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342 Cards in this Set
- Front
- Back
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haemophilus influenzae
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most common cause of bacterial meningitis in children under 4 years
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haemophilus influenzae
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name is misnomer. was once through to be cause of flu epidemics (which in fact were viral in origin; although they may have been a secondary invader)
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haemophilus influenzae
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small, gran-negative, non-motile, non-spore-forming bacillus (or coccobacillus) with complex nutritional requirements
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H. influenzae type b (Hib) and other encapsulated strains
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as a natural disease, occurs only in humans, experiementally in monkeys/rodents
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H. influenzae type b (Hib) and other encapsulated strains
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no known edotoxin (anti-endotoxin Abs not protective, but anti-capsular Abs are)
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H. influenzae type b (Hib) and other encapsulated strains
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produces IgA protease
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H. influenzae type b (Hib) and other encapsulated strains
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portal into humans is via respiratory tract generally by aerosols between children; often live there harmlessly, 30-50% carrier rate in children who may harbor unencapsulated strains
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H. influenzae type b (Hib) and other encapsulated strains
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disease starts as a nasopharyngitis (with otitis media--infection of the middle ear--or sinusitis)
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H. influenzae type b (Hib) and other encapsulated strains
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bacteremia with involvement of meninges
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H. influenzae type b (Hib) and other encapsulated strains
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less common but serious: epiglottitis and obstructive laryngitis, sudden onset, fatal within 24 hours, treatment must be prompt and airway ensured if necessary by tracheotomy
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H. influenzae type b (Hib) and other encapsulated strains
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sometimes bacteria spread to face (causing cellulitis)
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H. influenzae type b (Hib) and other encapsulated strains
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sometimes bacteria spread to joints, causing childhood pyarthrosis (pus in a joint)
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H. influenzae type b (Hib) and other encapsulated strains
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causes pneumonia
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meningitis, epiglottitis
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medical emergencies
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H. influenzae type b (Hib) and other encapsulated strains
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possesses a polysaccharide capsule that is antiphagocytic
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H. influenzae type b (Hib) and other encapsulated strains
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capsular carbohydrates provoke protective antibodies, capsule is basis for serotyping, six types a-f identified by agglutination, precipitation, or quellung (capsular swelling) tests with specific antisera
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H. influenzae type b (Hib) and other encapsulated strains
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most important. unlike a,c,d,e,f, which have hexose in polysaccharide capsular structure, this has ribose (5-carbon sugar)
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H. influenzae type b (Hib) and other encapsulated strains
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not known if or how unusual ring structure relates to pathogenicity of this type
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H. influenzae type b (Hib) and other encapsulated strains
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antigens and endotoxin exist, but not much known
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encapsulated virulent strains of Hib
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grow as smooth colonies
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encapsulated virulent strains of Hib
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spontaneously give rise to "rough" unencapsulated variants
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H. influenzae type b (Hib) and other encapsulated strains
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facultative anaerobe, requires 2 growth factors in blood.
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X growth factor
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growth factor present in blood, heat-stable;
hemin (precursor of heme groups of respiratory enzymes) |
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V growth factor
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growth factor present in blood, heat-labile;
NAD or NADP |
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staphylococcus
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secretes sufficient V factor so can promote growth of H. influenzae
on agar plates with no other source of V factor, such as blood agar plates, these colonies will be surrounded by small "satellite" colonies of H. influenzae detection of satellites cumberson and not used in hospital diag labs |
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X and V factors
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released from RBC by action of hemolysins secreted by some species of Staphylococci and Streptococci;
released when mild heat used in preparation of chocolate agar |
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H. influenzae type b (Hib) and other encapsulated strains
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chocolate agar used for culture
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H. influenzae type b (Hib) and other encapsulated strains
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sugar ferminentation reactions are not of diagnostic use
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H. influenzae type b (Hib) and other encapsulated strains
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very susceptible to disinfectants and drying
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H. influenzae type b (Hib) and other encapsulated strains
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passive immunity acquired from mother lasts only a few months
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H. influenzae type b (Hib) and other encapsulated strains
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after 3-4 years, most children have acquired active immunity from asymptomatic infections, and incidence of disease falls off--although some cases found in older children and, uncommonly, in adults
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H. influenzae type b (Hib) and other encapsulated strains
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conjugate capsular vaccine has been very effective.
vaccine is capsule (PRP=polyribosyl phosphate) linked to diphtheria toxoid so as to have inccreased dependence of "T cells and memory , as compared to previous formulation composed only of capsule. more immunogenic in very young children than previous versions |
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H. influenzae type b (Hib) and other encapsulated strains
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conjugate vaccine wherein the carbohydrate moiety is synthetic
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H. influenzae type b (Hib) and other encapsulated strains
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Diagnosis: history and age of patient most important
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meningitis from Hib
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blood and spinal fluid are cultured (spinal fluid centrifuged and sediment examined by gram stain)
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Diagnosis of Hib
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spinal fluid specimen streaked on chocolate agar and incubated in CO2 incubator or candle jar
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H. influenzae type b (Hib) and other encapsulated strains
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diagnosis: requirement of colonies for X and V factors demonstrated
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H. influenzae type b (Hib) and other encapsulated strains
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detection of capsular Ag in spinal fluid by immunofluorescence or immunoelectrophoresis (sensitive and accurate measure) establishes diagnosis
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H. influenzae type b (Hib) and other encapsulated strains
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diagnosis: latex-agglutination testq
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Hib meningitis
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ampicillin is drug of choice, 3rd generation cephalosporin for ampicillin-resistant;
Augmentin (ampicillin+clavulanate (B lactamase inhibitor)) renders ampicillin-resistant stains sensitive to antibiotic. if B-lactamase-negative, treatment switched to ampicillin |
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H. influenzae type b (Hib) and other encapsulated strains
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moratality rate low if treated early.
