General characteristic of intestinal infections. Typhoid fever
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Transcript General characteristic of intestinal infections. Typhoid fever
General
characteristic of
intestinal infections.
Typhoid fever,
paratyphoids
A and B
Intestinal infections are
characterized by location of causative
agents in intestine and their
distribution in the environment with
excrement's.
As a microbe is released into
the environment with feces, urine,
vomits (cholera), it can cause
disease in a healthy person only after
ingestion with food or water. In other
words, i.i. are characterized by
faecal-oral mechanism of
transmission.
On a global scale, intestinal infections
are second only to cardiovascular
diseases as a cause of death, they
are the leading cause of childhood
death, and in some populous,
developing areas, they are
responsible for many years of
potential life loss then all other
causes combined. Estimates are that
4.6-6 mln children die each year
(more than 12,600/day) in Asia,
Africa and Latin America and that
over 10,000 die from diarrhea each
year in the USA.
Typhoid fever
Typhoid fever is an acute disease
from the group of intestinal
infections. Characterized by cyclic
course, bacteremia, intoxication,
rash on the skin, lesions of the
lymphatic apparatus of the small
intestine.
Salmonella typhi
Antigens
О
Н
Vi
ІІІ
І
ІІ
1
2
3
Scheme of infection’s transmission:
Source:
1. Patient
2. Carrier
Mechanism of transmission – fecal-oral
Susceptibility – up to 40 – 50 %
Water epidemy characterized by:
1. Sudden beginning
2. Most of the patients were used the
same water-supply
3. Mild forms of disease mainly
4. Fast decreasing of epidemy after
disinfection of water
Food epidemy :
1. Acute or gradual begining after
consuming of contaminated food (milk)
2. Most patients fall ill after consuming of
unboiled milk (family outbreaks) from
the same source
3. Biggest part of sick contigent are
children
4. Severe forms of disease mainly,
because microorganisms replicates in
milk and create massive infectious dose
Phases of pathogenesis:
1. Penetration of the causative agent into the organism
2. Invasion of the small intestine through Peyer’s patches
and multiplication within macrophages
3. Spreading by bacteremia to the reticuloendothelia
system (liver, spleen, bone marrow) where furthe
multiplication occurs
4. Discharging of the agent from the organism (excretory
phase)
5. Re-invasion of the bloodstream and infection of othe
organs including the kidney and Peyer’s patches again
causing apparent relapse in the third week
6. Formation of immunity
A chronic asymptomatic carrier state persist in 1-2 %.
Prodromal period
fever
malaise
anorexia
headache
myalgias
Climax period
Constipation or diarrhea
Respiratory symptoms, including
cough and sore throat
Neuropsychiatries manifestations,
including confusion, dizziness,
seizures
Hepatosplenmegaly
Violation of cardiovascular system
Status typhosus is observed in
serious course of the disease
Rash
1.
2.
3.
4.
Appear on the 7-8th day of disease
Present only in half of the patients
Roseola-like
5.
Appear on the upper abdomen or on the lateral surface of
the body
Roseolas are few (5-15) in number
7.
Sometimes exist longer than a fever
6. Often new elements appear
Specific complications:
1. Intestinal bleeding
2. Intestinal perforation
3. Infectious-toxic shock
Signs of bleeding
1. Increase of pulse rate and decrease of
body temperature - “devil’s cross”
1. Clarification of consciousness
2. Other signs of posthaemorrhagic
anemia
Clinical signs of perforation
1. Mostly weak abdominal pain,
sudden acute pain occur rarely
2. Important symptom of peritonitis –
local tension of abdominal muscles
3. Signs of peritoneal irritation are
weak or absent
Factors, provoking relapses:
1. Violation of diet
2. Advanced cancellation of bed
regime
3. Emotional stress
4. Intercurrent diseases
5. Avitaminosis, immunodeficiency
state etc
Signs preceeding relapses
1.
