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81 Cards in this Set

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General Properties of the Streptococci
(gram + or -, arrangement, catalase?, oxygen use?, etc)
-Gram Positives
-Arranged in Chains or as diplococci
-Capsules impede phagocytosis--thus opsonins are primary mediator of immune response
-Catalase Negative (opposite Staph)
-Mostly facultative aerobes
-Close relation to lactococcus and enterococcus
What bacteria cause subacute endocarditis? Often a result of bacteremia caused by dental treatment.
-Alpha-hemolytic strep cause INFECTIVE endocarditis:
Includes all of Viridans group: mitor, salivarius, sanguis, mutans, pneumonia
-S. pyogenes (Beta-hemolytic) caues endocarditis by causing rheumatic fever--but NOT infective endocarditis usually.
Streptococcus pyogenes
(lancefield group, diseases caused, how spread, virulence factors, treatment, type of hemolysis)
-Lancefield Group A (most pathogenic)
-Diseases:
Pharyngitis (strep throat), Scarlet Fever, Rheumatic Fever, Acute Glomerulonephritis, Necrotizing Fascitis, Impetigo (pyoderma), ersypelas, cellulitis, Strep toxic shock syndrome, Bacteremia, endocarditis.
-Virulence Factors:
M protein, lipoteichoic acid, F-protein, Adhesins, Capsule, Strep pyrogenic exotoxins, superantigens, Streptolysins S and O (hemolysins), Streptokinases A & B, DNases, Hyaluronidase, C5a peptidase.
-Treatment:
Usually penicilin--if allergic then erythromycin or cephalosporins. Oxacillin or vancomycin if mixed with staph also. Pre med people with history of rheumatic fever or heart valve deformities with amoxicillin, or clindamycin if alergic
Beta Hemolytic
Streptococcus agalactiae
(lancefield group, disease, areas affecte)
-Lancefield group B
-Disease:
Septicemia, pneumonia and meningitis in newborns (acquired during birth), doesn't usually affect adults--but can colonize urinary tract or GI tract, associated with abscess formation.
-S. anginosus group is similar in disease causing
Streptococcus pneumoniae
(Lancefield group, disease, virulence factors, detection, treatment)
-Not grouped by Lancefield system
-Disease:
Usually infects lower respiratory tract--involving alveoli, often secondary infections since part of normal flora, can spread from oropharynx to lungs/ sinuses/ear/meninges, most common hospital fatality, spreads to meninges via blood stream causing a meningitis more severe than most--usually in kids, Lobar pneumonia in lower lungs is usually this bac.
-Virulence Factors:
Not as many as pyogenes--but can be invasive in respiratory tract and invoke immune respones. Pneumococci strains differentiated by distinct capsule polysaccharides, sIgA proteases, pneumolysin (lyses ciliated cells).
Detection:
Bile solubility test (bile lyses them); They release C polysaccharide--adding C reactive protein precipitates it.
Treatment:
Was penicillin--but resistance is emerging--some strains resistant to many antibiotics, there's a vaccine made from 8 strains.
Bacterial Endocarditis infections consist of:
fused platelets
fibrin
masses of bacteria
Scarlet Fever
How does it come about? Symptoms?
A complication of streptococcal pharyngitis
Expression of pyrogenic toxin under control of lysogenic phage
Toxin produces pink rash, initiates fever
Rheumatic Fever
Antibodies formed against streptococcus react with heart tissues. (mostly group A strep--pyogenes)
An autoimmune disease
Can damage heart valves thru cross antigenicity--damage can lead to endocarditis (bac growing on heart)
Recent S pyogenes infection may indicate. Often the infection has already been cleared.
Antibodies, not toxins cause this. And bac aren't on the heart, just antibodies (though can lead to damage, and then bac adhere)
Treat with penicillin and rest
Acute Glomerulonephritis
post-streptococcus pyogenes disease
(nonsuppurative) associated with streptococcal cross-antigenicity
acute inflammation of renal glmeruli
Resolves in 2-4 weeks
Impetigo
(pyoderma)
suppurative
Primarily caused by group A strep (S pyogenes)--followed by Staph aureus
Usually in hot/humid weather, in children with poor hygiene
Fluid filled pus vesicles on skin rupture easily.
Necrotizing Fascitis
Usually this gangrene flesh eating stuff is clostridium--but strep can do it also (pyogenes). (streptococcal gangrene)
Introduced by breaks in tissue
Causes extensive destruction
No antibiotic therapy works--have to aggressively remove infected tissue.
Erysipelas
Acute skin infection
Localized pain, inflammation, chills, fever
Often preceded by S pyogenes infection--see very red skin.
