typhoid

1. TYPHOID FEVER
AND
PARATYPHOID FEVER
Dr nawin kumarDr nawin kumar

2. Definition of Typhoid fever
• “mesenteric fever“ by BAGLIVI in 1696,
• typhoid fever was given its universal name in
1834.
• Potentially fatal, multi-systemic illness caused
primarily by Salmonella typhi and paratyphi”
• Earlier 100% death rate for the perforations
• Nowadays, 1 to 39%

3. Typhoid---ancient Greek Typhos, smoke
or cloud that was believed to cause disease
or madness

4. 430–426 B.C.
Killed 1/3 of the population of Athens,
including their leader Pericles. The power
shifted from Athens to Sparta. 2006 study
detected DNA sequences
similar salmonella

5. Etiology
Serotype: Dgroup of Salmonella
Gram-negative
rod
non-spore
flagella

6. 1. H(flagellarantigen).
2. O(Somatic orcell wall antigen).
3. Vi (polysaccharide virulence)
• “widel test”
Antigens: located in the cell capsule

7. Georges Fernand Isidor Widal (1862-1929)
Demonstrated specific agglutinins in the blood of Typhoid patient in 1896----
“The Widal Reaction”

8. Susceptibility and immunity
• all people equally susceptible to infection
• immunity is not associated with antibody
level of “H”, “O”and “VI”.
• No cross immunity between typhoid and
paratyphoid.

9. • 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

10. epidemiology
• sporadic occurusually, sometimes have
epidemic outbreaks.

11. Susceptibility and immunity
• All seasons, usually in summerand
autumn.
• Most cases in school-age children and
young adults.
• both sexes equally susceptible.

12. Infects roughly 21.6
million people each year
* International Estimate
Ramsden AE, Mota LJ, Münter S, Shorte SL, Holden DW. The SPI-2 type III secretion system
restricts motility of Salmonella-containing vacuoles. Cell
Kills 200,000 people
each year

13. 62% of these occurring in
Asia and 35% in
Africa
* International Estimate
* Taylor TE, Strickland GT. Malaria. In: Strickland GT, ed. Hunter’s
Tropical Medicine and Emerging Infectious Diseases. 8th ed.
Philadelphia: WB Saunders, 2000:614-43.
Highest in Pakistan & India in Asian
countries
(451.7 per 100,000)

14. •fecal-oral route
•close contact with
patients orcarriers
•contaminated water
and food
•flies and
cockroaches.

15. Best prevention Scrub of them off your handsBest prevention Scrub them off your hands

16. S. typhi are able to survive a
stomach pH as low as 1.5.
Antacids, (H2 blockers), PPI’s,
gastrectomy, facilitate
S typhi infection
TYPHOID FEVER RISK FACTORS

17. ingested orally
→ Stomach barrier(some
Eliminated)
→ enters the small intestine
→Penetrate the mucus layer
→ entermononuclearphagocytes
of ileal peyer's patches and
mesenteric lymph nodes
→ proliferate in mononuclear
phagocytes
spread to blood. initial
bacteremia (Incubation
period).
Pathogenesis

18. Pathogenesis
→ enterspleen, liverand
bone marrow
(reticulo-endothelial
system)
furtherproliferation
occurs "typhoid
nodules“
→ A lot of bacteria enter
blood again.(second
bacteremia).

19. S.Typhi.
stomach
Lower
ileum
peyer's patches &
mesenteric lymph nodes
thoracic
duct
1st bacteremia
(Incubation stage)
10-14d
(mononmonon
uclearuclear
phagocphagoc
ytesytes )
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 eliminated
convalvescence stage
(4-5w)
Enterorrhagia,i
ntestinal
perforation

20. PRESENTATION
Incubation period
is 7-14 days

21. FIRST WEEK TEMPERATURE PATTERN

22. Diffuse abdominal pain,
Inflamed Peyer patches
narrow the lumen--
Constipation.
Dry cough, dull frontal
headache, delirium,
increasingly Stupor &
malaise
FIRST WEEK OTHER SYMPTOMS

