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									Campylobacter
    Campylobacter

Among the most widespread cause of
infection in the world.
Cause both diarrheal and systemic
diseases
Campylobacter jejuni
      Typical Organisms
Gram-negative rods
with comma, S, or
“gull-wing” shapes.
Motive, with a single
polar flagellum
No spore & no
capsule
           Culture
An atmosphere with reduced O2 (5% O2)
with added CO2 (10% CO2)
At 42 ℃ (for selection)
Several selective media can be used
(eg, Skirrow’s medium)
Two types of colonies:
 watery and spreading
 round and convex
     Virulence Factor
Lipopolysaccharides (LPS) with
endotoxic activity
Cytopathic extracellular toxins and
enterotoxins have been found
         Pathogenesis
The infection by oral route from food, drink, or
contact with infected animals or animal
products(Milk, meat products ).
Susceptible to gastric acid (about 104
organisums)
Multiply in the small intestine   invade the
epithium      produce inflammation      cause
bloody stools
Occasionally, the bloodstream is invaded
    Campylobacter - symptoms
• Incubation: 4-8d
• Acute enteritis: 1w,         • diarrhea
  stools remain positive for   • malaise
  3w                           • fever
• Acute colitis                • abdominal pain
• Acute abdominal pain         • usually self-limiting
• Bacteremia: <1% C.           • antibiotics
  jejuni                       occassionally
• Septic abortion              • bacteremia
• Reactive arthritis              –small minority
Diagnostic Laboratory
       Tests
Specimens: Diarrheal stools
Smears: Gram-stained smears of stool
may show the typical “gull-shaped” rods.
Culture: (have been described above)
            Control
The source of infection may be food (eg,
milk, under-cooked fowl) or contract
with infected animals or humans and
their excreta.
         Helicobacter pylori
Curved bacilli –
Former name - Campylobacter pylori,
   H.   pylori
   Helicobacter pylori
Helicobacter pylori is the prototype
organism in this group. It is associated
with antral gastritis, gastric ulcers, and
gastric carcinoma.
Microbiology
 Gram negative rod, curved,
 Very Motile  corkscrew motion
 Microaerophilic, use amino acids and fatty
acids rather than carbohydrates to obtain energy
needs 10% CO2 and 5% O2
 Urease production
 Catalase production
 Oxidase positive
 Growth at 370C, not 250C or 420C
    Virulence factors

vacA (vacuolationg associated)
cytotoxin, Pathogenicity island: cag,
cytotoxin associated gene A+genes
related to bacterial secretion
Cag+ HP is much more associated
with peptic ulcer disease than Cag(--)
HP.
Pathogenesis

  Motility – it moves into the mucus
and produces adhesins on
gastric epithelial cells
(not intestinal epithelial cells)
  Urease production, breaks down
the urea to ammonia which buffers
the pH around the bacterium.
  Persists, escape defense
mechanisms – SOD, catalase,
Urease. Breack down free radicals
        Pathogenesis
H pylori invade the epithelial cell surface
to a certain degree
Toxins and LPS may damage the
mucosal cells
NH3 produced by the urease activity
may also damage the cells
Epidemiology
       Epidemiology
Prevalence related to socioeconomic level during
childhood.
Infection occurs in childhood, persists for
decades
Prevalence among adults – 20%-100%
Source – stomach of humans
Mode of transmission? Fecal-oral? Oral-oral?
Vomiting and aerosols ?
Incidence of HP colonization is declining in
developed countries
       Epidemiology
Under age 30        <20%
At age 60           40-60%
In developing countries      >80% in
adults
Acute epidemics of gastritis suggest a
common source for H pylori.
        Clinical features
  Acute acquisition - nausea, vomiting, abdominal pain
  last for 1w, later – gastritis.
  Persistent colonization - after acquisition,
  persist for years. Asymptomatic.
  Duodenal ulcer
- more than 90% with DU - carry HP.
- antimicrobial therapy response, eradication of
  HP - less recurrences
Gastric ulcer - 50-80% HP
Gastric carcinoma -HP induces gastritis,
gastritis is risk factor for Carcinoma.
Gastric lymphoma - MALToma: mucosa
associated lymphoid tumors, strong
association with HP. Stage 1 is cured by
antibiotics.
Esophageal diseases - HP protects
against: gastroesophageal reflux,
Barrette's esophagus and carcinoma of
esophagus.
          Immunity
An IgM antibody response to he
infection is developed
Subsequently, IgG and IgA are
produced
  Laboratory diagnosis
  Endoscopy and biopsy.
  Urease detection
  Culture
  Urea breath test - samples of breath air are
collected by having the patient blow into a
tube before and 30 min after ingestion of 13C-
labeled urea, rapid, noninvasive, for
assessing response 4-8w post therapy,
expensive but non invasive!!
  Serology
Principles of therapy
 Combination chemotherapy
  Some drugs are effective in vitro, not in
 vivo - due to acidic pH - erythromycin
  Resistance - not to bismuth salts or
 tetracyclines, 10-30% to metronidazole,
  Response - 1 month after cessation of
 therapy for breath test or biopsy, 6 month
 for serology
Principles of therapy
Triple therapy:
Bismuth+metronidazole+amoxicillin:
eradication 60-90%, tetracyclines, macrolides
- clarithromycin
PPI proton pump inhibitors therapy:
omeprazolone lansoprazole: inhibit HP,
urease, acid
PPI+amoxicillin+clarithromycin or
metronidazole
PPI+ Bismuth+metronidazole+amoxicillin-
very effective
PSEUDOMONAS
  假单孢菌属
Common Characteristics

