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Department of Infection Diseases

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Title: Department of Infection Diseases


1
  • C h o l e r a
  • Department of Infection Diseases
  • The Third Affiliated Hospital,
  • Sun Yat-sen University
  • Lai Jing

2
DEFINITION
  • Cholera was defined as Class A communi-cable
    diseases in the Law of the peoples Republic of
    China for Prevention and Control of Communicable
    Disease.
  • Its also one of the quarantinable diseases as
    stipulated by the International Health Regulation
    (IHRs) .

3
DEFINITION
  • Cholera is an acute infection of intestinal tract
    caused by Vibrio cholerae.
  • Clinical characteristics a sudden onset of
    severe watery diarrhea and vomiting, which lead
    to dehydration even hypovolemic.
  • Appropriate fluid replacement is the key of
    treatment and greatly reduces mortality.

4
ETIOLOGY Vibrio cholerae
Bacillus curved, facultative anaerobic,
gram-negative
5
motility with a single polar flagellum the
erratic movement
6
ETIOLOGY
  • Culture
  • sensitive to low PH
  • tolerant in alkaline condition
  • alkaline peptone water incubated in stool
    sample or rectal swab greater
    sensitivity
  • Antigenic type
  • flagellar H antigen
  • somatic O antigen

7
ETIOLOGY
  • Classification

  • V. cholerae O1
  • V. cholerae non-O1 V. cholerae
  • ( agglutination in antisera the O1 group
    antigen)
  • V. cholerae O1 biotype classic

  • biotype EL Tor
  • O139 strain agglutinate in O group 139 specific
    antiserum

8
ETIOLOGY
  • Serogroup O1 and O139 strain cause epidemic
  • Virulence Cholera toxin (CT )
  • Resistance
  • sensitive to
  • dryness
  • heat
  • sunlight
  • common disinfectants
  • acid, especially gastric acid

9
ETIOLOGY
  • When conditions in the environment such as
    temperature, salinity and availability of
    nutrients are suitable, V. cholerae can survive
    for years in a free-living cycle without the
    intervention of humans.

10
EPIDEMIOLOGY
  • A disease of antiquity
  • the ancestral home of classic biotype the
    Ganges Delta of India
  • subsequently spread to the world
  • seven global pandemics from 19th century to date
  • the biotype classic the initial six pandemics

11
EPIDEMIOLOGY
  • biotype EL Tor recognized first at the EL Tor
    quarantine station in the Persian Gulf in 1911
  • biotype EL Tor 7th pandemic which began in
    1961
  • V.cholerae O139 first designated in India in
    late 1992

12
The distribution of cholera in the world
13
EPIDEMIOLOGY
  • Sources of infection
  • patients
  • subclinical patients? carriers?
  • Routes of transmission
  • large numbers of vibrios sources from the
    voluminous liquid stools
  • contaminated food

14
EPIDEMIOLOGY
  • Contaminated water (river, seawater, wells, etc)
  • flies as media (contact
  • person to person)
  • the water-borne route

15
EPIDEMIOLOGY
  • Susceptibility of individuals
  • generally susceptible
  • more sensitive
  • individuals with low gastric production
  • persons of blood group O
  • children under 5 years

16
EPIDEMIOLOGY
  • non-sustain immunity from illness
  • naturally acquired immunity
  • V. cholerae O1 does not have cross-protect
    against the O139 strain.

17
EPIDEMIOLOGY
  • Seasonality
  • summer
  • autumn
  • Endemic
  • along the coast or the rivers
  • regions lacking of safe water supplies

18
  • River overflowed the villages and houses.
  • Drinking water was contaminated.
  • Cholera cases occured.

19
peddlers
Most of cholera cases had relation with
contaminated food.
20
The nearest epidemic happened in HaiNan
providence in China.
21
Cholera in Zimbabwe
  • A new large cholera outbreaks have happened in
    Zimbabwe since August 2008.
  • Cholera victims lie in a hospital ward in
    Zimbabwe.

22
  • until the end of January 2009
  • exceed 58, 000 cases reported
  • over 3, 000 people died
  • The number of cholera deaths continues to
    increase each day.

