TYPHOID FEVER

S.PAVITHRA
Msc Nursing

Definition of Typhoid fever

Acute enteric infectious disease

caused by Salmonella typhi (S.Typhi).

prolonged fever, Relative bradycardia, apathetic

facial expressions, roseola, splenomegaly,
hepatomegaly, leukopenia.

intestinal perforation, intestinal hemorrhage

Etiology
Serotype: D group of Salmonella
Gram-negative
rod
non-spore
flagella
Culture characteristics

Problem Statement World

Typhoid fever is endemic in India. A limited

study in an urban slum showed 1% of
children up to 17 years of age suffer from
typhoid fever every year. Reported data
for the year 2005 shows same picture with
6,53,580 cases and 417 deaths.

Cont

2004,WHO estimated the global

typhoid fever disease burden at 21
million case annually, resulting in an
estimated 216,000-600,000 deaths
per year, predominantly in children of
school age or younger. Majority of this
burden occurs in Asia.

Epidemiology

continues to be a global health problem

areas with a high incidence include Asia,

Africa and Latin America

affects about 6000000 people with more

than 600000 deaths a year. 80% in Asia .

sporadic occur usually, sometimes have

epidemic outbreaks.

EPIDIMIOLOGICAL
DETERMINENTS
Agent factors
AGENT: S. Tyhi is the major cause of
enteric fever, S. Para -A and S.
Para- B are relatively infrequent. S.
Typhi has three main antigens O,
H and Vi and a number of phage
types (at least 80).

RESERVOIR OF INFECTON

Man is the only known reservoir of

infection, viz cases and carriers.

(i). CASES
(ii) CARRIERS

(i). CASES

the case may be mild, missed

or severe. A case (or carrier) is
infectious as long as bacilli
appear in stools or urine.

CARRIERS:
the carriers may be temporary (incubatory,
convalescent) or chronic, convalescent carriers
excrete the bacilli for 6 to 8 weeks, after which
their numbers diminish rapidly.
By the end of three moths, nor more than 4 per
cent of cases are still excreting the organism;
and by the end of one year, the average carrier
rate is around 3 per cent persons who excrete
the bacilli for more than a year after a clinical
attack are called chronic carriers.

SOURCE OF INFECTION
The primary sources of infection are
faeces and urine of cases are carriers;
the
secondary sources contaminated
water, food, fingers and flies.
There is no evidence that typhoid bacilli
are excreted in sputum or milk.

Host factors:
Age:
Sex:
Immunity:

Environmental and social

factors:

Mode of transmission

1. Vehicle transmission:2. Direct contact:3. Flies:-

Transmission
fecal-oral route

close contact with patients or carriers

contaminated water and food

flies and cockroaches.

Susceptibility and immunity

all people equally susceptible to infection

acquired immunity can keep longer,
reinfection are rare
immunity is not associated with antibody
level of H, Oand VI.
No cross immunity between typhoid and
paratyphoid.

Susceptibility and immunity

All seasons, usually in summer and

autumn.
Most cases in school-age children and
young adults.
both sexes equally susceptible.

Pathogenesis
gastrointestinal tract hostpathogen interactions
The amount of bacilli infection
(>105baeteria).

Pathogenesis
ingested orally

Stomach barrier (some Eliminated)

enters the small intestine

Penetrate the mucus layer

enter mononuclear phagocytes of ileal peyer's
patches and mesenteric lymph nodes

proliferate in mononuclear phagocytes

spread to blood. initial bacteremia (Incubation
period).

Pathogenesis
enter spleen, liver and bone marrow
(reticulo-endothelial system)
further proliferation occurs

A lot of bacteria enter blood again.

(second bacteremia).

Recovery

S.Typhi.
2nd bacteremia

liverspleengall
BM ,ect
early stage&acme stage
(1-3W

stomach

(mono

Bac. In gall

nucle
ar
phago
cytes )

Bac. In
feces

Lower
ileum

S.Typhi eliminated
convalvescence stage
(4-5w)

peyer's patches &

mesenteric lymph nodes
LN Proliferate,swell
necrosis
defervescence stage

Enterorrhagia,i
ntestinal
perforation

3-4w

thoracic
duct

1st bacteremia
(Incubation stage)
10-14d

Pathology

essential lesion:

proliferation of RES (reticuloendothelial

system )
specific changes in lymphoid tissues
and mesenteric lymph nodes.
"typhoid nodules
Most characteristic lesion:
ulceration of mucous in the region of the
Peyers patches of the small intestine

Major findings in lower ileum

Hyperplasia stage(1st week):

swelling lymphoid tissue and
proliferation of macrophages.
Necrosis stage(2nd week):
necrosis of swelling lymph nodes
or solitary follicles.

