Bordetella and vibrio cholerae

1. 1
Bordetella and Vibrio cholerae
Bordetella pertussis Basics
 Aerobic, Gram negative coccobacillus
 Alcaligenaceae Family
 Specific to Humans
 Colonizes the respiratory tract
 Whooping Cough (Pertussis)
Transmission
 Very Contagious
 Transmission occurs via respiratory droplets
Human Disease & Associated Pathogens
Epidemiology of Bordetella pertussis Infection
 Man is only natural host; obligate parasites of man
 Disease is highly communicable (highly infectious)
 Person-to-person spread via inhalation of infectious aerosols
 Incidence in U.S.A. significantly reduced with required DPT vaccine;
Clinical Progression ofPertussis
Genus Species Disease
Bordetella pertussis Pertussis
Parapertussis Pertussis (milder form)
bronchiseptica Bronchopulmonary disease
Duration 7 – 10 Days 1 – 2c Weeks 2 – 4 Weeks 3–4 Weeks or longer
Symptoms None
Rhinorrhea,
malaise, fever,
sneezing,
anorexia
Repetitive
cough with
whoops,
vomiting,
leukocytosis
Diminished
paroxysmal cough,
development of
secondary
complication (
pneumonia, seizures,
encephalopathy)
Bacterial culture

2. 2
Virulence Factors Associated with Bordetella pertussis
Adhesions
 Filamentous - hemagglutinin
 Pertactin
 Fimbriae
Toxins
 Pertussis Toxin
 Adenylate Cyclase Toxin
 Trachealcytotoxin
 Dermonecrotic toxin
 Heat-labile toxin
Pertussis Toxin
Pertussis toxin (PTX) has a wide range of activities, including inhibition of chemotactic and phagocytic
abilities of leukocytes.
Adenylate Cyclase Toxin
 Invasive toxin
 During the initial stage of infection, B. pertussis releases an invasive adenylate cyclase toxin
(CYA) that impairs the bactericidal effects of immune effector cells by increasing the levels of
cAMP intracellularly.
 This impairment leads to an absence of fever in the host as well as a lack of adequate neutrophilic
response and high incidence of secondary bacterial pneumonia
Tracheal cytotoxin (TCT)
Trachealcytotoxin (TCT) is a disaccharide tetrapeptide that is derived from the cell wall. This toxin has
been observed to cause paralysis of the cilia and extrusion of ciliated cells.
Dermonectoric Toxin
Dermonectoric toxin is a heat stable toxin that induces inflammation, vasoconstriction, and dermonecrotic
lesions around colonies of B. pertussis in the respiratory tract .

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Heat-labile Toxin
Heat-labile toxin may also be involved in tissue damage during infection .
Virulence Factors Associated with Bordetella pertussis
Laboratory Culture, Prevention & Treatment of Bordetella
 Nonmotile
 Fastidious and slow-growing
 Requires nicotinamide and charcoal, starch,blood, or albumin to absorb toxic substances
 Requires prolonged growth
 Isolated on modified Bordet-Gengou agar
 Inactivated whole bacterial cells and toxoid are prepared in formalin for inclusion in DPT vaccine
 Subunit (acellular) vaccine also available
 Treatment with erythromycin, Azithromycin and clarithromycin
Differential Characteristics of Bordetella Species

4. 4
Vibrio cholerae
General Characteristics ofVibrio
 Similarities to Enterobacteriaceae
 Gram-negative
 Facultative anaerobes
 Fermentative bacilli
 Differences from Enterobacteriaceae
 Polar flagella
 Oxidase positive
Vibrio spp. (Family Vibrionaceae) Associated with Human Disease
Morphology & Physiology ofVibrio
 Comma-shaped (vibrioid) bacilli
 V. cholerae,V. parahaemolyticus,V. vulnificus are most significant human pathogens
 Broad temperature & pH range for growth on media
 18-37C
 pH 7.0 - 9.0 (useful for enrichment)
 Grow on variety of simple media including:
 MacConkey’s agar
 TCBS (Thiosulfate Citrate Bile salts Sucrose) agar
 V. cholerae grow without salt
 Most other vibrios are halophilic

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Vibrio spp. (Family Vibrionaceae) Associated with Human Disease
Epidemiology of Vibriospp.
 Vibrio spp. (including V. cholerae)grow in estuarine and marine environments worldwide
 All Vibrio spp. can survive and replicate in contaminated waters with increased salinity and at
temperatures of 10-30o
C
 Pathogenic Vibrio spp. appear to form symbiotic (?) associations with chitinous shellfish which
serve as an important and only recently recognized reservoir
 Asymptomatically infected humans also serve as an important reservoir in regions where cholera
is endemic
Taxonomy of Vibrio cholerae
 >200 serogroups based on somatic O-antigen
 O1 and O139 serogroups are responsible for classic epidemic cholera
 O1 serogroup subdivided into
 Two biotypes: El Tor and classical (or cholerae)
 Three serotypes: ogawa, inaba, hikojima
 Some O1 strains do not produce cholera enterotoxin (atypical or nontoxigenic O1 V. cholerae)
 Other strains are identical to O1 strains but do not agglutinate in O1 antiserum (non-cholera
(NCV) or non-agglutinating(NAG) vibrios) (non-O1 V.cholerae)
 Several phage types
Difference between El Tor & classical Vibrio cholerae
TEST CLASSICAL CHOLERA ELTOR CHOLERA
Haemolysis Negative Positive
Voges-Proskauer Negative Positive
Chick erythrocyte agglutination Negative Positive
Polymyxin B sensitivity Positive Negative
Group 4 Phage susceptibility Positive Negative
El Tor Phage 5 susceptibility Negative Positive

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Pathogenesis ofV.cholerae
 Incubation period: 2-3 days
 High infectious dose: >108
CFU
 103 -
105
CFU with achlorhydria or hypochlorhydria (lack of or reduced stomach acid)
 Abrupt onset of vomiting and life-threatening watery diarrhea (15-20 liters/day)
 As more fluid is lost, feces-streaked stoolchanges to rice-water stools:
 Colorless
 Odorless
 No protein
 Speckled with mucus
 Cholera toxin leads to profuse loss of fluids and electrolytes (sodium, potassium, bicarbonate)
 Hypokalemia (low levels of K in blood)
 Cardiac arrhythmia and renal failure
 Cholera toxin blocks uptake of sodium & chloride from lumen of small intestine
 Death attributable to:
 Hypovolemic shock (due to abnormally low volume of circulating fluid (plasma) in the
body)
 Metabolic acidosis (pH shifts toward acid side due to loss of bicarbonate buffering
capacity)
Virulence Factors Associated with Vibrio cholerae O1 and O139

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Cholera Toxin (A2-5B) (Vibrio cholerae)
 B-subunit binds to GM1 ganglioside receptors in small intestine
 Reduction of disulfide bond in A-subunit activates activates adenyl cyclase leading to an
increased cyclic AMP (cAMP) leveland hypersecretion of fluids and electrolytes
Mechanism ofAction ofCholera Toxin
Treatment & Prevention of V. cholerae
 Untreated: 60% fatality
 Treated: <1% fatality
 Rehydration & supportive therapy
 Oral
 Sodium chloride (3.5 g/L)
 Potassium chloride (1.5 g/L)
 Rice flour (30-80g/L)
 Trisodium citrate (2.9 g/L)
 Intravenous (IV)
 Doxycycline or tetracycline (Tet resistance may be developing) of secondary value
 Water purification, sanitation & sewage treatment
 Vaccines
Prepared by: AmjadKhan Afridi 15th
April, 2017