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General characteristic of intestinal infections. Typhoid fever, paratyphoids A and B

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Title: General characteristic of intestinal infections. Typhoid fever, paratyphoids A and B


1
General characteristic of intestinal infections.
Typhoid fever, paratyphoids A and B
2
  • 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.

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  • 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.

5
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.

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Salmonella typhi
  • Antigens

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Vi
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Scheme of infections transmission
  • Source
  • Patient
  • Carrier
  • Mechanism of transmission fecal-oral
  • Susceptibility up to 40 50

8
  • Water epidemy characterized by
  • Sudden beginning
  • Most of the patients were used the same
    water-supply
  • Mild forms of disease mainly
  • Fast decreasing of epidemy after disinfection of
    water

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  • Food epidemy
  • Acute or gradual begining after consuming of
    contaminated food (milk)
  • Most patients fall ill after consuming of
    unboiled milk (family outbreaks) from the same
    source
  • Biggest part of sick contigent are children
  • Severe forms of disease mainly, because
    microorganisms replicates in milk and create
    massive infectious dose

10
Phases of pathogenesis
  • 1. Penetration of the causative agent into the
    organism
  • 2. Invasion of the small intestine through
    Peyers patches, and multiplication within
    macrophages
  • 3. Spreading by bacteremia to the
    reticuloendothelial system (liver, spleen, bone
    marrow) where further multiplication occurs
  • 4. Discharging of the agent from the organism
    (excretory phase)
  • 5. Re-invasion of the bloodstream and infection
    of other organs including the kidney and Peyers
    patches again, causing apparent relapse in the
    third week
  • 6. Formation of immunity
  • A chronic asymptomatic carrier state persist
    in 1-2 .

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Prodromal period
  • fever
  • malaise
  • anorexia
  • headache
  • myalgias

14
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

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Rash
  1. Appear on the 7-8th day of disease
  2. Present only in half of the patients
  3. Roseola-like
  4. Appear on the upper abdomen or on the lateral
    surface of the body
  5. Roseolas are few (5-15) in number
  6. Often new elements appear
  7. Sometimes exist longer than a fever

17
Specific complications
  1. Intestinal bleeding
  2. Intestinal perforation
  3. Infectious-toxic shock

18
Signs of bleeding
  • Increase of pulse rate and decrease of body
    temperature - devils cross
  • Clarification of consciousness
  • Other signs of posthaemorrhagic anemia

19
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

20
Factors, provoking relapses
  1. Violation of diet
  2. Advanced cancellation of bed regime
  3. Emotional stress
  4. Intercurrent diseases
  5. Avitaminosis, immunodeficiency state etc

21
Signs preceeding relapses
  1. Subfebrile temperature
  2. Increasing of pulse rate
  3. Presence of rash
  4. Splenomegalia
  5. Aneozynophylia

22
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 scleras
    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.

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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.

24
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

25
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)

26
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

27
  • 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)

28
  • 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 - Widals 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

29
  • 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

30
  • 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

31
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.

32
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