Major findings in lower ileum

Ulceration stage(3rd week):
shedding of necrosis tissue and formation
of ulcer ----- intestinal hemorrhage,
perforation .
Stage of healing (from 4th week):
healing of ulcer, no cicatrices and no
contraction

Clinical manifestations
Incubation period: 360 days(714).
The initial period (early stage)
First week.
Insidious onset.
Fever up to 39~400C in 5~7 days
chillsailmenttiredsore throat
cough ,abdominal discomfort and
constipation et al.

The fastigium satge

second and third weeks.

Sustained high feverpartly remittent fever

or irregular fever. Last 1014 days.

Gastro-intestinal symptoms: anorexia

abdominal distension or paindiarrhea or
constipation

Neuropsychiatric manifestations: confusion

blunt respond even delirium and coma or
meningism

Circulation system:
relative bradycardia or dicrotic pulse.

splenomegalyhepatomegaly
toxic hepatitis.

roseola :30%, maculopapular rash

a faint pale color, slightly raised

round or lenticular, fade on pressure

2-4 mm in diameter, less than 10 in number

on the trunk, disappear in 2-3 days.

fatal complications:

intestinal hemorrhage
intestinal perforation
severe toxemia

defervescence stage

fever and most symptoms resolve by the

forth week of infection.
Fever come down, gradual improvement in
all symptoms and signs, but still danger.

convalescence stage

the fifth week. disappearance of all

symptoms, but can relapse

PATHOPHYSIOLOGY:

STOMACH

SMALL INTESTINE

BACILLI ENTER PAYERS PATCHES

MULTIPLY RAPIDLY

BILE/ GALBLADDER

CONT..

BILE CANALICULI

CLINICAL MANIFESTATIONS

BACTERAEMIA- TOXEMIA.

HEMOPOITIC SYSTEM, SPLEEN, BONE

MARROW, &ABDOMEN LYMPH NODES,
LUMPHOID TISSUE OF SMALL INTESTINE
INVOLVED

Clinical forms:

Mild infection:
very common seen recently
symptom and signs mild
good general condition
temperature is 380C
short period of diseases
recovery expected in 1~3 weeks
seen in early antibiotics users
young children mild more
easy to misdiagnose

Persistent infection:
diseases continue than 5 weeks

Ambulatory infection:
mild symptoms,early intestinal bleeding
or perforation.

Fulminate infection:
rapid onset, severe toxemia and
septicemia.
High fever,chill,circulation failure,
shock, delirium, coma, myocarditis,
bleeding and other complications, DIC

et all.

Special manifestations

In children

Often atypical
sudden onset with high fever.

Respiratory symptoms and diarrhea, dominant.

Convulsion common in below 3.
relative bradycardia rare.
Splenomegaly, roseola and leucopenia less common.

In the aged

temperature not high, weakness common.

More complications.high mortality.

Recrudescence

clinical manifestations reappear

less severe than initial episode

Its temperature recrudesce when temperature

start to step down but abnormal in the period of

2-3 weeks and persist 5~7 days then back to

normal.

seen in patients with short therapy of antibiotics.

relapse

serum positive of S.typhi after 13 weeks

of temperature down to normal.

Symptom and signs reappear

the bacilli have not been completely

removed

Some cases relapse more than once

Laboratory findings
Routine examinations:

white blood cell count is normal or decreased.

Leukocytopenia(specially eosinophilic
leukocytopenia).
recovery with improvement of diseases

decreased in relapse

Bacteriological examinations:

Blood culture:
the most common use
80~90% positive during the first 2 weeks of illness
50% in 3rd week
not easy in 4th week
re-positive when relapse and recrudesce

attention to the use of antibiotics

The bone marrow culture

the most sensitive test
specially in patients pretreated with antibiotics.

Urine and stool cultures

increase the diagnostic yield
positive less frequently
stool culture better in 3~4 weeks

The duodenal string test to culture bile

useful for the diagnosis of carriers.

Rose spots: Not use routinely

Serological tests(Vidal test):

five types of antigens:
somatic antigen(O),flagella(H) antigen, and paratyphoid fever
flagella(A,B,C) antigen.