1/3 used to havve resideual neurological damage but decreased with use of corticosteroids during antibiotic treatment to reduce inflammationa nd cytokine production due to LPS reelased as a result of lysis of bacteria |
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rifampin or single dose of cirprofloxacin or ceftraixone
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for prophylaxis of Hib in contacts
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non-typeable H. influenzae
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structure doesn't possess polysaccharide capsule
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non-typeable H. influenzae
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structure utilizes cell-surface adhesions and LPS to colonize cell surfaces
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non-typeable H. influenzae
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no known role for toxins
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non-typeable H. influenzae
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growth and metabolism identical to typeable strains
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typeable H. influenzae strains
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become systemic
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non-typeable H. influenzae
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generally restricted to respiratory tract and infections of the ear
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non-typeable H. influenzae
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2nd most common cause of otitis media (after S. pneumoniae) most common in children b/c iummune system of children doesn't fight infections of respiratory tract as effectively and structure of eustachian tube in young children is felt to make fluid and infections more likely due to a straighter angle and shorter length
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non-typeable H. influenzae
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typically causes respiratory tract infectiosn in pateitns with underlying respiratory issues (COPD, chronic bronchitis, CF), sinusitis, conjunctivitis, and otitis media (middle ear infections)
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non-typeable H. influenzae
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colonization starts in nasopharynx with preferential adhesion to respiratory mucus, non-ciliated cells and damaged epithelium
-peritrichous pili -cell-surface adhesions: Hap; Hia; HMW1/2; P2 and P5 porins, OapA OM protein; LPS |
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Hap adhesion, non-typeable H. influenzae
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found among typeable and non typeable
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HMW1/2 adhesion, non-typeable H. influenzae
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expressed by most non-typeable (but not typeable) strains
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Hia adhesion, non-typeable H. influenzae
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expressed in most non-typeable strains lacking HMW1/2
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Hsf adhesion, non-typeable H. influenzae
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homologue of Hia found in typeable strains
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LPS adhesions, non-typeable H. influenzae
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may bind to platelet activating factor (PAF) receptor
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non-typeable H. influenzae
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invasion via 3 routes: macropinocytosis, paracytosis, LPS binding to PAF
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macropinocytosis, non-typeable H. influenzae
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can manipulate host cell biology to surround bacteria with host cell membrane projections, formation of a vacuole and internalization of the bacterium. normal host cell behavior but the bacteria manipulates pathway
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paracytosis, non-typeable H. influenzae
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can pass between cells (via tight junctions?) to invade sub-epithelial space. unknown OM protein required for this process
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non-typeable H. influenzae
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any passive immunity acquired from mother lasts only a few months
adults are susceptible to infection - not clear that long term immunity develops immunity appears to be strain specific - variation in OM proteins |
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non-typeable H. influenzae
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no vaccine
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non-typeable H. influenzae
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requirement for X and V factors demonstrated
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non-typeable H. influenzae
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typing not typically performed unless isolates are from invasive infections, such as meningitis
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non-typeable H. influenzae
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treatment includes:
oral amoxicillin for out-patients for otitis media and sinusitis 20-35% isolates resistant to amoxicillin alternative: use amoxicillin with B-lactamase inhibitor (i.e., clavulanate) or ceftriaxone infections can be persistent and recurrent, can form antibiotic resistant biofilm OR can invade host cells and thus avoid antibiotics--controversial |
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otits media and sinusitis, non-typeable H. influenzae
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one of top reasons antibiotics are prescribed in the US
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H. ducreyi
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emerging sexually transmitted disease in the U.S.
cause of chancroid ("soft chancre" appearing as ragged ulcer on genitalia). venereal disease. |
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H. ducreyi
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uncommon in US but beginning to increase especially around cities that serve as major seaports; occurs more commonly in parts of Africa and Asia
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H. ducreyi
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type of haemophilus sensitive to sulfonamides, tetracycline, streptomycin
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H. aegypticus
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Koch-Weeks bacillus
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H. aegypticus
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tyep of haemophilus that produces purulent conjunctivitis.
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H. aegypticus
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type of haemophilus common in hot climates
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H. parainfluenzae
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type of haemophilus that is occasional cause of pharyngitis and bacterial endocarditis
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bordetella pertussis
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cause of whooping cough, a severe childhood disease
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whooping cough, bordetella pertussis
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begins with mild upper respiratory symptoms, followed by acute inflammation of trachea, bronchi, and bronchioles with paroxysmal cough, lasting 1-4 weeks. cough usually has characteristic sound
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bordetella pertussis
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small, gram-negative cocco-bacillus. similar in appearance to H. influenzae
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bordetella pertussis
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strict aerobe
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bordetella pertussis
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no requirement for X and V factors
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bordetella pertussis
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requires very fresh media for growth, so most clinical labs have switched to PCR based method to detect organism from washes of nasal cavity
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bordetella pertussis, neisseria meningitidis (meningococcus), Neisseria gonorrhoeae (gonococcus)
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found only in humans. no natural animal reservoir known
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pertussis toxin, bordetella pertussis
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ADP-ribosylating toxin that catalyzes transfer of ADP-ribose from NAD to inhibitory G protein that normally inhibits adenylate cyclase- this causes increased accumulation of cAMP
also affects control of phospholipase C and ion channels combined actions responsible for lymphocytosis, sensitization to histamine, enhancement of insulin secretion |
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cholera toxin
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ADP ribosylates stimulatory G protein also resulting in increased adenylate cyclase activity and cAMP level
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calmodulin-stimulated adenylate cyclase toxin, bordetella pertussis
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catalyzes production of cAMP from ATP, activated by endogenous calmodulin. results in supraphysiologic concentrations of cAMP that may impair leukocyte functions and even cause cell death
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dermonecrotic toxin, bordetella pertussis
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aka mous elethal toxin or heat-labile toxin
discovered when necrotic lesions developed following intradermal injection into suckling mice |
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dermonecrotic toxin, bordetella pertussis
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causes vascular smooth muscle contraction resulting in ischemic necrosis of lung tissue
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tracheal toxin, bordetella pertussis
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causes ciliostasis, inhibits DNA synthesis and ultimately kills tracheal epithelial cells
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pili, bordetella pertussis
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mediate attachment to ciliated epithelial cells of upper respiratory tract, cause diminished ciliary activity
also filus-like filmamentous hemagglutinin (FHA) |
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pertactin, bordetella pertussis
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surface molecule
acute local inflammation, increased mucous secretions, patchy ulceration of respiratory epithelium may result in diminished oxygen supply or pneumonia |
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bordetella pertussis
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do not invade blood stream but remain in respiratory tract
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bordetella pertussis
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expression of genes encoding virulence factors regulated at level of transcription by two-component system--composed of bacterial transmembrane sensor protein that responds to host environmental cues to phosphorylate cytoplasmic response regulator protein that binds DNA to activate transcription from appropriate promotors
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bordetella pertussis
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incubation period ~7-10 days
2 stages |
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catarrhal stage, bordetella pertussis
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runny nose, sneezing, low-grade fever, mild occasional cough (similar to cold)
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paroxysmal stage, bordetella pertussis
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bursts of coughing (probably to dislodge mucus), followed by high-pitched whoop and occasional vomiting
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paroxysmal stage, bordetella pertussis
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patients become cyanotic during cought attacks, which occur more frequently at night
infants don't make whooping sound |
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bordetella pertussis
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immunization in latter half of 20th century produced dramatic decline in disease
120,000 cases by 1950 but only 2,000 in 1977 |
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bordetella pertussis
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neither immunization nor disease produces lifelong immunity
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bordetella pertussis
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until recently, immunization was through one component of trivalent DTP (diphtheria toxoid + tetanous toxoid + heat killed pertussis organisms).
