Campylobacter Campylobacter Among the most widespread cause of infection in the world. Cause both...
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Campylobacter 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% O
2) 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
PathogenesisThe 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 stoolsOccasionally, the bloodstream is invaded
• diarrheadiarrhea• malaise malaise • feverfever• abdominal painabdominal pain• usually self-limiting • antibiotics occassionally• bacteremia
–small minoritysmall minority
CampylobacterCampylobacter - - symptomssymptoms
• Incubation: 4-8d• Acute enteritis: 1w,
stools remain positive for 3 w
• Acute colitis• Acute abdominal pain• Bacteremia: <1% C.
jejuni• Septic abortion• Reactive arthritis
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.
•Curved bacilli –•Former name - Campylobacter pylori,
H. pylori
Helicobacter 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 energyneeds 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
EpidemiologyPrevalence 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% HPGastric 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 - clarithromycinPPI proton pump inhibitors therapy: omeprazolone lansoprazole: inhibit HP, urease, acidPPI+amoxicillin+clarithromycin or metronidazolePPI+ Bismuth+metronidazole+amoxicillin-very effective
PSEUDOMONAS
假单孢菌属
Common Characteristics
Gram-negativeMotileAerobic rodSome produce water-soluble pigmentsWidely in soil, water, plants and animalsMore than 200 (up to now)
Some of the medically important pseudomonas
rRNA Homology Group and Subgroup Genus and Species
I. Fluorescent Group
Nonfluorescent Group
Pseudomonas aeruginosaPseudomonas aeruginosaPseudomonas fluorescensPseudomonas putidaPseudomonas stutzeriPseudomonas mendocina
II. Burkholderia pseudomalleiBurkholderia malleiBurkholderia cepaciaRalstonia pickettii
III. Comamonas speciesAcidovorax species
IV. Brevundimonas speciesV. Stenotrophomonas maltophilia
Pseudomonas aeruginosaPseudomonas aeruginosa
Pseudomonas aeruginosaPseudomonas 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 μmUnipolar flagellum (1~3) ---- actively mobile Occurs as single bacteria, in pairs, and occasionally in short chainCapsule 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
EndocarditisRespiratory infectionsBacteremiaCentral Nervous System infectionsEar infections including external otitisEye infectionsBone and joint infectionsUrinary tract infectionsGastrointestinal infectionsSkin 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
DiagnosisIsolation and laboratory identification.
blood agar plates eosin-methylthionine blue agar.
Gram morphology, Inability to ferment lactosePositive oxidase reactionFruity odorAbility 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
HaemophilusSmall 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 = hematinV factor = NAD Organisms: H. influenzae: H. ducreyi --( soft chancre); H. aegypticus -- (purulent conjunctivitis)
Characteristics and growth requirements of some haemophilus species
X=heme; V=nicotinamide-adenine dinucleotide
SpeciesRequires
Hemolysis X V
H influenzae (H aegyptius)
H parainfluenzae
H ducreyi
H haemolyticus
H parahaemolyticus
H aphrophilus
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Haemophilus influenzaePresent 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 strainsH. 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 (1.5μm) coccoid bacilli
sometimes in pairs or short chain
In culture: At 6~8 h on rich medium: small coccoid ba
cilli
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 phenomenonNot 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)
An infant with severe vasculitis with disseminated intravascular coagulation (DIC) with gangrene of the hand secondary to Haemophilus influenzae type b septicemia - prior to the availability
of the Hib vaccine
Child has swollen face due to Hib infection, tissue under the skin covering the jaw and cheek is infected, infection spr
eading into her face.
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
LPS
HemolysinIgA protease
PiliOuter membrane proteins
Gram stain and Laboratory GrowthGrowth 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 rodsCoccobacilli filamentous
Haemophilus ducreyi
Painful chancres become pustular, eroded, ulcerated andthere are NO defined borders
Legionella46 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-positiv
e Stain poorly by gram’s method,basic fuchsin s
hould be used as the counterstain Grow on BCYE(buffered charcoal-yeast extract
agar) with -ketoglutarate,at pH 6.9, 35 C,90% humidity3 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 productsProduce 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
PathogenesisAttach 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 aro
und vacuoles containing L pneumophila, Then cells are destroyedPontiac 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
ImmunityAntibodies 4-6 weeks after infectionCell-mediated response is important
Epidemiology1)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
DiagnosisClinical: 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
ErythromycinRifampicinPontiac fever requires no specific treatment
Treatment
ControlRegular 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
Classification – the genus contains three medially important speciesB. pertussisB. parapertussisB. bronchoseptica
Bordetella pertussis
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
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 coughwith whoops,vomiting,leukocytosis
DiminishedParoxysmal cough,Development of secondary complications(pneumonia,seizures,encephalopathy)
bacterial culture
Pertussis is generally a disease of infants (50% of cases occur in children less than 1 year old). Acquired by inhalation of droplets containing the organismThe organism attaches to the ciliated cells of the respiratory tract. During an incubation period of 1-2 weeks, the organism multiplies and starts to liberate its toxins.Next the catarrhal stage occurs - This last ~ 2 weeks.
Next is the paroxysmal stage that lasts ~ 4 weeks. The patient has rapid, consecutive coughs with a rapid intake of air between the coughs (has a whooping sound). The ciliary action of the respiratory tract has been compromised, mucous has accumulated, and the patient is trying to cough up the mucous accumulations. The coughs are strong enough to break ribs! Other symptoms due to the activity of the released toxins includeFinally there is a convalescent stage during which symptoms gradually subside. This can last for months.B. pertussis rarely spreads to other sites, but a lot of damage may occur, such as CNS dysfunction which occurs in ~10 % of the cases and is due to an unknown cause. Secondary infections such as pneumonia and otitis media are common.
B. Parapertussis & B. bronchoseptica
B. parapertussis – causes a mild form of whooping cough
B. bronchoseptica Widespread in animals where it causes kennel c
ough.Occasionally causes respiratory or wound infecti
ons
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