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TYPHOID FEVER
4th Medical students-
LIMU
2-5-2019
Dr. Ahmed Elhaddad
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
 Salmonellae are gram-negative bacilli belong
to enterobactereace which cause a spectrum
of characteristic clinical syndromes including.
 gastroenteritis.
 enteric fever.
 Bacteremia.
 Endovascular infections.
 And focal infections such as osteomyelitis or
abscesses.
 Antigens: located in the cell capsule
H (flagellar antigen).
O (Somatic or cell wall antigen).
Vi (polysaccharide virulence)
“widel test”
 Antigenic structure of Salmonella
H( flagella ) antigens
O (somatic) antigens
Vi (Virulence) capsular
polysaccharide antigens
Epidemiology of typhoid fever
Salmonellae are named for the pathologist Salmon,
who first isolated salmonella choleraesuis from
porcine intestine.
Salmonella are effective commensals and pathogens
that cause a spectrum of diseases in humans and
animals
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.
Risk factors
Defects in cellular-mediated immunity (AIDS, Transplant
patients & malignancy).
Defects in phagocytic function .
Altered stomach PH ( patients on anti-ulcer drug).
Prolonged use of antibiotics (altered gut flora).
Injured gut barrier (bowel disease or surgery).
Splenectomy or functional asplenia (sickle cell dis)
Source of infection
Cases and chronic carriers
Cases discharge from incubation, more in
2~4 weeks after onset, a few (about 2~5%)
last longer than 3 months
chronic carrier
Transmission
fecal-oral route
close contact with patients or
carriers
contaminated water and food
flies and cockroaches.
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
Diagnosis
Diagnosis of typhoid fever is made by
 Clinical examination
 Blood, bone marrow, or stool cultures for S.
typhi
 Serological Tests
Clinical manifestations
Incubation 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, tired、sore throat、
cough ,abdominal discomfort and
constipation .
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 .
 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
 Fulminate infection:
rapid onset, severe toxemia and
septicemia.
High fever,chill,circulation failure,
shock, delirium, coma, myocarditis,
bleeding and other complications,
DIC et all.
Laboratory findings
Routine examinations:
white blood cell count is normal or
decreased.
Leukocytopenia(specially eosinophilic
leukocytopenia).
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
 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
 Tube agglutination test.
 five types of antigens:
somatic antigen(O),flagella(H) antigen, and paratyphoid fever
flagella(A,B,C) antigen.
 Detects anti O and H antibodies in serum
 Diagnosis of Typhoid and Paratyphoid cases
 Carriers of typhoid bacilli possess antibody against the
Vi antigen of S. typhi. (Vi tires seem to correlate better
with the carrier state than do O or H titres).
 For this reason, the use of Vi agglutination for
detection of carriers was suggested .
WIDAL Test
Widal test
 Significance
 Ist week negative.
 Titers raise in 2nd week
 Raise of titers is diagnostic
How do you read Widal test results for
typhoid fever?
 The highest dilution of the patients serum in
which agglutinations occurs is noted, ex. if the
dilution is 1 in 160 then the titer is 160.
 Agglutination in dilution up to <1:60 is seen
in normal individuals . Agglutination in dilution
> 1:160 is suggestive of Salmonella infection
Complications
Intestinal hemorrhage
 Commonly appear during the second-third week of
illness
 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.
 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 .
Diagnosis
 Epidemiology data
 Typical symptoms and signs
 Laboratory findings.
Differential diagnosis
 Viral infections
 Malaria
 Leptospirosis
 Septicemia of Gram-negative bacilli
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.
 For delirium,coma or shock,
2-4mg dexamethasone in addition to
antibiotics reduces mortality.
Etiologic and special treatment
Antibiotics
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 (~14 days).
 Ofloxacin (10~14days).
 ciprofloxacin (14 days)).
2. Cephalosporines:
third generation effective(10~14 days).
3. Macrolides
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 or ciprofloxacin 4~6 weeks.
 Ampicillin plus probenecid 4~6 weeks.
 TMP+SMZ
2 tabs. Bid. 1~3 months.
 Cholecystitis may require cholecystectomy.
Nursing care
Isolation & barrier nursing is indicated
Trace source of infection.
Notification of the case to the infection control nurse in
the hospital.
Prevention
Education on hygiene practices like hand washing after
toilet use & avoidance of eating in non hygienic
restaurants.
Antibiotic prophylaxis is not needed for house-hold
contacts.
Proper handling & refrigeration of food even after
cooking.
Salmonella vaccine is available but affectivity is low
(50% protection).
Prognosis
With early diagnosis and prompt treatment most patients
with typhoid fever will recover in due time.
Fever & toxicity subsides within 72 hours of antibiotic
treatment.
Mortality is > 50% in untreated severe typhoid fever
particularly in children & elderly.
Recrudescence is rare but chronic carrier state is
reported in 10% of patients.

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typhoid fever.ppt on presentation on power point

  • 1. TYPHOID FEVER 4th Medical students- LIMU 2-5-2019 Dr. Ahmed Elhaddad
  • 2. 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
  • 3.  Salmonellae are gram-negative bacilli belong to enterobactereace which cause a spectrum of characteristic clinical syndromes including.  gastroenteritis.  enteric fever.  Bacteremia.  Endovascular infections.  And focal infections such as osteomyelitis or abscesses.
