to the modern techniques of community medicine to detect them, treat them and prevent them from acting as a source of infection to others. 

Carriers of typhoid are detected either serologically by blood examination for ‘Vi-antibody’ titer or bacteriologically by culture of urine and/or stools.

Treatment of Carriers of Typhoid Fever

Treatment of carriers–discussed under treatment of typhoid. 

Instructions to Typhoid Carriers

• They must abstain from working in food, water and milk establishments, till they are bacteriologically cured. 

• They must undergo periodical medical check-up including laboratory investigations to rule out their carrier state. 

• They must maintain a high standard of personal hygiene.

Prevention of Carrier State 

• Healthy carrier state cannot be prevented because they become carriers following subclinical infection. 

• Convalescent or chronic carrier state can be prevented by giving a correct and complete chemotherapy, with a follow-up to ensure their bacteriological recovery also. 

Source of Infection

The main source of infection is the feces of the infected person, to some extent urine also. Secondary sources are fecal contaminated water, food and fruits and vegetables.

Infective Material 

It is the feces of the cases and feces and/or urine of the carriers.

Period of Communicability

Varies from several days to months or even years. 

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Host Factors of Typhoid Fever

• Age incidence: Typhoid is common among children (5–15 years) often among adults and rare among elderly. Incidence is less above 30 years of age, because of development of immunity following subclinical infection.

• Sex incidence: Incidence of typhoid is more common among boys than among girls. However, the carrier state is more common among women than among men, in the ratio of 5:1.

• Immunity: There is an acquired, cell-mediated, partial immunity following a clinical illness. Hence reinfection and relapses are known to occur. 

• Environmental factors: The peak incidence is during monsoon season (July – September).

• Predisposing factors (Social factors): Typhoid is called a ‘Social disease’, because there are many social factors responsible for the prevalence of this disease in an endemic form in our country, such as poverty, illiteracy, ignorance, poor standard of living, lack of sanitation, lack of personal hygiene, open air defecation and urination, low standard of food hygienic practices, lack of protected water supply, etc. All these factors go hand-in-hand. When the conditions are favorable, the endemic disease becomes an epidemic disease 

Mode of Transmission of Typhoid Fever

The disease is mainly transmitted by ‘Feco-oral’ route, i.e. the pathogen is transmitted from one ‘F’, through six ‘Fs’ to a susceptible person.

Typhoid is mainly transmitted through fecal (sewage) contamination of water and often through contaminated food through house-flies, which act as mechanical vectors by flying from filthy substances to food substances. The disease is also transmitted through contaminated milk because water is added to milk or the milk-handler may be a carrier. Vegetables grown in sewage farms also favor the spread of the disease. Lack of personal hygiene such as non-trimming of nails, also favors the transmission through fingers. 

Pathology and Pathogenesis of Typhoid Fever

Having entered the body through the mouth, the pathogens enter the bloodstream, reach reticuloendothelial cells, where they multiply and after rupture of RE cells, they are poured into the blood resulting in bacteremia and circulate for one week. 

      After circulation, they lodge mainly in the Peyer’s patches of ileum. They also lodge in the spleen and gallbladder. However, any tissue or organ may be affected and may result in complications. 


Peyer’s patches are the most common site of involvement. These patches are all inflamed resulting in minute, innumerable ulcers with discharge of bacilli and pus into the lumen of the gut. The regional mesenteric lymph nodes are also inflamed and enlarged. 


There is lymphoid hyperplasia, resulting in splenomegaly. Presence of organisms in the spleen may act as a seed of future relapse. 


There will be chronic infection in the gallbladder resulting in cholecystitis and cholelithiasis (stones).

   On autolysis, the pathogens release endotoxin, which enters the circulation resulting in toxemia (fever). This endotoxin suppresses the activity of the heart and bone marrow; resulting in relative bradycardia and leucopenia. Antibodies are produced in the second week and subsequently, as the antibody titer increases, the patient recovers slowly after 3 weeks. 

Incubation Period of Typhoid Fever

10 to 15 days. 

Clinical Features of Typhoid Fever 

During the first week of illness, there is gradual onset of fever, continuous, raises day by day in a ‘step ladder’ fashion, associated with chills and severe prodromal symptoms such as headache, body ache, malaise, loss of appetite, joint pains with occasional vomiting. Fever will be in the range of 38 to 40°C. Often there will be dry cough. 

   During second week, temperature reaches its plateau (104°F), skin is dry and hot, tongue is coated, patient looks tired, abdomen is distended, spleen is enlarged and soft, tenderness in the right iliac fossa, relative bradycardia and often there will be transient appearance of rashes over the abdomen, which fade on pressure (Relative bradycardia means the heart-rate is lesser than what it should have been for that temperature). There may be diarrhea with ‘pea-soup’ stools. 