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bordetella pertussis
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potential side effects including encephalopaty and permanent neurological sequelae led to less infants receiving vaccine from late 80's into 90's, so disease cases actually began increasing
incidence rising since mid 1980's with nearly 9,000 cases reported in 1999 |
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bordetella pertussis
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acellular vaccines recently licsensed. each incorporated into one of several DTaP trivalent vaccines that are now the recommended vaccines DTP is essentially phased out
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bordetella pertussis
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transmitted by aerosolized droplets during sneezing or coughing. very contagious
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bordetella pertussis
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following prolonged series of coughs, inspiration through narrowed glottis produces whoop
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bordetella pertussis
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deaths have occurred mostly in infants, who are susceptible to disease b/c quantity of Ab crossing placenta is not adequate for protection by passive immunity
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bordetella pertussis
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antibodies in children found only after several weeks
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bordetella pertussis
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diagnosis includes history of contact, classic cough, marked lymphocytosis
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bordetella pertussis
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diagnosis includes isolation of organism by cough plate. colonies grow very slowly. identify by appearance of colony, gram stain, biochemical reactions
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bordetella pertussis
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rapid direct fluorescein-labeled antibody test for nasopharyngeal specimens
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bordetella pertussis
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erythromycin is drug of choice (alternatives: tetracycline, chloramphenicol).
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bordetella pertussis
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not sensitive to penicillin or ampicillin
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B. parapertussis
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other species of bordetella
produce a number of virulence factors similar to those of B. pertussis, but don't carry genes for pertussis toxin causes sporadic cases of whooping cough |
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B. bronchiseptica
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other species of bordetella
produce a number of virulence factors similar to those of B. pertussis, but don't carry genes for pertussis toxin causes respiratory illness in animals and only occasionally in humans |
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H. influenzae type B
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major infection: meningitis, epiglottitis, pneumonia, otitis media
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H. influenzae type B
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less common infection: arthirtis, osteomyelitis
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H. influenzae type B
B. pertussis Neisseria meningitidis Neisseria gonorrhoaea |
reservoir: humans
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H. influenzae type B
B. pertussis Neisseria meningitidis |
transmission: droplet
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H. influenzae type B
B. pertussis |
Gm-, coccobacilli
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H. influenzae type B
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growth requires X (hemin) and V (NAD) factors
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H. influenzae type B
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virulence: capsule, pili, IgA protease
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H. influenzae type B
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no exotoxins
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H. influenzae type B
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Diagnostics: Gram stain blood and spinal fluid; culture chocolate agar demonstrate XV req's confirm type b antigen
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H. influenzae type B
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treatment: 3rd generation cephalosporin, then amoxicillin if sensitive; contacts-rifampin, ciprofloxacin, or ceftraxone
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H. influenzae type B
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Hib vaccine
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B. pertussis
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major infection: pertussis (whooping cough)
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B. pertussis
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less common infection: pneumonia
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B. pertussis
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growth: Bordet-Gengou complex medium
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B. pertussis
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Virulence: FHA, pili, pertactin numerous toxins
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B. pertussis
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pertussis toxin, adenylate cyclase toxin, tracheal cytotoxin, dermonecrotic toxin
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B. pertussis
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Gram stain nasopharyngeal swab; direct antibody test; culture on B-G
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B. pertussis
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erythromycin and treat household contacts
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B. pertussis
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new acellular vaccine with PT, FHA, pertactin, pilli
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Neisseria meningitidis
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major infection: meningitis, septicemia
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Neisseria meningitidis
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less common infection: arthritis
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Neisseria meningitidis
Neisseria gonorrhoeae |
Gm-, diplococci, with adjacent sides slightly flattened
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Neisseria meningitidis
Neisseria gonorrhoeae |
+ oxidase
addition of drop of 1% solution of dye (dimethyl- or tetramethyl-p-phenylenediamine) to colony causes a pink and then a black color to appear within seconds. however, non-pathogenic also react positively. |
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Neisseria meningitidis
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Fermentation:
Glu+ Mal+ Lac- Suc- |
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Neisseria meningitidis
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virulence: capsule, meningitis usually assoc. with type B; IgA protease; pili
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Neisseria meningitidis
Neisseria gonorrhoeae |
toxins: LOS (LPS)-endotoxin; no exotoxins
in contrast to LPS, LOS has no O side chains |
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Neisseria meningitidis
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meningitis-fever, stiff neck, vomiting, lethargy, petechial rash
septicemia-fever, petechial rash, hypotension, W-F syndrome |
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Neisseria meningitidis
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Gram stain, spinal fluid, blood, nasopharyngeal or free-living and internalized bacteria; culture on chocolate agar and Thayer Martin.
