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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,
Skirrows 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)
produce inflammation
Campylobacter - symptoms
Incubation: 4-8d
Acute enteritis: 1w,
stools remain positive for
3w
Acute colitis
Acute abdominal pain
Bacteremia: <1% C.
jejuni
Septic abortion
Reactive arthritis
diarrhea
malaise
fever
abdominal pain
usually self-limiting
antibiotics
occassionally
bacteremia
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
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
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
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
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)
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 ---0.62 m
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 grapelike or corn taco-like odor
Culture
Obligate aerobic
Grow well at 37~42and 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
Invasins
Virulence Determinants
Motility/chemotaxis
Toxins
Flagella
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
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
Diagnosis
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)
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 months and 2 years.
Biological Characteristics
----Morphology of organism
In specimens of acute infections:
short (1.5m) 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:
(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)
Immunity
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 -lactamase; a thirdgeneration 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 -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
.
First defined Legionella pneumphila.
Morphology
Aerobic ,gram-negative, motile, catalase-positive
Stain poorly by grams method,basic fuchsin
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
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
Risk Groups
Diagnosis
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
duration
symptoms
bacterial
culture
Incubation
catarrhal
paroxysmal
convalescent
7-10 days
1-2 weeks
2-4 weeks
rhinorrhea
,
malaise,
fever,
sneezing,
anorexia
repetitive
coughwith
whoops,vomiting,
leukocytosis
Diminished
Paroxysmal cough,
Development of
secondary complications
(pneumonia,seizures,enc
ephalopathy)
none
B. Parapertussis & B.
bronchoseptica
B.
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