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Typhoid/Enteric fever
Enteric fever is a systemic syndrome
produced by a group of certain Salmonella
organisms
Typhoid feverS.Typhi
paratyphoid feverS.paratyphi- A,B or C
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Background: Typhoid fever, also known asenteric fever, is a systemic infection/syndromeby Salmonella typhiorSalmonella paratyphi
A,B,C(less virulent).
Since ancient times, these bacteria have thrivedduring wartime and during the breakdown ofbasic sanitation.
S typhi:developing nations where sanitation is
generally poor. Sporadic outbreaks occur in developed nations,
H/O travel to endemic areas
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Epidemiology
Of all Salmonella serotypes, only S typhi
and S paratyphiare pathogenic
exclusively in humans.
Typhoid fever is potentially fatal if
untreated
Humans are the only natural reservoir , so
direct or indirect contact with an infected
person (sick/carrier) is necessary for inf
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Mode of transmission
1)Ingestion of food or water contaminated with
human excreta/sewage-most common
2)Water borne outbreaks - poor sanitation
3) direct fecal-oral spread - poor personal hygiene
4)Oysters and shellfish cultivated in water (1)
5) International travellers to Asia, Latin America
6)Cong transmission-transplacental or intrapartum
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Pathogenesis
After ingestion the bacilli reach the intestine,passing the gastric barrier.
Attach to the microvilli of the ileal brush border &
invade the intestinal epth thru the peyerspatches
Reach the int lymph nodes,multiply within themononuclear cells
Monocytes unable to destroy the org.in earlystages of the dis.carry them to the mesentericlymph nodes and
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Thru the thoracic duct reach the blood
stream transient bacteremia
Reach the RES and other organs&
proliferate bacteremia recurs
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Pathogenesis
Hyperplasia of the peyers patches with
necrosis &sloughing of the epithelium,
produce ulcers(longitudinal) that may
bleed, but heal without scarring.
The inflammatory lesion may penetrate the
muscularis and the serosa of the intestines
perforation
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Mesenteric lymph nodes, liver, gall bladder(GB)
and spleen are inflammed with focal necrosis.
Local multiplication of the organism in the walls
of GBlarge no. of salmonellaintestines Hyperplasia of the reticuloendothelial tissues
with proliferation of mononuclear cells is the
predominant finding, areas of focal necrosis
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After a period of transient bactremia, the bacilli rseeded in various organs, liver, spleen,gallbladder, & bonemarrow, further multiply
This phase heralds the onset of clinical illness.
Bile serves a good culture media for the org tocontinue multiplying and the gall bladderdischarges large no. of org. into the intestines
Peyers patches and other lymphoid follicles get
inflammed and slough off to form typhoid ulcersand lead to the 2 most dreaded complications ,hemorrhage and perforation
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Salmonellae are grouped based on the somaticO antigen and further divided into serotypesbased on flagellar H and surface virulence (Vi)antigens.
S typhi, the cause of typhoid fever, has O and Hantigens, an envelope (K) antigen, and alipopolysaccharide macromolecular complexcalled endotoxin that forms the outer portion ofthe cell wall.
S typhi, S paratyphi C, and Salmonella Dublinare the only Salmonella serotypes that carry Viantigen
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It is an imp public health problem
Recently it has developed increasing bact
resistance to various antibiotics
Gram negative bacilli,motile and have
flagella.