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Neisseria meningitidis
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treatment with Penicillin G, ceftriaxone; rifampin prophylactically for close contacts b/c efficiently secreted into saliva, or ciprofoloxacin b/c so potent
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Neisseria meningitidis
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vaccine available epidemics or military for capsule types A, C, Y and W-135; but not for type B
type B capsule composed of sialic acid not recognized by C3b component of complement, so doesn't stimulate recruitment of phagocytes |
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Neisseria gonorrhoeae
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major infection: gonorrhea, PID
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Neisseria gonorrhoeae
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less common infection: arthritis, conjunctivitis
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Neisseria gonorrhoeae
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transmission: direct, STD
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Neisseria gonorrhoeae
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fermentation:
Glu+ Mal- Lac- Suc- |
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Neisseria gonorrhoeae
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virulence:
pili, IgA protease, Omp's?; Opa? |
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Neisseria gonorrhoeae
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men-urethritis
women-cervical gonorrhea, PID neonates-opthalmia neonatorum |
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Neisseria gonorrhoeae
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Gram stain urethral pus, fresh exudate for bacteria within WBC's
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Neisseria gonorrhoeae
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treatment: ceftriaxone and doxycycline for chlamydia trachomatis
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Neisseria gonorrhoeae
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no vaccine
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Neisseria meningitidis
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agent of meningococcal meningitis, also called meningococcus
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meningococcus
gonococcus |
require rich medium for isolation; grow better in 5-10% CO2
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Thayer-Martin selective medium
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permits recognition of N. meningitidis and N. gonorrhoeae from materials contaminated with other bacteria
contains chocolate agar, with vancomycin (to inhibit gram-positives) and colistin (to inhibit gram-negative enterics) and nystatin (anti-fungal) non-pathogenic Neisseria fail to grow on this media pathogenic species require blood products in medium, while nonpathogenic species do not |
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meningococcus
gonococcus |
readily killed by drying, heat, disinfectants
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non-pathogenic Neisseria
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ferment all the sugars except sucrose
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Neisseria meningitidis
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multiplies outside of cells, but not once phagocytized (although bacteria can be seen within leukocytes)
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Neisseria meningitidis
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endotoxin from organism damages walls of small vessels
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Neisseria meningitidis
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lives in nasopharynx. carrier rate varies; 5% in general population, higher in households where there has been a case of meningococcal meningitis
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Neisseria meningitidis
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differencies in composition of polysaccharide capsule are basis for classification into serogroups: bacteria of A, B, and C are most important
within each serogroup, there may be serotypes (e.g. group B has a dozen serotypes) based on differences between outer membrane proteins |
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Neisseria meningitidis
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encapsulated, Neisseria
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Neisseria gonorrhoeae
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not encapsulated, Neisseria
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Neisseria meningitidis
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virulent strains are encapsulated and have smooth colonies
on artificial media, rough colonies (unencapsulated, relatively avirulent) are often produced |
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Neisseria meningitidis
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carrier state may last from days to many months
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Neisseria meningitidis
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in some, mild pharyngitis and fever are all that occur
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Neisseria meningitidis
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transmission most often in crowded conditions (day care centers, military barracks)
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Neisseria meningitidis
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in small % of infected humans, bacteria progress from nasopharynx to bloodstream
incidence of severe disease--1 in 50,000 per years |
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Neisseria meningitidis
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incubation period: matter of days to a week
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Neisseria meningitidis
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predilection for children below 5. highest incidence in 1st year (but after protective maternal antibodies are gone; i.e. not neonates)
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group B Strep or E. coli K1
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most common meningitis in neonates due to this
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Neisseria meningitidis
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without treatment, mortality about 85%
with early treatment mortality <1% in otherwise healthy patients |
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Neisseria meningitidis
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capsule has antiphagocytic properties, contributing to virulence
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Neisseria meningitidis
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bacteria have organotropism, and localize in meninges preferentially. skin, eyes, lungs also sites in which bacteria localize
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Waterhouse-Friderichsen syndrome, Neisseria meningitidis
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uncommon: may cause adrenal failure, circulatory collapse, and shock, with rapid death
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Neisseria meningitidis
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most adults have antibodies that confer immunity. evoked within a week by the carrier state. when diverse groups are brought together--as in military camps--there is exposure to serotypes of bacteria not encountered before, hence outbreaks may occur
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Neisseria meningitidis
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clinical picture of upper respiratory infection followed by high fever and signs of meningitis
petechiae (small purplish-reddish spots caused by munte hemorrhages) may appear in skin, followed by large areas of ecchymosis (black and blue spots caused by leakage of blood from small vessels) |
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Neisseria meningitidis
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specimens from blood, spinal fluid, nasopharyngeal secretions cultured and examined for gram-negative diplococci
further identify organ by sugar fermentation test (4 hrs), and/or latex agglutination test (10 min) based on capsule antigen in CSF |
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Neisseria meningitidis
|
clinical picture is critical
presence of patechial rash in case of adult or child with neurological symptoms is indicative |
|
|
meningitis caused by H. influenzae and S. pneumoniae
|
hardest meningitis to diagnose in children
|
|
|
Neisseria gonorrhoeae
|
can be seen by gram stain in fluid of purulent exudate (pus)
|
|
|
Neisseria gonorrhoeae
|
can be seen inside of epithelial and phagocytic cells
|
|
|
Neisseria gonorrhoeae
|
lives primarily in genitourinary tract
|
|
|
Neisseria gonorrhoeae
|
endotoxin activity not major factor in disease state
|
|
|
Neisseria gonorrhoeae
|
more than 100 serotypes based on antigenicity of pilus protein
|
|
|
Neisseria gonorrhoeae
|
common mode of transmission: STD, direct genital contact, resulting in genitourinary tract infection
|
|
|
Neisseria gonorrhoeae
|
another mode of transmission through rectal and pharyngeal mucosa (non-pathogenic Neisseria also found in pharynx)
|
|
|
Neisseria gonorrhoeae
|
another mode of transmission in conjunctiva of newborns' eyes during passage of newborn through birth canal--ophthalmia neonatorium
|
|
|
Neisseria gonorrhoeae
|
infection established within hour of exposure.
bacteria anchor to surface fo epithelial cells using pili (which also impair phagocytosis by PMN's, non-piliated are non-virulent), then penetrate thru surface cells (intracellularly) and reach sub-epithelial CT in a few days. followed by inflammation and yellow purulent urethral discharge (with burning sensation on urination). symptoms in males typically appear in 2-3 days more variable and less well-defined in females. usually within 10 days; however high percentage of infected females remain asymptomatic in contrast to males. infection occasionally spreads to epididymis or prostrate in males and, more often, to Fallopian tubes in femails |
|
|
Neisseria gonorrhoeae
|
this disease--and infection with venereally-transmitted Chlamydia trachomatis--are probably the 2 most prevalent communicable bacterial diseases of humans
worldewide pandemic of this disease, not appreciably lessened by introduction of chemotherapy |
|
|
Neisseria gonorrhoeae
|
asymptomatic carrier states common. carriers can transmit infection
|
|
|
Neisseria gonorrhoeae
|
for males it is estimated that 1-10% of infected and able to transmit disease are asymptomatic.
