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.
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;
Size of inculums that is the larger dose the greater the chance of infection.
Presence of normal gastric acid which rapidly kills the bacteria bacilli
Virulence of the infecting strains
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;
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
Toxic damage leads to degeneration and focal necrosis of cardiac muscle.
The disease is of slow onset and common symptoms which normally occur early in other words known as prodrome, includes;
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;
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;
Slow pulseand fever,
Abdominal distension and tenderness
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
temperature is high and remains continous around 400c with relative bradycardia.
The patient may become dehydrated, delirious and exhausted.
The tongue is coated in the centre and the margins remain reddish.
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
Fever and toxemia continue
Complications set in during this period.
In uncomplicated cases temperature starts to fall in lysis, in the end of 3rd week and it touches normal within 7-10 days.
Abdominal symptoms subside.
Gradual improvement begins.
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
Peripheral circulatory collapse.
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.
Thrombophlebitis (inflammation of the wall of a vein leads to thrombosis)
Disease may relapse
Drug toxicity especially chloramphenicol
Perforation of the intestine resulting to peritonitis
Skin and appendage complication are bed sores and alopecia.
Other typhoid fever complication includes the following
Pyelonephritis ( i.e. inflammation of the renal pelvis)
Other disease that may confuse with typhoid fever includes;
How does clinicians/doctor diagnose typhoid fever
It can be through clinical suspicion ;
Continuous fever with relative Bradycardia
Timidity of the abdomen
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.
Stool-culture/positive in second week and urine-culture/third week of illness
Bone marrow culture-when other methods fail
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
Correct fluid and electrolytes
Adequate antibiotic therapy
Short course of corticosteroids.
2) Intestinal perforation
Use of antibiotics
3) Intestinal haemorrhage
Parenteral antibiotics and manage
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;
Avoid food contamination
Maintain good personal hygiene
Provision of protected water supply.
Personal prophylaxis through vaccination
This vaccine contains heat killed and phenol preserved Salmonella Typhi 1000 million and Salmonella Paratyphi A and B 750 million each/ml
-1 to 2 weeks apart
Booster dose every 2 or 5years type of typhoid fever vaccine.