They possess flagellar antigen H andsomatic antigen O
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Epidemiology: S.typhioccurs only in
humans
Transmission: feco oral route ,thru
contaminatedwater or food
Acutely infected patients excrete bacilli in
their stool or urine for a variable period
5% of the adults become chronic carriers
(resevoir)
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Food handlers and cooks are potent
source of infection
Most of the infected children stop
excreting the bacilli within 2 -3 mths and
rarely become carriers
Epidemics occur : contaminated drinking
water, poor sanitation and personal
hygiene, overcrowding & poverty
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Older children & young adults most
infected ,10% occur in under 5s and 1-2%
below 2yrs of age
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Clinical picture
Incubation period: 7- 14 days, (3-30days)
Clinical manifestations depend on age:
school-age &adolescents:
First week:
Onset is insidious, fever, malaise, anorexia,
myalgia, headache &abd pain over a period of 2
3 days,(more severe in the 2
nd
week)Diarrhea-pea soup consistency initially, later
constipation is prominent
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Temp rises in a step ladder pattern,
becomes unremitting ,high within a week
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Rose spots in 50% cases ,macular or
maculopapular,discreet,erythematous,1-5
mm, blanch on pressure
Appear in crops ,10-15 on the lower chest
and abdomen, last for 2 -3 days,culture of
the lesion positive forS.Typhi
Rhonchi and rales on auscultation
If no complications ,resolve in 2- 4 weeks
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Malaise and lethargy may persist for 1-2
mths
Patient may be emaciated by the end of
the illness
enteric fever by non typhoidal salmonella
is milder
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Infants and young children: RARE, milder,
present as acute gastroenteritis, LRTI, or
VF
Neonates: transmission is vertical. Begins
within 3 days of delivery.vomiting,
diarrhea, and abd distension are
common. temp variable 40.5 C seizures,hepatomegaly, jaundice, wt. loss
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Diagnosis: Culture of the organism is the
basis
1st week: Blood culture
2nd week: Agglutination test
3rd week: Stool culture
4th
week: Urine culture BASU
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LAB FINDINGS:anemia, normochromic,
normocytic blood loss/bonemarrow depression
Leucopenia , never below 2,500
leucocytosis,20,000-25,000(abscess)
Thrombocytopenia
LFT deranged
ProteinuriaPUS &RBCs in stool
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D/D: GE
VF
BRONCHITIS /BP LATER ; SEPTICEMIAS
ANICTERIC HEPATITIS
LEUKEMIAS /LYMPHOMAS
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Treatment
Antibiotic is essential for treating entericfever.
The fluoroquinolones and third generation
cephalosporins are the current mainstay oftherapy.
Ceftriaxone recommended for ped age grp
80mg/kg/day in a single dose
Relapse rate is low and prevents carrierstate
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Quinolones have the adv of dose and costeffective
Probable toxic effect on growing cartilage,
not recommended A short course of steroids improves the
survival rate of patients with shock,
obtundation, stupor/coma. initial dose of dexamethasone 3mg/kg
followed by 1mg/kg 6 hrly for 48 hrs
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Supportive treatment & maintenace of fluid
and electrolytes ,
Surgical intervention
Blood transfusion
Diet
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Complications
Intestinal hemorrhage & perforation after
the first week
Hemorrhage : drop in temp &blood
pressure increase in pulse rate
Perforation : marked increase in abd pain,
tenderness, vomiting& signs of peritonitis.
Pneumonias : superinf
Toxic myocarditis, myogenic shock
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Neurological :increased intracranial
tension, thrombosis, ataxia, chorea,
aphasia, deafness, psychosis& transverse
myelitis. Permanent sequlae are rare.
Osteomyelitis and septic arthritis are more
common in kids with hemoglobinopathies
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Prognosis
Depends on prompt therapy, age, previous
state of health, Salmonella serotype and
the appearance of complications
In developing coutries , mortality rate is
higher 10%.
Relapse known to occur in untreated
cases, (numerous), milder, shorter
duration
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Carriers :
Risk is low in kids and increases with age
Patients who excrete S.typhi@ 3mths orlonger,are excretors @ one yr &defined as
chronic carriers.
Incidence of biliary tract dis is higher.
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Prevention
Improved sanitation & clean water,
essential
Personal hygiene measures,
handwashing,
Attention to food prep practice
Course of 4-6 wks of high dose ampicillin(amoxycillin) plus probenecid or TMX-SMX
Ciproflox in adults, cholecystectomy
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Vaccines:3 types available
Parenteral , inactivated vaccine confers
limited protection(50-75%) ass with side
effects.
Approved for children 6 mths and above
2 doses (0.25ml -6mths-10yrs) &( 0.5ml-
above 10yrs),S/C, 4 weeks apart.
Boosters every 3 yrs necessary
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Oral live vaccine Ty21a strain (80%)
Three capsules given on alternate days,
repeated every 3yrs
Not recommended
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Vi polysacch typhoid vaccine : Vi antigen
is a capsular antigen
Effective after the age of 2 yrs
0.5 ml I/M deltoid area ,booster 2-3 yrs
yrs
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