higher for females |
|
|
Neisseria gonorrhoeae
|
complications of disseminated disease: arthritis-dermatitis syndrom, with spread to one of more joints, and with skin lesions; joint infection may occur in absence of prior overt genito-urinary symptoms
|
|
|
Neisseria gonorrhoeae
|
complication of disseminated disease: chronic pelvic inflammatory disease in females
|
|
|
Neisseria gonorrhoeae
|
clinical picture of discharge, plus history of exposure
|
|
|
Neisseria gonorrhoeae
|
stained smears of fresh exudate often show G- diplococci within PMN
|
|
|
Neisseria gonorrhoeae
|
culture should be done before treatment is started, if possible. colonies show oxidase-positive, gram- diplococci
chronic disease, diagnosis more difficult |
|
|
3 major forms of gonococcal resistance
|
drug resistant is major problem. recommended regimens have changed several times in past 10 years
a. plasmid-mediated penicillinase producing N. gon (PPNG) b. plasmid-mediated tetracycline resistant N. gon (TRNG)--TetR plasmid is conjugatieve and can mobilize PenR plasmid c. chromosome-mediated resistant N. gon (CMRNG). CMRNG is a broad based resistance--includes Pen, Tet, and some cephalosporins--related to mutations affecting permeability; level of resistance low; treatment failure rate |
|
|
Neisseria gonorrhoeae
|
b/c of widespread resistance, single-dose penicillin therapy no longer recommended
|
|
|
chlamydia trachomatis
|
IM ceftriaxone and 10day oral tetracycline or doxycycline
this is STD of highest incidence, so one assumes it's present in cases of gonorrhea |
|
|
opthalmia neonatorum, Neisseria gonorrhoeae
|
once the cause of 50% of blindness in children
prophylactic treatment of newborn required by law tetracycline or erythromycin ointment, or dilute (1%) silver nitrate from standardized ampules to prevent damaging effects of overdosing with silver nitrate |
|
|
Neisseria gonorrhoeae
|
immune response, although can be demonstrated after infection, is weak, for unknown reasons. hence repeated attacks are common. high degree of antigenic variation of surface components (for ex, 100's of antigenic pilus variants) may contribute to this
|
|
|
Koch's postulate
|
1. pathogen should be found in all cases of disease, with corresponding tissue distribution
2. microorganism should be grown in pure culture in vitro 3. a pure culture, inoculated into susceptible animals, the typical disease would ensue. the microorganism must be re-isolated from the lesion of such experimentally induced disease |
|
|
Molecular Koch postulate
|
1. the phenotype or molecular properties (e.g. DNA) should be associated with pathogenic strains and not with nonpathogenic strains
2. specific inactivation of the gene (or genes) associated with virulence trait should lead to a measurable decrease in pathogenicity 3. reversion or replacement of mutated gene with "wild type" should lead to restoration of pathogenicity or virulence |
|
|
adherence and colonization
invasion evasion of host defenses production of extracullular substances to facilitate bacterial spread |
bacterial infection is a multistep process
|
|
|
toxin mediated disease
|
tetanus
anthrax staphylococcal food poisoning |
|
|
nosocomial infections, gram-negative opportunistic bactera
|
hospital-acquired infections
carry multiple antibiotic resistances, making them difficult to treat lack of washing hands |
|
|
virulence factors, gram-negative opportunistic bactera
|
toxins and cell surface structures, contribute to disease caused by bacterium
|
|
|
pathogenecis or virulence determinants, gram-negative opportunistic bactera
|
factors or pathways required for organism to cause disease
may not be specific to bacterium-host interactions |
|
|
LPS, gram-negative opportunistic bactera
|
immune response to this gram-negative cell component causes symptoms
|
|
|
biofilms, gram-negative opportunistic bacteria, gram-negative opportunistic bactera
|
surface-attached microbial communities
65% nosocomial infections related to this device-related infections increased resistance to range of antimicrobial agents, associated with production of large quantities of extracellular polysaccharides |
|
|
Escherichia coli
|
part of our normal flora and most common opportunistic pathogen
|
|
|
Escherichia coli
|
most common cause of Gram-negative infections.
|
|
|
Escherichia coli
|
gastrointestinal infections
UTI bacteremia meningitis |
|
|
neonatal meningitis
|
capsular antigen of E. coli causes this disease
|
|
|
UTI, GI tract infections
|
pili of E. coli and other G- bacteria cause invasive and cell adhesive behavior, cause this disease
|
|
|
exotoxin
|
principal cause of GI tract symptoms, proteins produced by E. coli
|
|
|
E. coli
|
pathogenicity:
capsular antigen--neonatal meningitis pili-UTI, GI tract infecitons exotoxin--GI tract symptoms |
|
|
uropathogenic E. coli (UPEC)
|
95% of all non-hospital acquired UTI
60% women in U.S. will have one UTI during lifetime, 11% one per year |
|
|
uropathogenic E. coli (UPEC)
|
correlation between expression of certain virulence factors and site/type UTI. cell surface adhesins
Many UTI bacteria can bind mannosides that are common constituents of uroepithelial cells and urinary tract mucus. adhesion blocked by mannose, so mannose-sensitive |
|
|
bacteriurial infection
|
at least 10^5 bacteria/ml present in urine
|
|
|
cystitis
|
describes syndrome involving dysuria (burning feeling during urination), frequency, urgency, and occasionally suprapubic tenderness. typically involves infection of lower urinary tract but may include upper
|
|
|
acute pyelonephritis
|
results from UTI that has disseminated to kidney
clinical syndrome characterized by flank pain, tenderness and fever, dysuria, frequency and urgency |
|
|
uropathogenic E. coli (UPEC)
|
invasion and spread of bacteria into urinary tract almost always associated with ascending route of infection. urethra usually colonized with bacteria
|
|
|
UTI, uropathogenic E. coli (UPEC)
|
persistent infections due to formation of "pods" or biofilm-like structures that form within epithelial cells of urinary tract
can invade epithelial cells and replicate within cells |
|
|
hemagglutination
|
assay that uses RBC and series of dilution in microtiter dish or set of tubes to assay adherence or senstivity to mannose
|
|
|
adhesins
|
play role in colonization of urinary catheters. almost 100% catheters colonized with bacteria within 3 days
|
|
|
P pili
|
pili on E. coli strains associated with pylenonephritis
mediate attachment of bacteria to ( ) blood group globoseries Gal-Gal constituent of glycolipids present on uroepithelial cells and erythrocytes chromosomally located operon (pap genes) encodes functions necessary for biogenesis and function of this pilus system |
|
|
phase variation
|
stochastic switching of phenotypic trait to provide phenotypic diversity inside and outside host
controlled by variety of mechanisms: strand slippage, methylation, recombination influenced by environmental factors |
|
|
uropathogenic E. coli (UPEC)
|
virulence factors: LPS, capsule, motility, exotoxins including hemolysin
|
|
|
E. coli
|
major cause of bacteremia, leading cause of nosocomial bacteremia
|
|
|
E. coli
|
majority of isolates are noninvasive, but 2 routes that promote invasion are UTI and indwelling devices like intravenous catheters
|
|
|
E. coli
|
maybe ability to invade host cells allows crossing into bloodstream
|
|
|
E. coli
|
serum resistance is critical trait of strains and correlated with production of K1 capsule
|
|
|
gram-negative bacteremia
|
hallmark is systemic reaction to endotoxin or LPS
|
|
|
LPS
|
most toxic component of most bacteremic isolates of E. coli and is life-threatening
management of bacterial sepsis and accompanying endotoxic shock is difficult |
|
|
E. coli
|
most common neonatal pathogen, one of leading causes of neonatal meningitis
|
|
|
E. coli K1
|
isolated from 20-40% of healthy individuals including newborns. generally can colonize newborns ithin hours of birth via vertical transmission from mother or nursery staff
|
|
|
neonatal meningitis caused by E. coli K1
|
pathogenesis:
colonize host mucosal surfaces translocate across surfaces into bloodstream survive transport through bloodstream, serum resistance cross blood-brain barrier and survive in CSF proliferate and cause tissue damage |
|
|
E. coli
|
virulence determinants: K1 polysialic acid capsule (major) and S fimbriae, siderophores
|
|
|
E. coli capsule
|
outmost structure on bacterial surface
typically glycoconjugates allows it to evade nonspecific host immune defenses primarily anti-phagocytic mechanism |
|
|
Klebsiella pneumoniae
|
capsule can be used to help identify it based on mucoid colony
capsule allows reduced phagocytosis, reduced complement susceptibility |
|
|
Enterobacter cloacae
|
formerly lumped into Aerobacter and Klebsiella
differs from Klebsiella in that it is motile and generally less heavily encapsulated |
|
|
Enterobacter cloacae
|
infection occurs in hospital setting secondary to antibiotic therapy
associated with burn, wound, respiratory, urinary infectionws |
|
|
Enterobacter cloacae and E. agglomerans
|
associated with intravenous tubing contamination affecting hundreds of patients in 25 hospitals
|
|
|
Proteus vulgaris; proteus mirabilis
|
frequent cause of UTI
flagella, urease synthesis contribute to pathogenicity urea, urease>NH3+CO2> alkaline urine> salt crystalization and stone formation> chronic infection |
|
|
serratia marcesens
|
infections seen secondary to broad spectrum antigbiotic therapy or secondary to instrumentation (tracheostomy, indwelling catheters, renal dialysis, etc.)
