TYPHOID FEVER AND
PARATYPHOID FEVER
Dr nawin kumarDr nawin kumar
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%
Typhoid---ancient Greek Typhos, smoke or cloud that was
believed to cause disease or madness
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
Etiology
Serotype: D group of Salmonella Gram-negative rod non-spore flagella
1. H (flagellar antigen).
2. O (Somatic or cell wall
antigen).
3. Vi (polysaccharide
virulence)
• “widel test”
Antigens: located in the cell capsule
Georges Fernand Isidor Widal (1862-1929)
Demonstrated specific agglutinins in the blood of Typhoid patient in 1896----
“The Widal Reaction”
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.
• 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
• sporadic occur usually, sometimes have epidemic outbreaks.
Susceptibility and immunity
• All seasons, usually in summer and autumn.
• Most cases in school-age children and young adults.
• both sexes equally susceptible.
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
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)
•fecal-oral route
•close contact
with patients or
carriers
•contaminated
water and food
•flies and
cockroaches.
Best prevention
Scrub of them off your handsBest prevention
Scrub them off your hands
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
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 "typhoid
nodules“
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
PRESENTATION
Incubation period
is 7-14 days
FIRST WEEK TEMPERATURE PATTERN
Diffuse abdominal pain, Inflamed Peyer patches
narrow the lumen--Constipation.
Dry cough, dull frontal headache,
delirium, increasingly Stupor
& malaise
FIRST WEEK OTHER SYMPTOMS
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
Distended abdomen, Soft splenomegaly,
Relative bradycardia & dicrotic pulse
(double beat, the second beat weaker than the first)S
EC
ON
D W
EE
K
Patient may descend into the typhoid state---apathy,
confusion, and even psychosis
THIRD WEEK TYPHOID STATE
Necrotic Peyer patches, bowel perforation,
Peritonitis, intestinal hemorrhage
may cause death
THIRD WEEK Week of complications
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
Clinical forms: • Mild infection:
– symptom and signs mild– good general condition– temperature is 380C
– short period of diseases
• 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
• 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 back to normal.
• seen in patients with short therapy of antibiotics.
• Relapse
• serum positive of S.typhi after 1 ~ 3 weeks of temperature down to normal.
• Symptom and signs reappear
Diagnosis
• Epidemiology data
• Typical symptoms and signs
• Laboratory findings.
Laboratory findingsRoutine examinations:
white blood cell count is normal or decreased.
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 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.
BASU
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 higher supports 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.
MIN
OR
C
OM
PL
ICA
TIO
NS
Bilateral Salmonella typhi breast abscess
unmarried 35-year-old female without any predisposing
conditions
ME
DIC
AL
CO
MP
LIC
AT
ION
S
MA
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Morbidity 55.4%mortality 28.5 %
INTESTINAL PERFORATIONS
5% of people with typhoid 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 - 1515Published Online: 8 Dec 2005
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
(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
MECHANISM OF INTESTINAL PERFORATION
Intestinal peyer’s patches
Ileum especially distal ileum, jejunum usually does not perforate in typhoid,usually happens in the third week
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 PR
ES
EN
TA
TIN
PE
RF
OR
AT
ION
The bradycardia and leucopenia of typhoid may
occasionally mask the tachycardia and leucocytosis
of peritonitis
PA
TIE
NT
PE
RF
OR
AT
ION
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
“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
MDR-area
MDR+NAR-area
MEDICATION TREATMENT WHO RECOMMENDATIONS
Operate as early as possible,
Do as much as necessory & as little as possible
SURGICAL MANAGEMENT
PREPARATIONAdequately resuscitate,
Maintain good urine output, passnasogastric tube down,
Start chemotherapy.
Su
rgery
Ste
ps
Su
rgery
Ste
ps
Su
rgery
Ste
ps
Su
rgery
Ste
ps
INTESTINAL HEMORRHAGE
Occurs in 10-20
per cent of the cases
Intestinal bleeding is often marked
by a sudden drop in blood pressure and shock, followed by the appearance of blood in stoolH
em
orr
hag
e
pre
sen
tati
on
replace the blood loses. Bleeding usually stops
spontaneously
Only operate if bleeding is persistent, or
alarmingly
INTESTINAL HEMORRHAGE
Surgery Intestinal Hemorrhage
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 Cholecystitis
TYPHOID
Acute Acalculous Cholecystitis
TYPHOID
*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.
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
Mary Mallon (September 23, 1869 – November 11, 1938)
Forcibly quarantined twice, she infected 47 people,
three of whom died. She died in quarantine.
Chronic CholecystitisTYPHOID
Biliary anomalies, stones--requires cholecystectomy +
antibiotics4-6 weeks antibiotic treatment
MA
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MA
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• 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
Ty21a—Oral live attenuated vaccine
Vi-CPS— parenteral vaccine
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.
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:
• 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
• 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
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
Intestinal perforation: • 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.
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.
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