Typhoid fever causes, transmission and treatment

Typhoid fever/enteric fever ;lets today discuss about . One question that one may ask is, what is typhoid fever and how is transmitted. This is acute febrile infection/disease caused by Salmonella Typhi bacterium. This disease is transmitted through fecal oral route that is by eating or drinking water/milk that is contaminated  by human fecal matter. Another  source of infection is food handler and flies they can transmit the disease. This bacterium remain viable in water for long period of times. For one to be infected needs to ingest dose-107 organisms organism. Those organism are eliminated in feces and urine upto 9th weeks during convalescence (the process of getting well)-for convalescent carriers.

Healthy carriers

Are those who pass Salmonella typhi in feces (fecal carriers) or urine (Urinary carriers) without themselves suffering from the disease. Fecal carrier state is more likely to follow Salmonella typhi infection in 10% of cases above the age of 50 years.In many cases of fecal carriers, the gall bladder is the source of persistent S.typhi infection.

How does this disease establishes itself in body once  one get infected (pathogenesis)?

Several factor determine this;

  1. Size of inculums that is the larger dose the greater the chance of infection.
  2. Presence of normal gastric acid which rapidly kills the bacteria bacilli
  3. Virulence of the infecting strains
  4. The presence of bacterial flora in the jejunum

Following  ingestion of the Typhi Bacilli

  • The bacilli enter through the intestinal epithelial lining of the jejunum and ileum.
  • In the sub-mucosa they are phagocytosed by the polymorphs and macrophages. The organisms survive within the phagocytes and they reach the mesenteric lymph nodes.
  • There they multiply and enter the blood stream to produce a transient bactaraemia. They reach the spleen, gallbladder,  bone marrow, lymph nodes, lungs and kidneys, where further multiplication of the organisms occurs.
  • Large number of bacilli is discharged from the gall bladder into the intestines.
  • This time they enter the payer’s patches and lymphoid follicles of the ileum. These lymphoid structures undergo inflammation, necrosis and ulceration.
  • Clinical manifestation starts when bacteria begin to re-enter the blood steam from the intracellular sites. Usually asymptomatic.
  • The organism produces endotoxin which accounts for the fever and many of the systemic effects
  • Spleen and lymphoid tissue – proliferation of mononuclear cells.
  • Liver-Enlarge and show a cloudy swelling

In Payers patches;

  • Get swollen
  • There is Infiltrations by mononuclear cells undergoing necrosis and sloughing. Slough separate and form ulcers.
  • Blood vessels may be eroded leading to intestinal haemorrhage.
  • Erosion may extend to muscularis mucosa and serosa resulting to intestinal erosion and perforation.

Bactaremia  usually occurs with following features

  • Fever
  • Toxemia
  • Toxic damage leads to degeneration and focal necrosis of cardiac muscle.
  • Rectus abdominis muscle – Undergoes  Zenker’s degeneration.

Clinical manifestation of typhoid fever

The disease is of slow onset  and common symptoms which normally occur early in other words known as prodrome,  includes;

typhoid fever

  • Anorexia or loss of appetite
  • General body tiredness /malaise
  • Fever or hotness of the body
  • Lack of energy or lack of interest doing things or feeling lethargic
  • Headache may occurs from the beginning
  • Step-ladder rising temperature for first week
  • Relatively slow pulse/bradycardia
  • Nose bleeding/epistaxis may occurs
  • Non productive cough-in few case

Abdominal symptoms include;

  • Vague discomfort
  • Pain
  • Constipation/inability to pass stool for more than 3 days or passing hard stool
  • Less often diarrhea

On physical examination by a clinician/doctor

First week of illness patient experiences;

  1. Slow pulseand fever,
  2. Abdominal distension and tenderness
  3. Erythematatous macules, eg rose spot which are 2-3 mmin diameter. Are due to embolism and they last for few weeks. They normally difficult to find in darker.

By second week of illness

  1. temperature is high and remains continous around 400c with relative bradycardia.
  2. The patient may become dehydrated, delirious and exhausted.
  3. The tongue is coated in the centre and the margins remain reddish.
  4. Typhoid state – because of toxaemia

In this typhoid state patient shows;

  • Subsultus Tendinum. (abnormal twitching or tremor of muscles due to fever).
  • Muttering delirium (i.e. speaks in a quiet voice which is difficult to hear)
  • Tremulousness of the hands.
  • Carphology (floccillation) – i.e. Plucking of bedclothes by a delirious patient- it is a sign of extreme exhaustion and may be a prelude to death.
  • Picking movements of the hands.
  • Coma vigil ;This is when  patient is in comatose but the eyes are open.

Abdominal examination reveals the following;

  • Abdomen is Moderately distended (Tumidity/swollen/bulging) with vague tenderness, especially over the right iliac fossa.
  • Palpation may reveal gurgling due to mild distension of ileal loops.
  • Over 75% of the cases show moderate splenomegaly (3-4 cm) and is soft.
  • Stool is pea-soup coloured  since feces are loose and greenish in colour. It may contain blood streaks.

By third week of illness patient may recover or detorolate into severe state

  1. Fever and toxemia continue
  2. Complications set in during this period.
  3. In uncomplicated cases temperature starts to fall in lysis, in the end of 3rd week and it touches normal within 7-10 days.
  4. Abdominal symptoms subside.
  5. Gradual improvement begins.
  6. Convalescence is prolonged( recovery period)

Something to note is that, typhoid shows a wide variation in severity and duration of illness.