23. Rose spots, blanching,
truncal,
maculopapules usually 1-4
cm wide, < 5 in number;
these generally resolve
within 2-5 days
(bacterial emboli to the
dermis)
FIRST WEEK OTHER SYMPTOMS

24. Distended abdomen, Soft splenomegaly,
Relative bradycardia & dicrotic pulse
(double beat, the second beat
weaker than the first)
SECONDWEEK

25. Patient may descend into
the typhoid state---apathy,
confusion, and even psychosis
THIRD WEEK TYPHOID STATE

26. Necrotic Peyer patches, bowel
perforation,
Peritonitis, intestinal
hemorrhage
may cause death
THIRD WEEK Week of complications

27. Fever, mental state,
and abdominal distension slowly improve
over a few days,
complications may still occur
in surviving untreated individuals
FOURTH WEEK WEEK OF CONVALESCENCE

28. Clinical forms:
• Mild infection:
– symptomand signs mild
– good general condition
– temperature is 380
C
– short period of diseases
• Persistent infection:
diseases continue than 5 weeks
• Ambulatory infection:
– mild symptoms,early intestinal bleeding orperforation.
• Fulminate infection:
– rapid onset, severe toxemia and septicemia.
– High fever,chill,circulation failure, shock, delirium, coma,
myocarditis, bleeding and othercomplications, DIC

29. • Recrudescence
• 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 backto
normal.
• seen in patients with short therapy of antibiotics.
• Relapse
• serumpositive of S.typhi after 1～ 3 weeks of temperature down to
normal.
• Symptomand signs reappear

30. Diagnosis
• Epidemiology data
• Typical symptoms and signs
• Laboratory findings.

31. Laboratory findings
Routine examinations:
white blood cell count is normal ordecreased.
Leukocytopenia(specially eosinophilic leukocytopenia).
Blood culture:
80~90% positive during the first 2 weeks of illness
Serological tests (Widal test)
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 betterin 3~4 weeks
The duodenal string test to culture bile useful forthe diagnosis of
carriers.
BASU

32. Serological tests(Vidal test):
five types of antigens:
somatic antigen(O),flagella(H) antigen, and paratyphoid fever
flagella(A,B,C) antigen.
• "O"agglutinin antibody titer ≥1:80 and "H" ≥1:160 or"O" 4
times highersupports a diagnosis of typhoid fever
• "O"rises alone, not "H", early of the disease.
• Only "H"positive, but "O"negative
• nonspecifically elevated by immunization
• previous infections or
• anamnestic reaction.

33. MINORCOMPLICATIONS

34. Bilateral Salmonella typhi breast abscess
unmarried 35-year-old female without any predisposing conditions

35. MEDICALCOMPLICATIONS

36. MAJORSURGICALCOMPLICATIONS

37. Morbidity 55.4%mortality 28.5 %
INTESTINAL PERFORATIONS
5% of people withtyphoid fever experience
this complication
DS00538 April 10, 2008© 1998-2009 Mayo Foundation for Medical Education and
Research (MFMER).
Typhoid enteric perforation, Dr Y. Akgun *, B. Bac, S. Boylu, N. Aban, I.
Tacyildiz, British Journal of Surgery Volume 82 Issue 11, Pages 1512 - 1515
Published Online: 8 Dec 2005

38. Pathology in
ileum
• 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

39. (PEYER’S PATCHES)

40. (TYPHOID NODULE)

41. Majorfindings in lowerileum
• Hyperplasia stage(1st week):
swelling lymphoid tissue and
proliferation of macrophages.
• Necrosis stage(2nd week):
necrosis of swelling lymph nodes or
solitary follicles.