infections can involve most itssues pneumonia often contracted after use of contaminated respirator |
|
|
serratia marcesens
|
different from other enterobacteriaceae in that it is less likely to colonize GI tract, and is more associated with respiratory and urinary tract.
GI tract is important reservoir among neonates |
|
|
serratia marcesens
|
ouside hospital, associated with heroin addicts
|
|
|
serratia marcesens
|
outpatient setting, associated with septic arthritis
|
|
|
serratia marcesens
|
can produce Ig-specific protease that may influence pathogenicity
|
|
|
Pseudomonas aeruginosa
|
can cause both acute and chronic infections
|
|
|
Pseudomonas aeruginosa
|
acute infections:
bacteremia in immunocompromised patients eye infections burn infections |
|
|
Pseudomonas aeruginosa
|
chronic infections:
in lung in association with respiratory diseases like cystic fibrosis or implanted medical devices people with CF, chronic bacterial infection can't be cleared by current antimicrobial therapies, pt usually die of respiratory failure in mid-30's. bacteria grow in biofilms |
|
|
Pseudomonas aeruginosa
|
can't ferment sugars, so detection in blood culture requires aerobic incubation
|
|
|
Pseudomonas aeruginosa
|
can grow via anaerobic respiration with nitrate as electron acceptor, or ferment arginine
|
|
|
Pseudomonas aeruginosa
|
few nutritional requirements for growth and ability to grow at low temps 4degC
widespread distribution and great potential for contamination of many environments |
|
|
Pseudomonas aeruginosa
|
plasmid content. resistance to many antibiotics leads to its frequent overgrowth after antibiotic treatment. high natural resistance to many antibiotics for other Gram-
|
|
|
ExoA, Pseudomonas aeruginosa
|
ADP-ribosylates EF-2, stops protein synthesis, elicits apoptosis of affected cells
|
|
|
ExoS and ExoT
|
ADP-ribosylating enzymes that target host regulatory proteins
|
|
|
ExoU
|
cytotoxic, phospholipase activity; causes irreversible damage to cellular membranes and rapid necrotic death
|
|
|
Pseudomonas aeruginosa
|
elastases break down elastin, CT protein in lung, leads to tissue damage in lung
phospholipases break down phospholipids in lung surfactant and host cell membranes |
|
|
Pseudomonas aeruginosa
|
in chronic infections associated with CF, produces alginate capsule that makes strains appear mucoid. alginate thought to block phagocytosis
|
|
|
Pseudomonas aeruginosa
|
model organism for study of biofilm formation
|
|
|
Legionella pneumophila
|
elderly or immunocompromised most at risk
|
|
|
Legionella pneumophila
|
very strict growth requirements and grows slowly, rarely isolated from patients
|
|
|
E. coli
|
LPS (O-antigen)
Peritichous flagella (H-antigen) Capsule (K antigen) |
|
|
heat labile toxin (LT) and heat stable toxin (ST), E. coli
|
encoded on plasmids
|
|
|
Shiga-like toxin
|
encoded on lysogenic phage similar in many ways to phage lambda
|
|
|
virulence factors, E. coli
|
Adhesions: fimbrial including colonization factor antigens (CFAs) and bundle forming pili (BFP); and nonfimbrial
Toxins LT and ST; Shiga-like toxins Endotoxin (LPS) Nutrient uptake systems like sideropores hemolysins and cytotoxins K1 capsule |
|
|
Enterohemorrhagic E. Coli O157:H7
|
from contaminated farm products:
cattle feces ground beef: under-cooked hamburger leafy vegetables unpasteurized apple cider/juice, raw milk/dairy products, vegetables (spinach) large centralized processing facilities secondary person to person spread or contaminated wading pools, etc. petting zoos |
|
|
Enterohemorrhagic E. Coli O157:H7
|
asymptomatic carrier
diarrhea, frequently bloody severe, cramping abdominal pain vomiting in about 50% of the cases HUS (hemolytic uremic syndrome). hemolytic anemia, thrombocytopenia, acute renal failure. |
|
|
Enterohemorrhagic E. Coli O157:H7
|
preschool children and elderly are especially susceptible
|
|
|
Enterohemorrhagic E. Coli O157:H7
|
specific serogoup based on LPS and flagellar antigens
other serogoups: O111, O26, O157:H- |
|
|
Enterohemorrhagic E. Coli O157:H7
|
additional factors encoded on genetic elements:
intimin/Tir delivered by the TypeIII secretion system attaching and effacing lesion |
|
|
Enterohemorrhagic E. Coli O157:H7
|
Toxins: shiga-like toxin, hemolysin encoded on plasmid
|
|
|
secretion, Enterohemorrhagic E. Coli O157:H7
|
moving bacterial proteins from cytoplasm across cytoplasmic membrane
|
|
|
type III secretion system, Enterohemorrhagic E. Coli O157:H7
|
specialized form, where protein moves across bacterial cytoplasmic and outer membrane AND across the host cell membrane through an injection needle
|
|
|
type III secretion system, Enterohemorrhagic E. Coli O157:H7
|
allows bacterium to deliver proteins to host cytoplasm
|
|
|
type III secretion system, Enterohemorrhagic E. Coli O157:H7
|
genes often found together with other virulence genes in pathogenicity islands
|
|
|
