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TYPHOID FEVER AND
PARATYPHOID FEVER
Dr nawin kumarDr nawin kumar
Typhoid and Paratyphoid
• Definition• Etiology
• Pathogenesis • Epidemiology
• Clinical manifestations
• The laboratory and other examinations
• Complications
• Diagnosis and differential diagnosis
• Prognosis
• Treatment• Preventions• Paratyphoid Fever
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.
• haemorrhage;• perforation;• cholecystitis;• phlebitis;• genitourinary inflammation;• arthritis• osteomyelitis.
Etiology
Serotype: D group of Salmonella Gram-negative rod non-spore flagella Culture characteristics
• Antigens: located in
the cell capsule
H (flagellar
antigen).
O (Somatic or cell
wall antigen).
Vi (polysaccharide
virulence)
“widel test”
• Endotoxin
• A variety of plasmids
• Resistance: Live 2-3 weeks in
water. 1-2 months in stool. Die
out quickly in summer
Resistance to drying and
cooling
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.
Source of infection
Cases and chronic carriersCases discharge from incubation,
more in 2~4 weeks after onset, a
few (about 2~5%) last longer than
3 months
chronic carrier Typhoid Mary
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”, “O”and “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 host-pathogen interactions
• The amount of bacilli infection (>105baeteria).
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
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.
stomach
Lower ileum
peyer's patches &mesenteric lymph nodes
thoracic
duct
1st bacteremia(Incubation stage)
10-14d
(monomononuclenuclear ar phagophagocytescytes )
2nd bacteremia
liver 、 spleen 、 gall 、BM ,ect
early stage&acme stage(1-3W )
LN Proliferate,swell necrosis
defervescence stage
( 3-4w )
Bac. In gall
Bac. In feces
S.Typhi eliminatedconvalvescence stage
(4-5w)
Enterorrhagia,intestinal
perforation
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 Peyer’s patches of the small intestine
(PEYER’S PATCHES)
(TYPHOID NODULE)
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 manifestationsIncubation period: 3 ~ 60 days
(7 ~ 14).The initial period (early stage)• First week. • Insidious onset. • Fever up to 39~400C in 5~7 days
• chills 、 ailment 、 tired 、 sore throat 、 cough ,abdominal discomfort and constipation
The fastigium satge
• second and third weeks.
• Sustained high fever 、 partly remittent fever or irregular fever. Last 10 ~ 14 days.
• Gastro-intestinal symptoms: anorexia 、 abdominal distension or pain 、 diarrhea or constipation
• Neuropsychiatric manifestations: confusion 、 blunt respond even delirium and coma or meningism
• Circulation system:
relative bradycardia or dicrotic pulse.
• splenomegaly 、 hepatomegaly
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
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
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.
• clinical manifestations reappear
• less severe than initial episode
• It’s 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.
Recrudescence
relapse
• serum positive of S.typhi after 1 ~3 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 culturesincrease the diagnostic yieldpositive less frequentlystool 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 hemorrhageCommonly appear during the second-third
week of illness
difference between mild and greater bleeding
often caused by unsuitable food, diarrhea etc
serious bleeding in about 2~8%
a sudden drop in temperature 、 rise in
pulse 、 and 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.
Malariahistory 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 0.5 ~ 1%.
• but high in old ages 、 infant 、 and
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
it’s highly against S.typhi
penetrate well into macrophages,and achieve
high concentrations in the bowel and bile
lumens
• Norfloxacin (0.1 ~ 0.2 tid ~ qid/10 ~ 14 days).
• Ofloxacin (0.2 tid 10 ~ 14days).
• ciprofloxacin (0.25 tid)
caution: not in children and pregnant
2.Chloramphenicol:
• For cases without multiresistant S.typhi.
• Children in dose of 50 ~ 60mg/kg/per day.
• adult 1.5 ~ 2g/day. tid.
• Unable to take oral medication, the same
dosage given introvenously
• after defervescence reduced to a half.
complete a 10 ~ 14 day course.
• But ,drug resistance, a high relapse
rate,bone marrow toxicity.
3.Cephalosporines:
Only third generation effective
Cefoperazone and Ceftazidime.
2 ~ 4g/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, 4 ~6 weeks.
• Ampicillin 3 ~ 6g/day tid plus probenecid 1 ~ 1.5g/day. 4 ~ 6 weeks.
• TMP+SMZ2 tabs. Bid. 1 ~ 3 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.