Patient may develop the following complications

  1. Peripheral circulatory collapse.
  2. Disseminated intravascular coagulation. A  condition resulting from overstimulation of blood-clotting mechanisms in responds to a disease or injury leading into overstimulation. This results to generalised blood coagulation and excessive consumption of clotting factors leading into spontaneous bleeding.
  3. Thrombophlebitis (inflammation of the wall of a vein leads to thrombosis)
  4. Disease may relapse
  5. Drug toxicity especially chloramphenicol
  6. Perforation of the intestine resulting to peritonitis
  7. Bleeding from the intestine
  8. Toxic Hepatitis
  9. Suppurative paroditis – (parotid salivary  gland inflammation)

Neurological complication includes;

  1. Meningitis
  2. Peripheral neuritis
  3. Deafness and
  4. Comatose state.

Skin and appendage complication are bed sores and alopecia.

Other typhoid fever  complication includes the following

  • Myocarditis
  • Pyelonephritis  (  i.e. inflammation of the renal  pelvis)
  • Glomerulonephritis
  • Osteomyelitis
  • Arthritis

Other disease that may confuse with typhoid fever includes;

  • Hepatic amoebiasis
  • Tuberculosis
  • Infective endocarditis
  • Urinary infections
  • Malaria
  • Rheumatic fever
  • Lymphomas

How does clinicians/doctor diagnose typhoid fever

It can be through clinical suspicion ;

  • Continuous fever with relative Bradycardia
  • Coated tongue
  • Timidity of the abdomen
  • Mild Hepatosplenomegaly
  • Tenderness and gurgling in the right lower quadrant of the abdomen

Doctor may order following test to assist in making diagnosis

1.  Blood for complete blood count shows low leukocyte count and relative lymphocytosis

2.Blood culture-1st week


  • Culture of blood clot yield better results and is gold standard.
  1. Stool-culture/positive in second week and urine-culture/third week of illness
  2. Bone marrow culture-when other methods fail
  3. widal test to demonstrate rising titers

  • Widal Test- Used to detect and measure the H and O agglutinins of typhoid and paratyphoid bacilli in patients’ serum.
  • Rising titers demonstrated by repetition of tests at weekly intervals, IS SUGGESTIVE.
  • H’ antibody is non specific, can rise when a person has received TAB inoculation. ( i.e. a combined vaccine used to produce immunity against  the disease typhoid,  Paratyphoid A, Paratyphoid B).
    • agglutinins are of greater value in diagnosis and titer of 1:200 or more is very suggestive.
  • Paratyphoid A and B share the same type of agglutinins.

Also healthcare provider should trace contacts and investigate epidermic/ disease ourbreak through liaising with disease surveillance team in the hospital so as to contain the spread of typhoid fever.

Trearment of typhoid fever

For severe cases of typhoid fever patient needs to be admitted in hospital for bed rest. Needs proper nursing care to prevent bed sore and oral sepsis. Maintenance of nutrition  fluids and electrolytes balance. Diet should be easily digestable low residue type, 1500-1800 calories/day and 2-3 liters of fluids/day. Fever and headache to be relived by paracetamol. Constipation;  Opened once in 3-4 days with Glycerine enema. Laxatives are contraindicated. Diarrhoea stops when milk is withdrawn from the diet.

Specific drugs for treatment of typhoid includes;

One may use one of the following medication.

  • Chloramphenicol 30-40 mg/kg (1gm) QID x 14/7
  • Ciprofloxacin-400-500mg IV-6-7/days then 15-20mg/kg/BW bd/tds x 15/7
  • Ceftriaxone- 1-2g IV or IM od or bd x 7-10/7
  • Ofloxacin 400mg bd x 10-12/7
  • Pefloxacin 400mg bd x 7-12/7

Other medication includes;

  • Ampicillin 1g/day QID x 2/52
  • Amoxicillin 1gm tds X 2/52
  • Cotrimoxazole 400mg trimethoprin + 2400mg of sulphamethoxazole
  • Furazolidone 100mg Tab QID

Sometimes patient may develop complications and this is how they managed

1)Typhoid state

  • Correct fluid and electrolytes
  • Adequate antibiotic therapy
  • Short course of corticosteroids.

2) Intestinal perforation

  • Surgical operation
  • Use of antibiotics

3) Intestinal haemorrhage

  • Blood transfusion
  • Parenteral antibiotics and manage
  • Toxaemia


  • similar to primary attack

(5)Treatment of carriers

  • Ampicillin and cotrimoxazole given in repeated courses
  • Add probenecid to improve eradication rate
  • Ciprofloxacin  for four weeks
  • Cholecystectomy is curative in over 85% of the cases with Gall bladder disease

General preventive measures/prophlayxis includes;

  1. Avoid food contamination
  2. Maintain good personal hygiene
  3. Provision of protected water supply.
  4. Personal prophylaxis through vaccination

TAB vaccine

  • This vaccine contains heat killed and phenol preserved Salmonella Typhi 1000 million and Salmonella Paratyphi A and B 750 million each/ml
  • Dose 0.5mls

-Two doses

-1 to 2 weeks apart

  • Booster dose every 2 or 5years type of typhoid fever vaccine.

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