23
  • Cholera is closely linked to
  • inadequate environmental management.
  • lacking of sanitary water
  • people drink contaminated water.

24
  • Recent interruptions to the water supplies,
    together with overcrowding

25
PATHOGENESIS
  • Whether the disease develops or not depends
    on
  • the hosts non-specific immunity (gastric
    acidity )
  • the amount of the bacteria ingested

26
Ingestion of V. cholerae Resistant to gastric
acid Colonize small intestine
Illness occurs when viable organisms reach the
duodenum and jejunum.
27
PATHOGENESIS
  • Active motile vibros penetrate mucous layers and
    attach to the brush border of the intestinal
    epithelium where they secrete cholera toxin (CT ).

28
Cholera toxin binds to intestinal cells
Chloride channels activated
Chloride ion-driven secretion, malabsorption of
sodium ion and water
Release large quantities of electrolytes
bicarbonates
Fluid hypersecretion
Diarrhea
Dehydration
29
PATHOGENESIS
  • Watery stool
  • non-fecal
  • enriched in water, potassium and bicarbonate
  • no plasma protein or formed elements of the blood
  • no cellular damage or inflammation

30
PATHOLOGY
  • The most prominent pathological findings
  • dehydration in heart, liver, skin, etc
  • mild pathological changes in small intestine

31
CINICAL MANIFESTATIONS
  • Incubation several hours 7 days.
  • Clinical course of typical cases three stages
  • Stage of diarrhea and vomiting
  • Stage of dehydration
  • Stage of reaction and convalescence
  • All signs and symptoms drive from the fluid
    losses.

32
CINICAL MANIFESTATIONS
  • Stage of diarrhea and vomiting
  • sudden onset with severe diarrhea and vomiting,
    several times to more than 10 times per day.

33
CINICAL MANIFESTATIONS
  • Fluid loss may be extreme, exceeding 1 liter per
    hour.
  • rice-water stools yellowish and watery or clear
    with flecks of mucus
  • no abdominal pain or tenesmus
  • no fever in general

34
CINICAL MANIFESTATIONS
  • Stage of dehydration
  • acidosis (loss of sodium bicarbonate )
  • muscle cramps
  • circulatory failure and renal failure (
    hypovolumia )
  • dehydration hoarse voice exteme thirst

35
depletion-sunken eyes scaphoid abdomen
poor skin turgor loss of skin elasticity
36
Table 1 Clinical findings according to degree of
dehydration
Finding Mild Dehydration Moderate Dehydration Severe Dehydration
Loss of fluid lt5 510 gt10
Mentation Alert Restless Drowsy or comatose
Radial pulse rate Normal Rapid Very rapid
Stystolic blood pressure Normal Low Very low
Skin elasticity Retracts rapidly Retracts slowly Retracts very slowly
Eyes Normal Sunken Very sunken
Urine prouduction Normal Scant oliguria
37
CINICAL MANIFESTATIONS
  • Stage of reaction and convalescence
  • recover from the disease if dehydration corrected
    promptly.
  • pyretic reaction

38
CINICAL MANIFESTATIONS
  • In rare instances cholera sicca shock and
    death occur before diarrhea appears.

39
COMPLICATIONS
  • Acute renal failure
  • Acute pulmonary edema

40
DIAGNOSIS
  • Tentative diagnosis clinical manifestations and
    epidemiologic data
  • Patient develops or dies from severe watery
    diarrhea and dehydration in an area where cholera
    is not endemic.
  • Patient develops acute watery diarrhea in an area
    where there is an epidemic or cholera is endemic.
  • Definitive diagnosis the isolation of the
    V.cholerae from stool, vomit or rectal swab

41
DIFFERENTIAL DIAGNOSIS
  • Bacterial food poisonings
  • Gastroenteritis
  • enterotoxigenic E. coli
  • enteropathogenic E. coli
  • shigellosis

42
LABORATORY FINDINGS
  • Stool examinations
  • stool routine test mucus and WBC
  • dark-field microscopic examination darting
    motility of vibrios in fresh wet preparations