   Gram-negative
   Motile
   Aerobic rod
   Some produce water-soluble
   pigments
   Widely in soil, water, plants and
   animals
   More than 200 (up to now)
         Some of the medically important
                       pseudomonas
 rRNA Homology Group
    and Subgroup                 Genus and Species
I. Fluorescent Group      Pseudomonas   aeruginosa
                          Pseudomonas   fluorescens
                          Pseudomonas   putida
     Nonfluorescent Group Pseudomonas   stutzeri
                          Pseudomonas   mendocina
II.                      Burkholderia pseudomallei
                         Burkholderia mallei
                         Burkholderia cepacia
                         Ralstonia pickettii
III.                     Comamonas species
                         Acidovorax species
IV.                      Brevundimonas species
V.                       Stenotrophomonas maltophilia
Pseudomonas aeruginosa
    Pseudomonas aeruginosa


Widely distributed in nature
Frequently present in small numbers in the normal
intestinal flora and on the skin
Commonly present in moist environments in
hospitals
It is primarily a nosocomial pathogen
     Typical Organisms

Gram-negative rod ----
0.6×2 μm
Unipolar flagellum (1~3) -
--- actively mobile
Occurs as single bacteria,
in pairs, and occasionally
in short chain
Capsule
Pili in strains obtained
from clinical specimens
   Culture
Grow readily on many
types of culture media
Smooth and round colonies
Multiple colony types in one culture
Fluorescent greenish color
Sometimes produce a sweet or grape-
like or corn taco-like odor
     Culture

Obligate aerobic
Grow well at 37~42℃and no growth at 4℃
Produce water-soluble pigments
Pyocyanin; Pyoverdin; Pyorubin; Pyomelanin
Produce hemolysin
Oxidase-positive
Ferment glucose but not other carbohydrates
Virulence Determinants
    Virulence Determinants

Adhesins   fimbriae (N-methyl-phenylalanine pili)
           polysaccharide capsule (glycocalyx)
           alginate slime (biofilm)
Invasins   elastase
           alkaline protease
           hemolysins (phospholipase and lecithinase)
           cytotoxin (leukocidin)
           siderophores and siderophore uptake systems
           pyocyanin diffusible pigment
   Virulence Determinants
Motility/chemotaxis    Flagella
Toxins                 Exoenzyme S
                       Exotoxin A
                       Lipopolysaccharide
Antiphagocytic surface properties
                       Capsules, slime layers
                       LPS
Defense against serum bactericidal reaction
                       Slime layers,capsules
                       LPS
                       Protease enzymes
     Virulence Determinants
Defense against immune responses
       Capsules, slime layers
       Protease enzymes
Genetic attributes
       Genetic exchange by transduction and conjugation
       Inherent (natural) drug resistance
       R factors and drug resistance plasmids
Ecologic criteria
      Adaptability to minimal nutritional requirements
      Metabolic diversity
      Widespread occurrence in a variety of habitats
Inhibition of protein synthesis
in susceptible cells ----Toxin A