  During third week, the patient will have signs of toxemia such as very high temperature, rapid thready pulse, mentally dull, delirious, disoriented, sleepy, confused, talks irrelevantly,w will have toxic face, later becomes stuporous, develops coma and dies. Case fatality rate is 10 percent in untreated cases. 

    Those who recover following the development of antibodies and with or without treatment, temperature falls by lysis, appetite improves, distension of abdomen disappears, strength improves and the convalescence is slow. 

During First week of illness - blood for culture.

During Second week of illness - blood for widal, TC (Leucopenia) 

During Third week of illness - blood for repeat widal and stool and urine for culture. 

Note: Blood for widal will be negative during first week of illness because sufficient antibodies are not produced and blood for widal will be positive only during second week and blood for repeat widal during third-week shows increase in antibody titer, which is confirmative. Stool and urine for culture will be positive only during third week onwards. 

Complications of Typhoid Fever

No other disease has so many complications, as much as it is in typhoid because any organ may be affected. Recognized complications are mainly three—Relapse, Hemorrhage (from the intestinal ulcers) and Perforation (of these ulcers). Hemorrhage in the gut is characterized by Malena and perforation is characterized by acute peritonitis, which constitutes an acute surgical emergency. 

  Other complications of typhoid are meningitis, myocarditis, gallstones, pneumonia, hepatitis, osteomyelitis, arthritis, thrombophlebitis, and others. 

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Treatment of Typhoid Fever

• Isolation: Preferably in the isolation ward till 2 to 3 stool culture report comes as negative. It may take about 2 weeks. 

• Concurrent disinfection: Of mainly the excreta (urine and stools) by collecting it in a container containing 10 percent cresol or 8 percent bleaching powder. 

• Chemotherapy: Now the drug of choice is cefotaxime, 200 mg twice a day for adults and 100 mg twice a day for children, for about 10 days. Ceftriaxone can also be given. Resistance has been observed against quinolone drugs. Antipyretics are also given. 

• Follow-up: Itis done by sending three consecutive samples of stool and urine for culture, to ensure bacteriological recovery of the patient. 

• Treatment of carriers: Depends upon the type of carriers. 

Biliary carriers–Cholecystectomy 

Intestinal carriers–Resection of loop of gut.

 Urinary carriers–Partial or total nephrectomy depending upon the damage of the kidney. 

Thus, since the carriers invariably suffer from surgical problem, surgery followed by chemotherapy is the rule. This offers 70 to 90 percent cure.

Prevention and Control of Typhoid Fever

Elimination of Reservoir 

This consists of making the infectious persons non-infectious by giving treatment for cases and carriers.

 Breaking the Channel of Transmission( Interruption of transmission). 

Since the mode of transmission is by feco-oral route, it is interrupted by construction of ‘Sanitation barrier’. It consists of construction and use of sanitary latrine, which prevents the access of the pathogens from feces to six F’s.

  The construction and use of sanitary latrine will be more effective, when it is supplemented with the following measures.

• Chlorination of water for drinking purposes

• Pasteurization of milk

• Adoption of food-hygienic measures 

• Disinfection of fruits and vegetables with KMnO4

• Disinfection of fomites like utensils, plates 

• Adopting high standard of personal hygienic measures (such as trimming of nails, washing the hands with soap and water after the using toilet and before eating the food)

• Control of house flies by keeping the environment clean. 

Protection of Susceptibles

Protection of susceptibles is mainly by Health promotion and Immunization. 

Health promotion: This consists of: 

• Provision of protected (chlorinated) water supply 

• Sanitary disposal of sewage 

• Health education of the people about hazards of open-air defecation, importance of sanitation in and around the house, importance of personal hygiene, use of sanitary latrines, spread of the disease, etc. 

Specific protection is by vaccination. 

There are three types of vaccines—Killed vaccines, Live vaccines and Cellular extract vaccines. 

• Killed vaccines are of three types – Trivalent (TAB) vaccine 

 – Bivalent (TA) vaccine 

 – Monovalent antityphoid vaccine. 

These are all less effective and outdated vaccines. Not used. 

Live vaccine: It was first developed by Germanier and Furer in 1975. It is a live, lyophilized vaccine, made available in a pack of 3 capsules, each capsule containing not less than 109, viable, attenuated, Salmonella typhi-21 a Strain. It is indicated for all adults and children above 6 years of age. (because children below 6 years may not swallow capsules).

Schedule consists of one capsule, to be swallowed, on alternate days, preferably 1 hour before meals, irrespective of age and sex, above 6 years, for 3 days, i.e. on Day 1, 3 and 5. 

Immunity is developed about 2 weeks after taking the third capsule and lasts for 3 years. It is 60 percent effective. Booster dose consists of the same 3 capsules, recommended once in 3 years. 

Side effects are nil. Acute febrile disease is a contraindication. A note of caution is that oral antibiotics should not be given alongwith oral typhoid vaccine because they may destroy the live vaccine strain, resulting in vaccine failure. 

The capsule is marketed as Typhoral, best stored at 2 to 8°C.

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