Antibody reaction appear during first week

70% positive in 3~4 weeks and can prolong to

several months

in some cases, antibodies appear slowly, or

remain at a low level,

some(10~30%) not appear at all.

"O" agglutinin antibody titer 1:80 and "H"

1:160 or "O" 4 times higher supports a
diagnosis of typhoid fever

"O" rises alone, not "H", early of the

disease.Only "H" positive, but "O" negative, often
nonspecifically elevated by immunization or
previous infections or anamnestic reaction.

Antibody level maybe lower when have used

antibiotics early.

Some cross reaction between group D and

A.

False positive in some infectious diseases.

Some positive in blood culture ,but negative in

vidal test.

'Vi" often useful for carrier (1:40)

molecular biological tests:

DNA probe or polymerase chain reaction
(PCR)

Complications
Intestinal hemorrhage
Commonly appear during the second-third week of
illness
difference between mild and greater bleeding

often caused by unsuitable food, diarrhea et al

serious bleeding in about 2~8%
a sudden drop in temperature rise in pulseand
signs of shock followed by dark or fresh blood in the
stool.

Intestinal perforation:

The more serious .Incidence,1-4%

Commonly appear during 2-3 weeks.

Take place at the lower end of ileum.

Before perforation,abdominal pain or

diarrhea,intestinal bleeding .

When perforation, abdominal pain, sweating, drop in

temperature, and increase in pulse rate, then, rebound
tenderness when press abdomen,
abdomen muscle entasia, reduce or disappear in the
sonant extent of liver, leukocytosis .

Temperature rise .peritonitis appear.

celiac free air under x-ray.

Toxic hepatitis:
common,1-3 weeks
hepatomegaly, ALT elevated
get better with improvement of diseases in 2~3
weeks

Toxic myocarditis.
seen in 2-3 weeks, usually severe toxemia.

Bronchitis, bronchopneumonia.
seen in early stage

Other complications:

toxic encephalopathy.

Hemolytic uremic syndrome.

acute cholecystitis

meningitis

nephritis et al.

Diagnosis

Epidemiology data

Typical symptoms and signs

Laboratory findings.

Differential diagnosis

Viral infections:
such as upper respiratory tract infection.
abrupt onset with fever, headache, leucopenia,
sore throat, cough, coryza.
no rose spots, no enlargement of liver & spleen.
The course of illness no more than 2 wks.

differential diagnosis depends on typical

manifestations and blood culture.

Malaria
history of exposure to malaria.
Paroxysms(often periodic) of sequential
chill,high fever and sweating.
Headache, anorexia, splenomegaly, anemia,

leukopenia
Characteristic parasites in
erythrocytes,identified in thick or thin blood
smears.

Leptospirosis

Endemic area,contacted with urine of mice.

Abrupt fever,chills,severe headache,and myalgias,
especially of the calf muscles.
Leptospires can be isolated from
blood,cerebrospinal fluid.
Special agglutination titers develop after 7 days
and may persist at high levels for many years.

Epidemic Louse-Borne typhus

prodromal of malaise and headache followed by

abrupt chills and fever.

headaches,prostration,persisting high fever.

Maculopapular rash appears on the forth to

seventh days on the trunk and in the axillas,

spreading to the rest of the body but sparing the
face,palms,and soles.

Laboratory confirmation by proteins OX19

agglutination and specific serologic tests.

Tuberculosis

continuous high or low fever,fatigue,weight

loss,night sweats.

Mild cough

pulmonary infiltration on chest radiograph

positive tuberculin skin test reaction(most

cases)

acid-fast bacilli on smear of sputum

sputum culture positive for mycobacterium

tuberculosis.

Septicemia of Gram-negative bacilli

abrupt onset,high fever,symptom of toxemia.

Chill,sweats.

Shock.

Positive of gram-negative bacilli from blood

culture.

Prognosis:

Case fatality 0.51%.

but high in old agesinfantand serious

complications

Have immunity for ever after diseases

About 3% of patients become fecal carriers .

TREATMENT
General treatment

isolation and rest

good nursing care and supportive treatment

close observation T,P,R,BP,abdominal

condition and stool .
suitable diet include easy digested food or
half-liquid food.drink more water

intravenous injection to maintain water and

acid-base and electrolyte balance

Symptomatic treatment:

for high fever:

physical measures firstly

antipyretic drugs such as aspirin should be

administrated with caution

delirium,coma or shock,2-4mg
dexamethasone in addition to antibiotics
reduces mortality.

