Campylobacter
Campylobacter
Among the most widespread cause of in fection in the world.
Cause both diarrheal and systemic dise ases
Typical Organisms
Gram-negative rods with comma, S, or “gull-wing” shapes. Motive, with a single polar flagellum
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
Virulence Factor
Lipopolysaccharides (LPS) with endotoxi c activity
Pathogenesis
The infection by oral route from food, drink, or contact with infected animals or animal p roducts(Milk, meat products ).
Susceptible to gastric acid (about 104 organisums)
Multiply in the small intestine invade the epithium produce inflammation cau se bloody stools
• diarrheadiarrhea
• malaise malaise • feverfever
• abdominal painabdominal pain
• usually self-limiting • antibiotics occassio
nally
• bacteremia
–small minoritysmall minority
Campylobacter
Campylobacter
- -symptoms
symptoms
• Incubation: 4-8d
• Acute enteritis: 1w,
stools remain positive for 3 w
• Acute colitis
• Acute abdominal pain
• Bacteremia: <1% C. jejuni
Diagnostic Laboratory
Tests
Specimens: Diarrheal stools
Smears: Gram-stained smears of stool may show the typical “gull-shaped” rods .
Control
•Curved bacilli –
•Former name - Campylobacter pylori,
H. pylori
Helicobacter pylori
Microbiology
•Gram negative rod, curved,
•Very Motile corkscrew motion
•Microaerophilic, use amino acids and fatty acid
s rather than carbohydrates to obtain energy needs 10% CO2 and 5% O2
•Urease production •Catalase production •Oxidase positive
Virulence factors
vacA (vacuolationg associated) cytot oxin, Pathogenicity island: cag, cytot oxin associated gene A+genes relate d to bacterial secretion
Cag+ HP is much more associated
with peptic ulcer disease than Cag(--)
Pathogenesis
•Motility – it moves into the mucus
and produces adhesins on gastric epithelial cells (not intestinal epit helial cells)
•Urease production, breaks down t
he urea to ammonia which buffers t he pH around the bacterium.
•Persists, escape defense mechani
Pathogenesis
H pylori invade the epithelial cell surfac e to a certain degree
Toxins and LPS may damage the muco sal cells
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 ?
Epidemiology
Under age 30 <20% At age 60 40-60%
In developing countries >80% in adults
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.
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
Immunity
An IgM antibody response to he infectio n is developed
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 13 C-labeled urea, rapid, noninvasive, for
assessing response 4-8w post therapy, expensive but non invasive!!
Principles of therapy
Combination chemotherapy
Some drugs are effective in vitro, not in vivo - due to acidic pH - erythromycin
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
PSEUDOMONAS
Common Characteristics
Gram-negative Motile
Aerobic rod
Some produce water-soluble pigments
Widely in soil, water, plants and animals
Some of the medically important pseudomonas
rRNA Homology Group and
Subgroup Genus and Species I. Fluorescent Group
Nonfluorescent Group Pseudomonas aeruginosa Pseudomonas aeruginosa Pseudomonas fluorescens Pseudomonas putida Pseudomonas stutzeri Pseudomonas mendocina
II. Burkholderia pseudomallei
Burkholderia mallei Burkholderia cepacia Ralstonia pickettii
III. Comamonas species
Acidovorax species
IV. Brevundimonas species
Pseudomonas aeruginosa
Pseudomonas aeruginosa
Pseudomonas aeruginosa
Widely distributed in nature
Frequently present in small numbers in the normal in testinal flora and on the skin
Commonly present in moist environments in hospi tals
Typical Organisms
Gram-negative rod ---- 0.6 ×2 μm
Unipolar flagellum (1~3) ---- actively mobile
Occurs as single bacteria , in pairs, and occasionall y in short chain
Capsule
Culture
Grow readily on many types of culture media
Smooth and round colonies
Multiple colony types in one culture
Fluorescent greenish color
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
Virulence Determinants
Adhesins fimbriae (N-methyl-phenylalanine pili) polysaccharide capsule (glycocalyx) alginate slime (biofilm)
Invasins elastase
alkaline protease
hemolysins (phospholipase and lecithinase) cytotoxin (leukocidin)
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
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
Inhibition of protein synthesis in
susceptible cells ----Toxin A
The resultant ADP-ribosyl-EF-2 complex is inactiv e in protein synthesis.
Diverse sites of infection by
Disease caused by
Pseudomonas aer
uginosa
Endocarditis
Respiratory infections Bacteremia
Central Nervous System infections Ear infections including external otitis Eye infections
Bone and joint infections Urinary tract infections
Gastrointestinal infections
Who are at risk?
People with cystic fibrosis Burn victims
Individuals with cancer
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 ℃
Control and Treatment
The spread of Pseudomonas is best controlled b y 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 markedl y reduced sepsis.
Susceptibility testing is essential.
Review
General characteristics: Gram negative rod, unipola r flagellum, actively motile; produce diffusible pigment s -- pyocyanin,gluorescin and pyorubin; aerobic, prod uce hemolysin.
Pathogenicity: cause suppurative infections in burn, trauma, etc.
Endotoxin: main pathogenic substance Exotoxin A
Extracellular enzymes:phospholipase, proteinase, e tc.
Bacteriological diagnosis:
Specimens
Common Characteristics
Small, gram-negative Pleomorphic
Require enrich media (usually containin g blood for isolation)
No flagellum, no spore
Haemophilus
Small Gram-negative coccobacilli , facultative anaerobes, non motil e
often resemble cocci, eg pneumo cocci,
most non-encapsulated strains --- virulent forms encapsulated
fastidious (require blood facto rs)
X factor = hematin V factor = NAD
Characteristics and growth requirements of s ome haemophilus species
X=heme; V=nicotinamide-adenine dinucleotide Species
Requires
Hemolysis
X V
H influenzae (H aegyptius)
-Haemophilus influenzae
Present in the nasopharynx of approximately 75 p ercent of healthy children and adults (non encaps ulated strains as the normal flora)
Rarely encountered in the oral cavity
Has not been detected in any other animal specie s
6 types(a-f) according to capsular polysaccharide type in the encapsulated strains
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 ba cilli
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
Biological Characteristics
---- Growth
Aerobic or facultative anaerobic Grow well at 33~37℃
Require X and V factors
Virulence factor
Endotoxin
Lipooligosaccharide Neuraminidase
IgA protease
Fimbriae
Disease caused by H. influenzae
Naturally-acquired disease caused by H. infl uenzae seems to occur in humans only.
Bacteremia
Acute bacterial meningitis
Epiglottitis (obstructive laryngitis),
Cellulitis
Osteomyelitis Joint infections
Ear infections (otitis media)
An infant with severe vasculitis with di sseminated intravascular coagulation (DIC) with gangrene of the hand secon
dary to Haemophilus influenzae type b septicemia - prior to the availability
of the Hib vaccine
Child has swollen face due to Hib infection, tissue under th
e skin covering the jaw and c heek is infected, infection spr
Immunity
Relation of the age incidence of bacterial meningitis caused by
Host resistance to infection
Bactericidal antibody directed against P RP capsule of H. influenzae type b
Who is at risk?
Young children under 5 years (most case s occurring in infants between 6-11 month s of age)
Day-care attendees
Those in contact with household cases of Hib disease
Diagnosis
The history and the physical exam.
Detecting the bacteria in blood, spinal fluid, or other body fluid
Treatment
H. influenzae meningitis: ampicillin for strains of the b acterium that do not make ß-lactamase; a third-gener ation cephalosporin or chloramphenicol for strains tha t do.
Chloramphenicol for penicillin-resistant H. influenzae
Third-generation cephalosporins, such as ceftriaxone or cefotaxime: effective against H. influenzae and pen etrate the meninges well
Tetracyclines and sulfa drugs: sinusitis or respiratory i nfection caused by nontypable H. influenzae.
Control
LPS
Hemolysin IgA protease Pili
Outer membrane proteins
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.
DIAGNOSIS:
Generally made on presentation only. Soft, very painful chancre.
Gram negative pleomorphic rods
Coccobacilli filamentous
Haemophilus ducreyi
Painful chancres become pustular, eroded, ulcerated and
Legionella
46 species of Legionella and 68 sero groups.
1976 outbreak of pneumonia occurred a
mong persons attending a convention o f the American Legion in Philadelphia 费
城 .
Morphology
Aerobic ,gram-negative, motile, catalase-positive
Stain poorly by gram’s method,basic fuchsin sho
uld be used as the counterstain
Grow on BCYE(buffered charcoal-yeast extract a
gar) with -ketoglutarate,at pH 6.9, 35 C,90% hu
midity
3 days of incubation,colonies are round or flat wit h entire edges.
Cell products
Produce distinctive 14-17 carbon branc hed-chain fatty acid.
Produce proteases, phosphatase, lipas e, Dnase,& Rnase
Transmission
contaminated air
infected water supply
Pathogenesis
Attach to phagocytic cell surface
1).no antibody : C3 deposite on the bacterial surface,attac hed to CR1 or CR3
2).antibody is present : Fc-mediated phagocytosis
• fail to fuse with lysosomal granules and ribosomes,mitochondria aro
und 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
Epidemiology
1)When legionellosis occur?
they are are usually occur in the summer and early fall, but cases m ay occur year-round. About 5% to 30% of people who have Legionn aires' disease die.
2)How is legionellosis spread?
Legionella are typically associated with aerosolized water (central ai r conditioning, cooling towers, showers, whirlpool spars).
Disease is generally waterborne; transmission occurs via airborne dr oplets.
3)Where is the Legionella bacterium found?
The organisms exist in many types of water systems in nature; hum ans are an accidental host.
Risk Groups
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
Erythromycin Rifampicin
Pontiac fever requires no specific treatment
Treatment
Control
Bordetella
Classification – the genus contains thr ee medially import ant 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 re spiratory tract.
Incubation catarrhal paroxysmal convalescent
duration 7-10 days 1-2 weeks 2-4 weeks 3-4 weeks or longer
symptoms none rhinorrhea , malaise, fever, sneezing, anorexia
repetitive coughw ith whoops,vomiti ng,leukocytosis Diminished Paroxysmal cough, Development of secondary complications (pneumonia,seizures,enc ephalopathy) bacterial culture
Pertussis is generally a disease of in fants (50% of cases occur in children less than 1 year old).
Acquired by inhalation of droplets co ntaining the organism
The organism attaches to the ciliated cells of the respiratory tract. During an incubation period of 1-2 weeks, th e organism multiplies and starts to li berate its toxins.
Next the catarrhal stage occurs - Thi s last ~ 2 weeks.
Next is the paroxysmal stage that lasts ~ 4 weeks. The patient has rapid, consecutive coughs with a rapid inta ke of air between the coughs (has a whooping sound). The ciliary action of the respiratory tract has been com promised, mucous has accumulated, and the patient is trying to cough up the mucous accumulations. The co ughs are strong enough to break ribs! Other symptoms due to the activity of the released toxins include
B. Parapertussis
&
B. bronchoseptic
a
B. parapertussis – causes a mild form of wh ooping cough
B. bronchoseptica
Widespread in animals where it causes kennel c
ough.
Occasionally causes respiratory or wound infecti
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.
