thyphoid fever.ppt

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TYPHOID FEVER

ND

P R TYPHOID FEVERGuoli Lin

Department of Infectious Diseases

The Third Affiliated Hospital of SYSU



Typhoid and Paratyphoid

Definition

Etiology

Pathogenesis

Epidemiology

Clinicalmanifestations

The laboratory andother examinations

Complications

Diagnosis anddifferential

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.



Etiology

Serotype: D group of Salmonella

Gram-negativenon-spore

flagella

aerob/fakultatif anaerob



Antigens: located in the cell capsule

H (flagellar antigen) Protein,

termolabil

O (Somatic or cell wall antigen)

lipopolisakarida, termostabil

Vi (polysaccharide virulence)

S.Typhi, S. Paratyphi C



A schematic diagram of a single Salmonella typhi cell

showing the locations of the H (flagellar), 0 (somatic), and

Vi (K envelope) antigens.



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.



• InfeksiSalmonella peroral

Masa Inkubasi10-14 hari

•

GejalaProdromal

Minggu I• Bradi relatif•

Typhoid tounge• Organomegali

Minggu II danselanjutnya

Gang. KesadaranRoseole spot

Demam,anoreksia, mual,

muntah, obstipasi,cefalgia, myalgia



Transmissionfecal-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

(monon

uclear

phagoc

ytes )

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



Pathology

essential lesion:proliferation of RES (reticuloendothelial

system )

specific changes in lymphoid tissuesand mesenteric lymph nodes.

"typhoid nodules“

Most characteristic lesion:

ulceration of mucous in the region of the

Peyer’s patches of the small intestine



回肠：

集淋巴结(PEYER’SPATC

HES)增生



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 nocontraction



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 ailment tired sore throat

cough ,abdominal discomfort and

constipation et al.



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 perforationsevere 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

Cli i l f



Clinical forms:

Mild infection:

very common seen recentlysymptom and signs mild

good general condition

temperature is 380Cshort 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.



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 recrudesceattention to the use of antibiotics



The bone marrow culture

the most sensitive testspecially in patients pretreated with antibiotics.

Urine and stool cultures

increase the diagnostic yieldpositive less frequently

stool culture better in 3~4 weeks

The duodenal string test to culture bileuseful 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 feverflagella(A,B,C) antigen.

Antibody reaction appear during first week

70% positive in 3~4 weeks and can prolong toseveral 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 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 thesonant 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.



DIAGNOSTIK TYPHOID Typhoid Cardinal Sign

Febris continua Bradikardi relatif

Organomegali

Typhoid tounge

Roseole

Konstipasi/diare

Pemeriksaan lab hanya penunjang

Leukopenia Trombositopenia ringan

SGOT/SGPT meningkat

Widal Test + (dapat + pada 6 bulan-1 tahun post typhoid)



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 toseventh 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 oftoxemia.

Chill,sweats.

Shock.

Positive of gram-negative bacilli fromblood 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 fecalcarriers .

TREATMENT



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.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 antibioticsreduces 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:



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 C h l i



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,andattention 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:



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+SMZ

2 tabs. Bid. 1～3 months.

Cholecystitis may require cholecystectomy.

P h l i



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:



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:



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.

thyphoid fever.ppt

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