Cellulitis
-S pyogenes can cause
-Similar to erysipelas--but involves deeper subcutaneous tissues
-Local inflammation, and systemic signs.
-Can be treated with antibiotics
-Diffuse infection of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin. Caused by normal skin flora or by exogenous bacteria, and often occurs where the skin has previously been broken. Erysipelas is the term used for a more superficial infection of the dermis and upper subcutaneous layer that presents clinically with a well defined edge. Erysipelas and cellulitis often coexist, so it is often difficult to make a distinction between the two
Streptococcal Toxic Shock Syndrome
S. pyogenes
similar to staph toxic shock, except here you expect to see bac in blood. (bacteremia) And with strep often have necrotizing fascitis with it.
Leads to shock and organ failure
Tissue destruction from pyrogenic exotoxins produced
S. pyogenes virulence factors:
M protein
Lipoteichoic Acid
Adhesins
Capsule
Streptococcal Pyrogenic Exotoxins
Streptolysin O
Streptolysin S
Streptokinases A and B
DNases
Hyaluronidase
C5a peptidase
-M Protein: Antiphagocytosis, Adhesion promoting, Anti-complement (degrades C3b).
-Lipoteichoic Acid: facilitates adherence
-F-protein: part of cell wall, for adherence
-Adhesins: M and F proteins, and lipoteichoic acids.
-Capsule: antiphagocytic, composed of hyaluronadate--which is in ground substance--so body doesn't see as foreign.
-Pyrogenic Exotoxins--superantigens, inappropriately activate T cells = too many cytokines. Cause rash of scarlet fever. Phage conversion is responsible--non toxogenic strep throat strains infected by phage--become toxogenic.
-Streptolysin O: a hemolysin--lyses RBC's, WBC's, platelets. immunogenic. Oxygen labile. ASO test finds. But skin infections may give false negs because cholesterol in skin lipids deactivates it.
-Streptolysin S: stable in O. responsible for beta hemolysis in blood agar. non immunogenic. Lyse phagocytes if eaten. lyse same things as streptolysin O.
-Streptokinases: A and B. Cleave plasminogen to plasmin--which is an active proteolytic enzyme--and lyse clots to enable spreading.
-DNases: enable spreading--depolymerize nucleic acid of lysed cells to make less viscous so can move.
-Hyaluronidase: spreading factor--breaks up ground substance
-C5a peptidase--degrades C5a compliment protein, which activates phagocytic cells and promotes inflammation.
Pneumonia
caused by bac, viruses, or fungi
characterized by chills/fever, cough, blood tinged sputum.
Bronchopneumonia
inflammation of smaller bronchial tubes, caused by many microbes:
S aureus, Haemophilus influenzae, klebsiella pneumoniae, etc.
S. viridans
(group, hemolysis, nutrition required, disease caused, etc)
No lancefield grouping
Contains cariogenic strep
S. mutans, S. salivarius, S. mitis
All are alpha hemolytic--most streptococcal species of mouth are.
Require enriched blood agar for growth
Can be found in oropharynx, GI tract, and Urinary tract as well as mouth.
Disease: dental caries, subacute endocarditis (acute is staph aureus), intra-abdominal infections.
Most susceptible to PCN
Named viridans because can make green pigment in culture.
Enterococcus
(Grouping, disease, treatment, etc)
Previously grouped as group D strep--possess group D antigen.
Part of normal GI flora.
A dangerous nosocomial pathogen--has resistance to Abx.
Often causes disease as result of broad spec Abx. (usually cephalosporins--naturally resistant).
2 key species: Enterococcus faecalis & faecium
Disease: leads to bacteremia, endocarditis, peritonitis, UTI's, wound infections. 10% of all nosocomials.
Treatment typically with vancomycin, but resistance is growing--so often combine Abx--aminoglycosides + cell wall inhibitor.
Streptococcus classification schemes.
Lancefield grouping (serological): Groups A,B,C, etc. Carbohydrates (C carbohydrates) of cell wall/capsule act as immunogens. Allows some rapid clinical tests. S. pyogenes is group A--which is most likely to cause disease. pneumoniae and viridans not grouped.
Hemolytic Patterns:
Alpha hemolysis: incomplete hemolysis. Blood agar can turn green from loss of K from RBC's.
Beta Hemolysis: complete lysis of RBC's--see clear zones.
Gamma Hemolysis: non hemolytic strep. produce no phenotype on blood agar.
Biochemical and physical properties.
Endospores
(what bac produce, diseases caused, structure)
Made by gram + (Clostridium & Bacillus)
Resistant to heat/drying--autoclaves best.
Structure: Spores are dormant--no metabolic action taking place. Water removed. