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Typhoid Fever
Acute infectious disease caused by the typhoid bacillus Salmonella typhi. The bacillus is
transmitted by milk, water, or solid food contaminated by feces of typhoid victims or of
carriers, that is, healthy persons who harbor typhoid bacilli without presenting symptoms.
The World Health Organization (WHO) estimates that globally more than 16 million
cases of typhoid fever occur annually, causing 600,000 deaths.
An infection of the GIT affecting the lymphoid tissues (Peyer’s Patches) of the small
intestines.
Sign and symptoms
The bacteria collect in the small intestine, from which they enter the bloodstream. This
induces the first symptoms, chills followed by high fever and prostration. Victims may
also experience headache, cough, vomiting, and diarrhea. The disease spontaneously
subsides after several weeks in most instances, but in about 20 percent of untreated
cases the disease progresses to pneumonia, intestinal hemorrhage, and even death.
Onset
1. Headache, chilly sensation, aching all over the body,
2. Nausea and vomiting and diarrhea
3. By the 4th and 5th day all symptoms are worst
4. Fever is higher in the morning than it was in the afternoon.
5. Breathing is accelerated, tongue is furred,the skin is dry and not, abdomen is
distended and tender.
6. Rose spots appear on the abdominal wall on the 7th to the 9th day.
7. On the second week symptoms become more aggravated. Temperature remains
in uniform level. Rose spots become more prominent.
Typhoid state
1. Intense symptoms decline in severity
2. The tongue protrudes, become dry and brown.
3. Teeth and lips accumulate a dirty-brown collection of dried mucus and bacteria
known as soreds.
4. Patients seems to be staring blankly (coma vigil)
5. Twitching of the tendon sets in specially the wrist (subsultus tendinum)
6. Patient mutters deliriously and picks up aimlessly at bedclothes with his fingers
in continuous fashion (Carphlogia)
7. There is constant tendency for the patient to slip down to the foot part of bed.
8. In severe cases rambling delirium sets in often ending in death.
TYPHOID FEVER AND CHOLERA
Incubation period
The incubation period of typhoid fever usually lasts one to three weeks.
5-40 days; means 10-20days
Period of communicability
Variable. As long as the patient is excreting the microorganism, he is still capable of
infecting others.
Source of infection
Carriers could be one who recovered from the disease or one who have cared for a
patient with typhoid and was infected.
Ingestion of shellfish (oysters) taken from waters contaminated by sewage disposal.
Stool and vomitus of infected individual.
Mode of transmission
Fecal-oral transmission
Organism can be transmitted through the 5 F’s (Foods,Fingers,Flies,Formites,Feces)
Ingestion of contaminated food, water and milk.
Pathogenesis
The organism gain access to the blood stream through the bowel, principally through the
infected Peyer’s patches of the lymphoid tissues.
First week these lymph nodes are swollen
Second week they from sloughs which are often bile colored.
Third week, the sloughs separates and leave an ulcerated surface then; Hemorrhage
and perforation may occur due to extension of the lesion and continuous erosion of the
epithelial lining of the small intestines.
Since toxin is absorbed by the blood stream, almost all organs of the body are effected,
most commonly the heart, liver, spleen and mesenteric lymph glands are red and
swollen.
Complications
Hemorrhage or perforation- the two most dreaded complications
Peritonitis
Bronchitis and pneumonia
Meteorism or excessive distention of the bowels (tympanites)
Thrombosis and embolism
Early heart failure
“typhoid spine” or neuritis
Septicemia
Reiter”s syndrome- joint pain, eye irritation, painful urination that can led to chronic
arthritis.
TYPHOID FEVER AND CHOLERA
Diagnostic procedure
Typhidot
ELISA
Widal
Rectal swab
Salmonella Enzyme Immuno-assay (SEIA) considered confirmatory test.
Treatment
First antibiotic effective against the typhoid bacillus, Chloromycetin, or chloramphenicol,
derived from a South American mold in the late 1940s. Because of widespread
resistance to chloramphenicol, antibiotics from the fluoroquinolone and cephalosporin.
groups, such as ciprofloxacin and ceftriaxone, are currently the drugs of choice in the
treatment of typhoid.
Chloramphenicol- drug of choice
Ampicillin
Co-trimoxazole
Ciprofloxacin or ceftriaxone
If patient does not respond to chloramphenicol, 3rd and 4th generation drugs are
administered.
Nursing management
Maintain or restore fluid and electrolyte balance
Monitor patient’s V/S.
Prevent from further injury(fall) in patient with typhoid psychosis
Maintain good personal hygiene and mouth care
Cooling measures during febrile state
Watch for signs of intestinal bleeding
Proper disposal of excreta
Control
Compulsory inspection of milk and water supplies, and the pasteurization of milk in
particular, have greatly reduced the incidence of the typhoid bacilli. Of equal importance
in the control of typhoid fever has been the recognition of carriers, who can then be
prevented from handling food, and improvement of sewage facilities.
Sanitary/ proper disposal of excreta
Proper supervision of food handlers
Enteric isolation.
Adequate protection or provision of safe drinking water supply
Reporting of cases to health authorities.
TYPHOID FEVER AND CHOLERA
The fluid loss is attributed to the enterotoxin elaborated by the organism as they lie in
opposition to the lining cells of the intestines.
The toxin stimulates adenylate cyclase, resulting in conversion of the adenosine
triphosphate (ATP) to Cyclic Adesine Monophosphate (CAMP).
This stimulates the mucosal cell to increase secretion of chloride, associated with water
and bicarbonate loss.
The toxins act upon the intact epithelium on the vasculator of the bowel, thus, results to
outpouring of intestinal fluids.
Fluid loss of 5%-10% of the body weight results in dehydration and metabolic acidosis.
If treatment is delayed or inadequate, acute renal failure and hypokalemia become
secondary problem.
Clinical manifestations
There is an acute, profuse, watery diarrhea with no tenesmus or intestinal cramping.
Initially, the stools are brown and contain fecal materials but soon become pale gray,
“rice water”, in appearance with an inoffensive, fishy odor.
Vomiting often occurs after the diarrhea has been established.
Diarrhea causes fluid loss amounting to 1-30 liters per day owing to subsequent
dehydration and electrolyte loss.
Tissue turgor is poor; eyes are sunken into the orbit.
The skin is cold, the fingers and toes are wrinkled, assuming the characteristics “washer-
woman’s-hand”.
Radial pulses become imperceptible and the blood pressure unobtainable.
Cyanosis is present.
The voice become hoarse and then, is lost, so that the patient speaks in whisper.
(aphonia)
Breathing is rapid and deep.
Despite marked diminished peripheral circulation, consciousness is present.
Patient develops oliguria and may even develop anuria.
Temperature could be normal at the onset of the disease but become sub-normal in later
stage especially if the patient is in shock.
When the patient is in deep shock, the passage of diarrhea stops.
Death may occur on the first or the second day if not properly treated. Or as short as 4
hours after onset.
Diagnostic exams
Rectal swabs
Dark field or phase microscopy
Stool exam / fecalysis
Medical Treatment
Consists mainly of intravenous or oral replacement of fluids and salts. Packets for
dilution containing the correct mixture of sodium, potassium, chloride, bicarbonate, and
glucose have been made widely available by the WHO. Most patients recover in three to
TYPHOID FEVER AND CHOLERA