LEE (locus for enterocyte effacement), Enterohemorrhagic E. Coli O157:H7
|
pathogenicity island that encodes T3SS, intimin, and tir
|
|
|
type III secretion systems, Enterohemorrhagic E. Coli O157:H7
|
secretion apparatus to deliver proteins to host cell
effector proteins delivered into host cell via secretion apparatus, alter host cell biology |
|
|
Tir, type III secretion systems, Enterohemorrhagic E. Coli O157:H7
|
T3ss-secreted bacterial that is delivered to surface of epithelial cell to allow for E. coli attachment
|
|
|
Intimin, type III secretion systems, Enterohemorrhagic E. Coli O157:H7
|
Tir binding protein on surface of E. coli
|
|
|
type III secretion systems, Enterohemorrhagic E. Coli O157:H7
|
toxin, proteins can recruit host cell actin, causing altered morphology, impact signal transduction pathways in host cell to form A/E lesions
|
|
|
Shiga-like toxin, Enterohemorrhagic E. Coli O157:H7
|
toxin, also called verotoxin
encoded on a phage comprised of 2 subunits |
|
|
Shiga-like toxin, Enterohemorrhagic E. Coli O157:H7
|
toxin, interferes with protein synthesis via its RNA cleavage activity (subunit A) and may impact cytoskeleton (subunit B)
|
|
|
Hemolysin, Enterohemorrhagic E. Coli O157:H7
|
toxin, nutrient acquisition
cytotoxic-pore formation in cells |
|
|
Enterohemorrhagic E. Coli (EHEC)
|
large inestine (food borne pathogen)
moderately invasive, produces Shiga toxin, forms A/E lesions complicated by hemolytic uremia |
|
|
Enterophathogenic E. coli (EPEC)
|
small intestine (major cause of infantile diarrhea)
forms A/E lesions, no known hemolysin, no shiga-like toxin or other toxins identified |
|
|
Enteroaggregative E. coli (EAEC)
|
small intestine
no A/E lesions, non-invasive, produces heat stable-like toxin, produces hemolysin, causes persistent diarrhea in children |
|
|
enteroinvasive E. coli (EIEC)
|
large intestine (important cause of diarrhea)
non-fimbrial adhesins, replicate within enterocytes leading to lysis, no Shiga toxin |
|
|
enterotoxigenic E. coli (ETEC)
|
small intestine (major cause of diarrhea world wide)
fimbrial adhesins, non-invasive, produce LT and/or ST, watery diarrhea, no inflammation |
|
|
Enterohemorrhagic E. Coli O157:H7
|
biochemical identification based on carbohydrate fermentation patterns and other reactions
Lac+, discerned on EMB or MacConkey agar |
|
|
Enterohemorrhagic E. Coli O157:H7
|
sorbitol-negative (colorless)
commensal strains are positive direct or latex agglutination tests to identify antigen biochemical tests to confirm ID serology and toxin analysis |
|
|
diagnosis of other diarrheagenic E. coli:
|
serotyping-pulsed field gel electrophoresis
PCR analysis of virulence factors |
|
|
Enterobacteriaceae family (enterics)
|
normally as part of human gut flora
gram negative rods, including E. coli, salmonella, shigella, etc facultative anaerobes, ferment glucose, oxidase negative (no cytochrome oxidase) |
|
|
Salmonella
|
gram negative rods, non-spore-forming, facultative anaerobes
ferment glucose under anaerobic conditions DO NOT FERMENT LACTOSE (distinguishing characteristic PRODUCE H2S |
|
|
Salmonella
|
more than 1500 species
antigenic analysis of O antigen, sugar part of LPS analysis of H antigen, part of flagella, two types, phase I and phase II antigens |
|
|
Salmonella typhi
|
unique antigen called Vi antigen
|
|
|
Salmonella typhi, S. choleraesuis
|
typhoid fever or enteric (typhi)
one serotype |
|
|
salmonella enteriditis
|
many serotypes, named by city in which microorganism discovered
|
|
|
Salmonella
|
feces, blood, urine
primary isolation from feces on media containing lactose (EMB and MacConkey agar) biochemical and serological tests to identify organism for diagnostic and epidemiologic purposes, using type specific sera against O, H, Vi antigens |
|
|
Salmonella
|
requires high inoculum for disease (10^5 CFU)
|
|
|
Salmonellosis, 3 distinguishable syndromes
|
enteric fevers, septicemias, acute gastroenteritis (most)
|
|
|
typhoid fever, Salmonella
|
prototype of enteric fevers, caused by S. typhi/paratyphi (facultative intracellular organisms)
|
|
|
typhoid fever, Salmonella
|
acquired by ingestion of contaminated food or water, common in developing countries
many infections subclinical, 7-14 day incubation malaise, anorexia, headache, onset of fever with stepwise increase to 104 F diarrhea usually absent but abdominal tenderness and distention present, due to enlarged liver and spleen, sepsis skin rash on trunk called rose spots, lasting few days leukopenia is common fever subsides after third week severe intestinal hemorrhages in later stages osteomyelitis in patients with sickle cell anemia |
|
|
typhoid fever, Salmonella
|
ingested organisms survive gastric acid, reach small intestine, multiply within mononuclear cells of Peyer's patches, enter intestinal lymphatics, travel via thoracic duct to blood where disseminated into spleen, bone marrow, gall bladder.