  • 4.  Antigens: located in the cell capsule H (flagellar antigen). O (Somatic or cell wall antigen). Vi (polysaccharide virulence) “widel test”
  • 5.  Antigenic structure of Salmonella H( flagella ) antigens O (somatic) antigens Vi (Virulence) capsular polysaccharide antigens
  • 6. Epidemiology of typhoid fever Salmonellae are named for the pathologist Salmon, who first isolated salmonella choleraesuis from porcine intestine. Salmonella are effective commensals and pathogens that cause a spectrum of diseases in humans and animals
  • 7. 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.
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  • 9. Risk factors Defects in cellular-mediated immunity (AIDS, Transplant patients & malignancy). Defects in phagocytic function . Altered stomach PH ( patients on anti-ulcer drug). Prolonged use of antibiotics (altered gut flora). Injured gut barrier (bowel disease or surgery). Splenectomy or functional asplenia (sickle cell dis)
  • 10. Source of infection Cases and chronic carriers Cases discharge from incubation, more in 2~4 weeks after onset, a few (about 2~5%) last longer than 3 months chronic carrier
  • 11. Transmission fecal-oral route close contact with patients or carriers contaminated water and food flies and cockroaches.
  • 12. Susceptibility and immunity  All seasons, usually in summer and autumn.  Most cases in school-age children and young adults.  both sexes equally susceptible.
  • 13. Pathogenesis  gastrointestinal tract host- pathogen interactions  The amount of bacilli infection (>105baeteria).
  • 14. 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
  • 15. Pathogenesis  enter spleen, liver and bone marrow (reticulo-endothelial system) further proliferation occurs  A lot of bacteria enter blood again. (second bacteremia).  Recovery
  • 16. Diagnosis Diagnosis of typhoid fever is made by  Clinical examination  Blood, bone marrow, or stool cultures for S. typhi  Serological Tests
  • 17. Clinical manifestations Incubation 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, tired、sore throat、 cough ,abdominal discomfort and constipation .
  • 18. 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
  • 19.  Circulation system: relative bradycardia .  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.
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  • 22.  Fulminate infection: rapid onset, severe toxemia and septicemia. High fever,chill,circulation failure, shock, delirium, coma, myocarditis, bleeding and other complications, DIC et all.
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  • 24. Laboratory findings Routine examinations: white blood cell count is normal or decreased. Leukocytopenia(specially eosinophilic leukocytopenia).
  • 25. 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
  • 26.  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
  • 27.  Tube agglutination test.  five types of antigens: somatic antigen(O),flagella(H) antigen, and paratyphoid fever flagella(A,B,C) antigen.  Detects anti O and H antibodies in serum  Diagnosis of Typhoid and Paratyphoid cases  Carriers of typhoid bacilli possess antibody against the Vi antigen of S. typhi. (Vi tires seem to correlate better with the carrier state than do O or H titres).  For this reason, the use of Vi agglutination for detection of carriers was suggested . WIDAL Test
  • 28. Widal test  Significance  Ist week negative.  Titers raise in 2nd week  Raise of titers is diagnostic
  • 29. How do you read Widal test results for typhoid fever?  The highest dilution of the patients serum in which agglutinations occurs is noted, ex. if the dilution is 1 in 160 then the titer is 160.  Agglutination in dilution up to <1:60 is seen in normal individuals . Agglutination in dilution > 1:160 is suggestive of Salmonella infection
  • 30. Complications Intestinal hemorrhage  Commonly appear during the second-third week of illness  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.
  • 31.  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
  • 32. Other complications:  toxic encephalopathy.  Hemolytic uremic syndrome.  acute cholecystitis、  meningitis、  nephritis .
  • 33. Diagnosis  Epidemiology data  Typical symptoms and signs  Laboratory findings.
  • 34. Differential diagnosis  Viral infections  Malaria  Leptospirosis  Septicemia of Gram-negative bacilli
  • 35. 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 .
  • 36. 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
  • 37.  Symptomatic treatment: for high fever.  For delirium,coma or shock, 2-4mg dexamethasone in addition to antibiotics reduces mortality.
  • 38. Etiologic and special treatment Antibiotics 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 (~14 days).  Ofloxacin (10~14days).  ciprofloxacin (14 days)).
  • 39. 2. Cephalosporines: third generation effective(10~14 days). 3. Macrolides 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.
  • 40.  Perforation: early diagnosis. stop diet. decrease down the stomach pressure. intravenous injection to maintain electrolyte and acid-base balances. use of antibiotics. sometimes operative.
  • 41.  Toxic myocarditis: bed rest, cardiac muscle protection drugs, dexamethasone, digoxin. 5.Chronic carrier:  Ofloxacin or ciprofloxacin 4~6 weeks.  Ampicillin plus probenecid 4~6 weeks.  TMP+SMZ 2 tabs. Bid. 1~3 months.  Cholecystitis may require cholecystectomy.
  • 42. Nursing care Isolation & barrier nursing is indicated Trace source of infection. Notification of the case to the infection control nurse in the hospital.
  • 43. Prevention Education on hygiene practices like hand washing after toilet use & avoidance of eating in non hygienic restaurants. Antibiotic prophylaxis is not needed for house-hold contacts. Proper handling & refrigeration of food even after cooking. Salmonella vaccine is available but affectivity is low (50% protection).
  • 44. Prognosis With early diagnosis and prompt treatment most patients with typhoid fever will recover in due time. Fever & toxicity subsides within 72 hours of antibiotic treatment. Mortality is > 50% in untreated severe typhoid fever particularly in children & elderly. Recrudescence is rare but chronic carrier state is reported in 10% of patients.