  The resultant ADP-ribosyl-EF-2 complex is
  inactive in protein synthesis.
  This intracellular mechanism of action of
  toxin A is identical to that of diphtheria toxin
  fragment A .
Diverse sites of infection by
        P aeruginosa
    Disease caused by
Pseudomonas aeruginosa
Endocarditis
Respiratory infections
Bacteremia
Central Nervous System infections
Ear infections including external otitis
Eye infections
Bone and joint infections
Urinary tract infections
Gastrointestinal infections
Skin and soft tissue infections, including
wound infections, pyoderma and dermatitis
  Who are at risk?

People with cystic fibrosis
Burn victims
Individuals with cancer
Patients requiring extensive stays in
intensive care units
             Diagnosis
Isolation and laboratory identification.
      blood agar plates
      eosin-methylthionine blue agar.
Gram morphology,
Inability to ferment lactose
Positive oxidase reaction
Fruity odor
Ability to grow at 4 2 ℃
Fluorescence under ultraviolet radiation helps
in early identification of P aeruginosa colonies
and also is useful in suggesting its presence in
wounds.
   Control and Treatment
The spread of Pseudomonas is best controlled
by cleaning and disinfecting medical equipment.
In burn patients, topical therapy of the burn with
antimicrobial agents such as silver sulfadiazine,
coupled with surgical debridement, has
markedly reduced sepsis.
Susceptibility testing is essential.
The combination of gentamicin and carbenicillin
can be very effective in patients with acute P
aeruginosa infections.
               Review
General characteristics: Gram negative rod,
unipolar flagellum, actively motile; produce
diffusible pigments -- pyocyanin,gluorescin and
pyorubin; aerobic, produce hemolysin.
Pathogenicity: cause suppurative infections in
burn, trauma, etc.
   Endotoxin: main pathogenic substance
   Exotoxin A
   Extracellular enzymes:phospholipase,
proteinase, etc.
Bacteriological diagnosis:
   Specimens
   Culture and identification
   Unusual bacteria
Haemophilus influenzae
Common Characteristics

Small, gram-negative
Pleomorphic
Require enrich media (usually
containing blood for isolation)
No flagellum, no spore
Divided into 17 species according to
different requirement to X and V factor
 Haemophilus
Small Gram-negative
coccobacilli, facultative
anaerobes, non motile
often resemble cocci, eg
pneumococci,
most non-encapsulated strains --
- virulent forms encapsulated
fastidious (require blood
factors)
X factor = hematin
V factor = NAD
Organisms: H. influenzae: H.
ducreyi --( soft chancre); H.
aegypticus -- (purulent
conjunctivitis)
Characteristics and growth requirements
     of some haemophilus species
                             Requires
         Species              X    V    Hemolysis
H influenzae (H aegyptius)    +    +        -
H parainfluenzae              -    +        -
H ducreyi                     +    -        -
H haemolyticus                +    +        +
H parahaemolyticus            -    +        +
H aphrophilus                 -    -        -

  X=heme; V=nicotinamide-adenine dinucleotide
Haemophilus influenzae
Present in the nasopharynx of approximately
75 percent of healthy children and adults
(non encapsulated strains as the normal flora)
Rarely encountered in the oral cavity
Has not been detected in any other animal
species
6 types(a-f) according to capsular
polysaccharide type in the encapsulated
strains
H. influenzae type b (Hib) encapsulated
strain is the most common cause of
meningitis in children between the ages of 6
   Biological Characteristics
 ----Morphology of organism
In specimens of acute infections:
          short (1.5μm) coccoid bacilli
          sometimes in pairs or short chain
In culture:
          At 6~8 h on rich medium: small coccoid
bacilli
     Later: longer rods, lysed bacteria,
pleomorphic
Biological Characteristics
      ---- Colonies
On brain-heart infusion agar with blood:
         Small, round, convex, iridescence
(24h)
On chocolate agar:
         Takes 36~48h to develop 1mm
colony
Satellite phenomenon
Not hemolytic
                              satellite phenomenon
  Biological Characteristics
         ---- Growth
Aerobic or facultative anaerobic
Grow well at 33~37℃
Require X and V factors
Grow better on chocolate agar than on
blood agar
     Virulence factor
Endotoxin
Lipooligosaccharide
Neuraminidase
IgA protease
Fimbriae
Polyribosyl ribitol phosphate (PRP)
capsule (the most important)
          Disease caused by H. influenzae