endotoxin (lipid A of LPS) released into bloodstream causes some of symptoms |
|
|
typhoid fever, Salmonella
|
stool cultures positive very early in course of infection. culture may be missed b/c no GI symptom, becomes negative after 1st week
blood cultures positive after 7-14 days stool cultures positive again when excreted into intestine from gall bladder where it resides in late stage of disease or in carrier state, particularly in pateints with gallbladder diseases |
|
|
typhoid fever, Salmonella
|
3% patients excrete large number of oragnisms from suppurative focus in biliary tract over extended periods
important sources for spreading infection if sewage disposal is incorrect or compromised |
|
|
typhoid fever, Salmonella
|
isolate from blood, stool, or urine
test for elevated or rising O and H agglutinins between 1st and 3rd week--febrile agglutinins test rise in Ab to Vi antigen to diagnose |
|
|
typhoid fever, Salmonella
|
fluoroquinolones (ciprofloxacin or 3rd generation cephalosporins
chloramphenicol, ampicillin, tremethoprim plus sulfa chronic: ampicillin or cipro, cholecystectomy |
|
|
typhoid fever, Salmonella
|
only infects man, not animals
vaccination only for those at high risk: deficiency in gastric acid, defects in cell-mediated immunity, HIV patients, patients with splenectomy, sickle cell disease |
|
|
typhoid fever, Salmonella
|
old vaccine is saline suspension of heat/phnol-killed S. typhi, 51-67% vaccine efficacy
two available currently: oral live (4 doses), attenuated not for children less than 6 years Vi capsular polysaccharide vaccine (ViCPS) for intramuscular use, 2 weeks prior to exposure, 50-80% of recipients protected |
|
|
Salmonella choleraesuis, septicemia
|
high fever and bacteremia usually without GI involvement
may occur in patients with sickle cell anemia, cancer, or young childre. osteomyelitis due to bacteria in child with sickle cell anemia |
|
|
Salmonella choleraesuis, septicemia
|
suppurative lesions during bacteremia almost anywhere in body: local abscesses, cholecystitis, pericarditis, meningitis, osteomyelitis. extra-intestinal infection in association with underlying chronic diseases or impairment of host defense
|
|
|
Salmonella typhimurium, enterocolitis
|
confined to GI tract, blood cultures positive in 5-10% patients
most common form of Salmonella infections 8-48 hrs after contaminated food consumption sudden onset with headache, chills, abdominal pain, nausea, vomiting, diarrhea, accompanied by fever. endotoxin release upon invasion of epithelial tissues of small and alrge intestins 6-8 hr after ingestion lasts 1-4 days, selflimited |
|
|
S. typhi (enteric fever) and S. choleraesuis (septicemia)
|
blood cultures positive in these types of Salmonella
|
|
|
Salmonella typhimurium, enterocolitis
|
almost all of 1500 seotypes cause gastroenteritis
transmission patterns differ from typhpoid fever, reservoir determined by serotypes in domestic animals |
|
|
Salmonella typhimurium, enterocolitis
|
domestic nanimals fed bacteria-laden meat scraps
poultry, eggs, pork, dog food, domestic turtles, pork sausage are common sources of contamination |
|
|
Salmonella typhimurium, enterocolitis
|
Salmonella common in developed and developing countries
|
|
|
Salmonella typhi
|
Salmonella common in developING countries
|
|
|
Salmonella enteritidis
|
Salmonella serotype most frequently involved in egg contamination
|
|
|
Salmonella typhimurium, enterocolitis
|
fruits when contaminated in field by animal or human fecal matter, spread this type of Salmonella
|
|
|
Salmonella typhimurium, enterocolitis
|
diagnosis dependent on finding organism in feces or fecal swab
H and O agglutinins useful at late stage, for species ID |
|
|
Salmonella typhimurium, enterocolitis
|
mostly self limiting
replace fluid and electrolytes treatment with antibiotics where underlying predisposing conditions type of salmonella |
|
|
shigella and salmonella
|
doesn't ferment lactose
|
|
|
Shigella (contrast with Salmonella)
|
non-motile
|
|
|
Shigella (contrast with Salmonella)
|
do not produce gas from glucose
|
|
|
Shigella (contrast with Salmonella)
|
doesn't produce H2S
|
|
|
Shigella (contrast with Salmonella)
|
LPS polysaccharide O antigens only, no H antigents (no flagella)
|
|
|
Shigella
|
more difficult to recover from feces
|
|
|
Shigella
|
produces disease only in humans, inhabits human intestinal tract, no animal reservoir
spread by Food, Feces, Fingers, Flies, especially in overcrowded conditions once ingested, invades intestinal epithelial cells after 1-4 days incubation |
|
|
Shigella
|
facultative intracellular organism, growing within host cells during infection
|
|
|
Shigella
|
penetration beyond submucosa rare, rarely cause bacteremia
|
|
|
Shigella (contrast with Salmonella)
|
inoculum needed to initiate disease is low, easily transmitted by fecal-oral route in daycare and mental hospitals
can resist killing by stomach acid, can infect at low numbers |
|
|
Shigella (contrast with Salmonella)
|
produces bloody diarrhea by invading cells in terminal ileum and colon )mucosal ulcerations with PMN and bacteria enmeshed in fibrin)
|
|
|
S. dysenteriae
|
exotoxin, cytotoxin called Shiga toxin
contains A/B polypeptide subunits B=receptor binding subunit to bind to intestinal epithelial cells, A enters cell to inactivate 60S ribosome, stopping protein synthesis |
|
|
Shiga toxin, Shigella
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causes fluid secretion
blocks fluid absorption in intestine kills absorptive epithelial cells, bloody diarrhea from invasion of epithelial cells and blockage of lfuid absorption (in cholera there is active fluid secretion) |
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Bacillary dysentery, S. dysenteriae
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characterized by sudden onset of abdominal cramps, diarrhea and fever following incubation of 1-4 days. diarrhea watery at first but later contains blood and mucus
diarrhea may occasionally be severe; may cause dehydration and electrolyte imbalance, particularly in infants and young children diarrhea usually self-limiting last a few days mucus and blood and PMN in stool are common, blood cultures usually negative send stool for PMN's, indicator of invasive disease |
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Bacillary dysentery, S. dysenteriae
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identification of organism from feces, Gram- rods, non lactose fermenting, no gas, no H2S, nonmotile
clinical symptom difficult to differentiate from other GI diarrheal diseases. get stool culture for diagnosis |
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Bacillary dysentery, S. dysenteriae
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most important therapy is fluid and electrolyte replacement
antibiotics effect not dramatic (cipro, trimethoprim-sulfa) no antibiotics for mild cases. many strains carry R factors for ampicillin resistance |
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Bacillary dysentery, S. dysenteriae
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caused by Food, Fingers, Feces, Flies
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Bacillary dysentery, S. dysenteriae
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vaccine: little immunity, not very effective. organisms clear in week but small % people have more persistent carriabge
live avirulent oral vaccines not successful |
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Rickettsia and Chlamydia
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small, 300nm
obligate intracellular growth NOT viruses contain both DNA and RNA binary fission susceptible to antibiotics, esp tetracyclines own protein synthetic machinery bacteria-like cell walls, related to gram neg |
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Rickettsia and Chlamydia, Mycobacterium leprae
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only obligate intracellular bacteria (others are facultative intracellular)
intracellular during infection but can grow extracellularly both in vivo and in vitro |