Etiologic and special treatment

1.Quinolones:
first choice

its highly against S.typhi

penetrate well into macrophages,and achieve high
concentrations in the bowel and bile lumens

Norfloxacin (0.10.2 tidqid/1014 days).

Ofloxacin (0.2 tid 1014days).

ciprofloxacin (0.25 tid)

caution: not in children and pregnant

2.Chloramphenicol:

For cases without multiresistant S.typhi.

Children in dose of 5060mg/kg/per day.

adult 1.52g/day. tid.

Unable to take oral medication, the same dosage

given introvenously

after defervescence reduced to a half. complete a

1014 day course.

But ,drug resistance, a high relapse rate,bone

marrow toxicity.

3.Cephalosporines:
Only third generation effective
Cefoperazone and Ceftazidime.

24g/day .10~14 days.

4.Treatment of complication.

Intestinal bleeding:
bed rest, stop diet,close observation T,P,R,BP.
intravenous saline and blood transfusion,and
attention to acid-base balances.
sometimes,operative.

Perforation:
early diagnosis.

stop diet.
decrease down the stomach pressure.
intravenous injection to maintain electrolyte
and acid-base balances.
use of antibiotics.
sometimes operative.

Toxic myocarditis:

bed rest, cardiac muscle protection drugs,

dexamethasone, digoxin.
5.Chronic carrier:

Ofloxacin 0.2 bid or ciprofloxacin 0.5 bid, 46

weeks.

Ampicillin 36g/day tid plus probenecid 1

1.5g/day. 46 weeks.

TMP+SMZ
2 tabs. Bid. 13 months.

Cholecystitis may require cholecystectomy.

Prophylaxis

1.control source of infection

Isolation and treatment of patients
stool culture one time per 5 days.
if negative continued two times ,without isolation.

Control of carriers.
observation of 25 days(15 days in paratyphoid)
when close contact

2. Cut of course of transmission

key way
avoid drinking untreated water and food.
3.Vaccination
side-effect more, less use

Paratyphoid fever A,B,C

Caused by Salmonella paratyphoid

A,B,C.respectively.

in no way different from typhoid fever in

epidemiology, pathogenesis,
pathology,clinical manifestations,
diagnosis, treatment and
Prophylaxis

Paratyphoid A,B:

incubation period 2~15days, in genaral,8~10 days.

milder in severity

fewer in complications.

Better in prognosis,

relapse more common in Paratyphoid A.

Treatment same as in typhoid fever.

Paratyphoid C:

Always sudden onset.

Rapid rise of temperature.

Presented in different forms-- Septicemia,

Gastroenteritis and Enteric fever

Complications--arthritis, abscess formation,

cholecystitis, pulmonary complications are
commonly seen.

Intestinal hemorrhage and perforation not as

common as in typhoid fever.

RASH ON ABDOMEN

Sore throat

Typhoid fever rash

Petechial rash

Laboratory diagnosis:

Microbiological procedures

Serological procedure

New diagnostic tests

CONTROL OF TYPHOID REVER

control of reservoir
control of sanitation, and
immunization

Typhoid fever prevention.

Prevention of flies

CONTROL OF RESERVOIR.
cases:

Early diagnosis
Notification
Isolation
Treatment
Disinfection
Follow up

Cont..

Carrier:

Identification
Treatment
Survey
Surveillance
Health education

2. CONTROLOF SANITATION

3. IMMUNIZATION

Cont..

It is recommended to
those living in endemic areas
household contacts
groups at risk of infection such as school
children and hospital staff
travelers proceeding to endemic areas,
and
Those attending melas and yatras.

Anti typhoid vaccines

The Vi polysaccharide vaccine

Schedule:- the vaccine licensed for individuals
aged less than or equal 2 years. Only one dose
is required, and the vaccine confers protection 7
days after injection. To maintain protection, revaccination is recommended every 3 years.

The Ty2vaccine

Schedule:- the capsules are licensed for

use in individuals aged more than or
equal to 5 years. The liquid vaccine can
be administered from the age of 2 years.
the Ty 21 a vaccines, including live
vaccines against polio, cholera, and
yellow fever, or the measles, mumps, and
rubella (MMR) combination.

Complications:Endocarditis,
Meningitis,
Pneumonia,
Osteomyelitis,
Intestinal perforation and hemorrhage.
Septicemia,
Parodists,
Cerebral dysfunction.

Immunization.

Prevention of flies

Fluid therapy

Hospitalization

TYPHOID BREAKOUT