43
LABORATORY FINDINGS
  • stool hanging drop examinations and motility
    inhibition test
  • The bacteria can be discerned by immobilization
    with its serotype antiserum.
  • culturealkaline peptone water or
    thiosulfate-citrate-bile salt-sucrose (TCBS) agar

44
Opaque flat yellow colonies form on TCBS agar in
18 hours at 37?.
45
LABORATORY FINDINGS
  • Blood examinations
  • increased RBC, hemoglobin and WBC
  • normal or decreased serum sodium, serum
    potassium, increased BUN
  • decreased CO2CP
  • Urine test RBC, WBC, albumin, casts.

46
LABORATORY FINDINGS
  • Specific antibody in immobilization test
    epidemiological studies
  • Several other methods
  • latex agglutination
  • enzyme immunoassay
  • polymerase chain reaction (PCR)

47
TREATMENT
  • Isolation
  • 6 days after the symptoms disappear
  • before 3 negative stools cultures taken once
    every other day

48
TREATMENT
  • Fluid replacement
  • The goal restore the fluid losses
  • start as soon as diarrhea begins
  • two phases rehydration phase maintenance phase
  • two routes intravenous fluids, oral fluids

49
TREATMENT
  • Intravenous fluids
  • severe or moderate cases
  • or in shock
  • the main principles early, rapid and enough
  • infuse of salt solution according to the
    reaction to the treatment
  • correct of the metabolic acidosis
  • give potassium if patients without oliguria

50
Table 2 The volume of intravenous fluids in first
24 hours
Volume of infusion Mild Dehydration Moderate Dehydration Severe Dehydration
adult(ml) 30004000 40008000 800012000
child(ml/kg) 120150 150200 200250
salt solution(ml/kg) 6080 80100 100120
(5 4 1 solution NaCl 5g, NaHCO3 4g, KCl 1g and
50 GS 20 ml in per liter of water. )
51
TREATMENT
  • Oral fluids
  • mild cases
  • severe cases in
  • which the patients condition has improved after
    giving intravenous fluids

52
TREATMENT
  • Oral rehydration solution (ORS)
  • NaCl 3.5, NaHCO3 2.5, KCl 1.5 and GS 20 in
    grams per liter of water per liter water
  • The volume in the initial 6 hours adult 750ml/h
    child 1520ml/kg
  • The total volume is decided as the degree of
    dehydration and ongoing fluid loss.

53
TREATMENT
  • Antibiotics
  • reduce the duration of diarrhea
  • decrease excretion of the V. cholerae
  • norfloxacin, doxycycline, berberine or SMZ-TMP
  • Treatment of complications
  • acute renal failure
  • acute pulmonary edema

54
PREVENTION
  • Control of sources of infection
  • The diarrhea clinic need be established.
  • Case must be reported to CDC within 6 hours in
    towns or within 12 hours in villages.
  • all patients strictly isolated in wards

55
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56
PROGNOSIS
  • Without treatment, mortality approaches 60 per
    cent of those affected.
  • Management
  • The clinical type

57
PROGNOSIS
  • The mortality is always in greater among
  • the aged and young children
  • the intemperate and those poorly nourished
  • treatment is not vigorous in the early stage of
    the disease

58
PREVENTION
  • close contacts
  • medical surveillance for 5 days
  • take SMZ-TMP or norfloxacin for 2 days
  • all carriers
  • detection and treatment

59
PREVENTION
  • Interruption of the routes of transmission
  • correct the water supply and sewage system as a
    matter of urgency

60
PREVENTION
  • provision of facilities for sanitary disposal of
    human waste
  • education on good personal hygiene
  • a wide variety of disinfectants are effective
    bleaching power, soap
  • adhering to proper food safety practices

61
PREVENTION
  • Increase the immunity of individuals
  • Vaccination different vaccine strains
  • Once an outbreak has started, WHO does not
    recommend oral cholera vaccine or parenteral
    cholera vaccine.
  • The vaccines limited efficacy is at least
    partially due to its failure to induce a local
    immune response at the intestinal mucosal surface.

62
  • Thank you !
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