  Naturally-acquired disease caused by H.
influenzae seems to occur in humans only.
 Bacteremia
 Acute bacterial meningitis
 Epiglottitis (obstructive laryngitis),
 Cellulitis
 Osteomyelitis
 Joint infections
 Ear infections (otitis media)
  Sinusitis associated with respiratory tract
infections (pneumonia)
 Child has swollen face
  due to Hib infection,    An infant with severe vasculitis
  tissue under the skin    with disseminated intravascular
  covering the jaw and     coagulation (DIC) with gangrene
    cheek is infected,        of the hand secondary to
                            Haemophilus influenzae type b
infection spreading into
                               septicemia - prior to the
       her face.            availability of the Hib vaccine
                   Immunity




Relation of the age incidence of bacterial meningitis caused by
H influenzae to bactericidal antibody titers in the blood
Host resistance to infection

Bactericidal antibody directed against
PRP capsule of H. influenzae type b
Antibody to somatic (cell wall) antigens
       Who is at risk?
Young children under 5 years (most
cases occurring in infants between 6-11
months of age)
Day-care attendees
Those in contact with household cases of
Hib disease
Immune deficiencies that lower the body's
resistance to infection
            Diagnosis

The history and the physical exam.
Detecting the bacteria in blood, spinal
fluid, or other body fluid
Satellite phenomenon
                Treatment
H. influenzae meningitis: ampicillin for strains of the
bacterium that do not make ß-lactamase; a third-
generation cephalosporin or chloramphenicol for
strains that do.
Chloramphenicol for penicillin-resistant H. influenzae
Third-generation cephalosporins, such as ceftriaxone
or cefotaxime: effective against H. influenzae and
penetrate the meninges well
Tetracyclines and sulfa drugs: sinusitis or respiratory
infection caused by nontypable H. influenzae.
Amoxicillin plus clavulanic acid (Augmentin): effective
against ß-lactamase producing strains.
                    Control
Hib conjugate vaccines licensed for use among children
Haemophilus ducreyi

Gram negative pleomorphic rods
   Coccobacilli            filamentous

                                                    Painful chancres become pustular,
                                                    eroded, ulcerated and
                                                    there are NO defined borders




      LPS
      Pili
      Outer membrane proteins
      Hemolysin
      IgA protease
                                              DIAGNOSIS:
                                   Generally made on presentation only.
                                       Soft, very painful chancre.
  Gram stain and Laboratory Growth
  Growth REQUIRES X (hemin) factor only (H. influenzae needs X and V)
  Organisms also grow best in an increased CO2 environment.
  Legionella
46 species of Legionella and 68
serogroups.
1976 outbreak of pneumonia occurred
among persons attending a convention
of the American Legion in Philadelphia
费城.
First defined Legionella pneumphila.
    Morphology
 Aerobic ,gram-negative, motile, catalase-
  positive
 Stain poorly by gram’s method,basic fuchsin
  should be used as the counterstain
 Grow on BCYE(buffered charcoal-yeast extract
  agar) with -ketoglutarate,at pH 6.9, 35 C,90%
  humidity
  3 days of incubation,colonies are round or flat
  with entire edges.
  Color vary from colorless to pink or blue
0.5-1 um wide ,2-50 um long
Cell products
Produce distinctive 14-17 carbon
branched-chain fatty acid.
Produce proteases, phosphatase, lipase,
Dnase,& Rnase
Produce a metalloprotease
    Transmission
contaminated air
 infected   water supply