2.
3.
4.
5.
Subfebrile temperature
Increasing of pulse rate
Presence of rash
Splenomegalia
Aneozynophylia
Clinical peculiarities of paratyphoid A
1. In paratyphoid A incubation period is
shorter than in typhoid fever. It's
duration is 8-10 days.
2. The onset of the disease is an acute.
Sometimes, the onset of the disease is
accompanied by cough, catarrh.
3. Facial hyperemia, blood injection of the
sclera’s vessels, herpes on the lips are
observed during examination.
4. The temperature is wave-like or
remittent. The fever is accompanied by
chills and than by diaphoreses.
Clinical peculiarities of paratyphoid A
5. In paratyphoid A the rash appears more
early than in typhoid fever. The rash is
polymorphic. Roseolas, petechias and
measles-like rash may be observed. The
intoxication is temperate.
6. There is no status typhosus.
7. There is normal quantity of leukocytes in
peripheral blood. But leukocytosis and
lymphocytosis may occur too.
8. In majority of the patients the disease
has a moderate course. The relapses are
frequently
observed
in
case
of
paratyphoid A.
Clinical peculiarities of paratyphoid B
•
•
•
•
•
Paratyphoid B incubation period is 5-10 days.
The onset of the disease is acute, with
expressive chill, myalgia and weakness
At the initial period of the disease the
intoxication may be combined with symptoms
of acute gastroenteritis
The temperature is not prolonged. Status
typhosus is absent in majority of the patients.
The symptoms of intoxication disappears very
quickly
The rash is polymorphic, plenty. It appears at
the earlier period. In some cases the course
of paratyphoid B may be severe with septic
manifestations
Diagnostics
Positive blood culture during first
two weeks
From the third week positive faecal,
bile and urine cultures are obtained
Widal serology test is most helpful in
non-endemic areas
RIHA with erythrocyte diagnostics
(O-, H-, Vi-antigens)
Treatment
1. Etiotropic:
Ciprofloxacin, Ceftriaxone, Ampicillin,
Co-Trimoxazole or Chloramphenicol,
Levomycetin, Bactrim, Azitromicin,
Ofloxacin , Cefotaxim (depending on
sensitivity tests)
Vi – antigen
2. Pathogenetic: diet № 2, bed regime,
desintoxication remedies, inhibitors of
proteases, probiotics, desensibilizing
remedies, vitamins
Treatment of infectious-toxic shock:
Rheopolyglukin
Quartasault (Lactosault)
Dopamine
Prednisolone
Treatment of intestinal bleeding:
Precise bed regime, laying on the back during
24 h
Water-tea diet 10 -12 h
Cooling of abdominal area during first hours
after bleeding detection
Medicinal treatment (Vicasol, Calcium chloride,
blood transfusion, amynobutyrum acid etc)
Ant epidemic measures:
Examination on typhoid fever and
paratyphoids all patient with fever, which
last more than 5 days (once on
hemoculture, and if fever continue more
than 10 days - Widal’s hemaglutination
reaction or RIHA)
Examination of all persons, who are
working at the industried dealing with
food for detection of bacteriocarriers
Obligatory hospitalization of patients and
carriers into infectious hospital
Obzervation of contact
persons during 25 days
and their isolation from
other people
Every day thermometry,
interrogation and medical
examination
One test of feces on
coproculture and blood on
Vi-antigene
Reconvalescents are discharged from
the hospital after clinical recovering
and three-times analysis of feces and
urine with 5-days interval, and bile
after 10 days of disappearing of
clinical signs
three-month observation and 2-years
registration in sanitary-epidemic
department with several times
bacterial examination during a year
Current and final disinfection
Control and prevention
Depends on personal hygiene, safe
food and water, and good sewage
disposal facilities to control endemic
disease.
Carrier detection and treatment help
to control outbreaks, and killed or
live v accine will protect travellers.