42. Majorfindings in lowerileum
• Ulceration stage(3rd week):
shedding of necrosis tissue and formation
of ulcer----- intestinal hemorrhage,
perforation .
• Stage of healing (from4th week):
healing of ulcer, no cicatrices and no
contraction

43. MECHANISM OF INTESTINAL PERFORATION
Intestinal peyer’s patches

44. Ileum especially distal ileum,jejunum usually doesnot perforate in typhoid,
usually happens in the third week

45. 2 or 3 weeks hx of disease,
with suddenly worsening
of pain & general conditions,
Tenderness starts in his right lower
quadrant, spreads and eventually
becomes generalized, Guarding ,
(seldom the board-like rigidity)
Erect film, shows gas
Under diaphragm (50% positive)
lateral decubitus film, shows gas
under his abdominal wall
PRESENTATINPERFORATION
The bradycardia and leucopenia of
typhoid may occasionally mask the
tachycardia and leucocytosis of
peritonitis

46. PATIENTPERFORATION

47. If peritonitis seems to be localized, signs
confined to only part abdomen, general
condition is good, patient not deteriorating,
consider non-operative treatment.
CONSERVATIVE SURGICALVS
If signs of generalized peritonitis,
do a laparotomy

48. “Suck and drip”
Resuscitation, antibiotics, pass a NG-tube,
Monitor abdominal tenderness, pulse,
temperature, white blood count.
If any of these rise, suspect that peritonitis is
extending, so take an erect
X-ray film of his abdomen
CONSERVATIVE MANAGEMENT

49. MDR-area
MDR+NAR-area
MEDICATION TREATMENT WHO RECOMMENDATIONS

50. Operate as early as possible,
Do as much as necessory & as little as possible
SURGICAL MANAGEMENT
PREPARATION
Adequately resuscitate,
Maintain good urine output, pass
nasogastric tube down,
Start chemotherapy.

51. SurgerySteps

52. SurgerySteps

53. SurgerySteps

54. SurgerySteps

55. INTESTINAL HEMORRHAGE
Occurs in 10-20
per cent of the cases

56. Intestinal bleeding is often marked
by a sudden drop in blood
pressure and shock, followed by
the appearance of blood in stool
Hemorrhagepresentation

57. replace the blood loses.
Bleeding usually stops
spontaneously
Only operate if bleeding is
persistent, or alarmingly
INTESTINAL HEMORRHAGE

58. Surgery Intestinal Hemorrhage

59. Occurs in 1-2% of cases
*According to Indian study 8%
More common in children
Antibiotic resistance & virulence of bacteria
*M.L. Kulkarni, SJ. Rego, Department of Pediatrics, J.J.M. Medical College, Davangere 577 004.
Acute Acalculous CholecystitisTYPHOID

60. Acute Acalculous CholecystitisTYPHOID
*Thickened gall bladder wall,
sonographic Murphy's sign,
pericholicystic collection in the
absence of gall stones
*Subha Rao SD, LewinS, Shetty B, et al. Acute acalculous cholecystitis in typhoid fever. Indian Pediatr 1992, 29: 1431-1435.

61. Chronic Cholecystitis (Carriers)TYPHOID
Excretes bacteria in stools for
more > 1 year1-4% of non-
treated infected patients become
chronic carriers
Patients with cholelithiasis,
biliary anomalies, females,
Salmonella can be cultured from
stools, duodenal aspirate, gall
stones

62. Mary Mallon
(September 23, 1869 – November 11, 1938)
Forcibly quarantined twice, she infected 47 people,
three of whom died. She died in quarantine.

63. Chronic CholecystitisTYPHOI
D
Biliary anomalies, stones--requires
cholecystectomy + antibiotics
4-6 weeks antibiotic treatment

64. MAJORSURGICALCOMPLICATIONS

65. MAJORSURGICALCOMPLICATIONS

66. • Prophylaxis
1.control source of infection
Isolation and treatment of patients
stool culture one time per5 days.
if negative continued two times ,without isolation.
Control of carriers.
observation of 25 days(15 days in paratyphoid) when
close contact

67. 2. Cut of course of transmission
key way
avoid drinking untreated waterand
food.
3.Vaccination
side-effect more, less use

68. Ty21a—Oral live attenuated vaccine

69. Vi-CPS— parenteral vaccine

70. Paratyphoid feverA,B,C
• Caused by Salmonella paratyphoid
A,B,C.respectively.
• in no way different fromtyphoid feverin
epidemiology, pathogenesis,
pathology,clinical manifestations,
diagnosis, treatment and
Prophylaxis

71. Paratyphoid A,B:
• incubation period 2~15days, in genaral,8~10 days.
• milderin severity
• fewerin complications.
• Betterin prognosis,
• relapse more common in Paratyphoid A.
• Treatment same as in typhoid fever.