not spread person-person
Pathogenesis
   Attach to phagocytic cell surface
    1).no antibody : C3 deposite on the bacterial
   surface,attached to CR1 or CR3
    2).antibody is present : Fc-mediated phagocytosis
• fail to fuse with lysosomal granules and ribosomes,mitochondria
   around vacuoles containing L pneumophila, Then cells are
   destroyed
   Pontiac fever
  marked by fever, chills, headache and malaise that lasted 2-5
   days
   Legionnaire's disease
  the more severe form of infection which includes pneumonia
Immunity
  Antibodies 4-6 weeks after infection
  Cell-mediated response is important
Epidemiology
1)When legionellosis occur?
  they are are usually occur in the summer and early fall, but
  cases may occur year-round. About 5% to 30% of people who
  have Legionnaires' disease die.
2)How is legionellosis spread?
  Legionella are typically associated with aerosolized water
  (central air conditioning, cooling towers, showers, whirlpool
  spars).
  Disease is generally waterborne; transmission occurs via
  airborne droplets.
3)Where is the Legionella bacterium found?
  The organisms exist in many types of water systems in nature;
  humans are an accidental host.
Risk Groups
   The elderly, cigarette smokers, persons with chronic lung or
  immuno-compromising disease, and persons receiving
  immunosuppressive drugs
Diagnosis
    Clinical: Symptoms include headache, malaise, rapid
    fever, nonproductive cough, Chest X-rays show pneumonia
    Laboratory: immunofluorescent(IF) ,silver stain.
   Legionella antigens in urine samples
   Legionella-specific serum antibody
Treatment
    Erythromycin
    Rifampicin
    Pontiac fever requires no specific treatment

Control
    Regular maintenance of air conditioning or the inclusion of
    biocidal compounds into water cooling towers reduces the
    reservoir. Similarly, hyperchlorination of the water supply
    eliminates the source.
Bordetella

              Bordetella pertussis

  Classification – the
  genus contains
  three medially
  important species
   B. pertussis
   B. parapertussis

   B. bronchoseptica
Virulence
 factors

Pili for attachment
Pertactin, an outer membrane protein also acts as an adhesion
FHA: Filamentous hemagglutinin
PT: Pertussis toxin
Bacterial adenylate cyclase
Dermonecrotic toxin –causing strong vasoconstrictive effects.
Tracheal cytotoxin –the killing and sloughing off of ciliated cells in the
respiratory tract.
Lipooligosaccharide associated with the surface of the bacteria and has
potent endotoxin activity
pertussis toxin
Pertussis is generally a disease of          Next is the paroxysmal stage that lasts ~ 4 weeks. The
infants (50% of cases occur in               patient has rapid, consecutive coughs with a rapid
                                             intake of air between the coughs (has a whooping
children less than 1 year old).              sound). The ciliary action of the respiratory tract has
Acquired by inhalation of droplets           been compromised, mucous has accumulated, and the
                                             patient is trying to cough up the mucous
containing the organism                      accumulations. The coughs are strong enough to
The organism attaches to the ciliated        break ribs! Other symptoms due to the activity of the
                                             released toxins include
cells of the respiratory tract. During
                                             Finally there is a convalescent stage during which
an incubation period of 1-2 weeks,           symptoms gradually subside. This can last for months.
the organism multiplies and starts to        B. pertussis rarely spreads to other sites, but a lot of
liberate its toxins.                         damage may occur, such as CNS dysfunction which
                                             occurs in ~10 % of the cases and is due to an unknown
Next the catarrhal stage occurs -            cause. Secondary infections such as pneumonia and
This last ~ 2 weeks.                         otitis media are common.


                  Incubation     catarrhal          paroxysmal                   convalescent

 duration         7-10 days      1-2 weeks           2-4 weeks               3-4 weeks or longer

                                rhinorrhe       repetitive                Diminished
                                a,              coughwith                 Paroxysmal cough,
symptoms            none        malaise,        whoops,vomiting,          Development of
                                fever,          leukocytosis              secondary complications
                                sneezing,                                 (pneumonia,seizures,enc
                                anorexia                                  ephalopathy)
 bacterial
  culture
    B. Parapertussis & B.
         bronchoseptica

 B. parapertussis – causes a mild form of
  whooping cough
 B. bronchoseptica
     Widespread in animals where it causes kennel
      cough.
     Occasionally causes respiratory or wound
      infections
          CONTROL
Sanitary: This very contagious disease
requires quarantine for a period of 4-6
weeks.
Immunological: Pertussis vaccine is a
part of the required "DPT" schedule.
Chemotherapeutic: Antibiotic
prophylaxis (erythromycin) may be used
for contacts. Treatment of disease with
antibiotics does not affect its course

								
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