72. 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.

74. Complications
Intestinal hemorrhage
Commonly appearduring the second-third week of illness
difference between mild and greaterbleeding
often caused by unsuitable food, diarrhea etc
serious bleeding in about 2~8%
a sudden drop in temperature 、 rise in pulse 、 and
signs of shockfollowed by darkorfresh blood in the stool.

75. Intestinal perforation:
• a very severe condition in tropical countries
• incidence ranges from 0.9 to 39% (8),
• mortality rate ranging from 27% to 77%
• the mortality and the morbidity rate depend
– on the general status of the patient,
– the virulence of the germs
– the duration of disease evolution
– Less on the surgical technique,
• adequate pre-operative management
• aggressive resuscitation with antibiotherapy

76. • Rent closure
• Resection anastomosis
– Last 60 centimeters of the ileum -high
concentration of peyer’s patches whose infection
is a source of intestinal perforation
– Digestive fistula - most threatening
– anastomotic leakage- suturing is performed in a
septic environment
– new perforation

77. postoperative complications
• Resection with temporary ileostomy
– avoiding any intestinal suture in septic tissues
– management of stoma
– Peristomal ulceration – awful skin pain –self
limitation of food intake. denutrition, cachexia
and death
• postoperative septic shock

78. Intestinal perforation:
• Commonly appear during 2-3 weeks.
• Take place at the lowerend 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 ordisappearin the sonant extent of liver,
leukocytosis .
• Temperature rise .peritonitis appear.
• celiac free airunderx-ray.

79. • Toxic hepatitis:
common,1-3 weeks
hepatomegaly, ALT elevated
get betterwith improvement of diseases in 2~3
weeks
• Toxic myocarditis.
seen in 2-3 weeks, usually severe toxemia.
• Bronchitis, bronchopneumonia.
seen in early stage

80. Othercomplications:
• toxic encephalopathy.
• Hemolytic uremic syndrome.
• acute cholecystitis 、
• meningitis 、
• nephritis et al.

81. 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 orhalf-
liquid food.drinkmore water
intravenous injection to maintain waterand acid-
base and electrolyte balance

82. • Symptomatic treatment:
forhigh fever:
• physical measures firstly
• antipyretic drugs such as aspirin should be
administrated with caution
• delirium,coma orshock,2-4mg dexamethasone
in addition to antibiotics reduces mortality.

83. 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

84. 2.Chloramphenicol:
• Forcases without multiresistant S.typhi.
• Children in dose of 50～ 60mg/kg/perday.
• adult 1.5～ 2g/day. tid.
• Unable to take oral medication, the same dosage
given introvenously
• afterdefervescence reduced to a half. complete a 10
～ 14 day course.
• But ,drug resistance, a high relapse rate,bone
marrow toxicity.

85. 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.

86. • Perforation:
early diagnosis.
stop diet.
decrease down the stomach pressure.
intravenous injection to maintain electrolyte
and acid-base balances.
use of antibiotics.
sometimes operative.

87. • Toxic myocarditis:
bed rest, cardiac muscle protection drugs,
dexamethasone, digoxin.
5.Chronic carrier:
• Ofloxacin 0.2 bid orciprofloxacin 0.5 bid, 4～ 6
weeks.
• Ampicillin 3～ 6g/day tid plus probenecid 1～
1.5g/day. 4～ 6 weeks.
• TMP+SMZ
2 tabs. Bid. 1～ 3 months.
• Cholecystitis may require cholecystectomy.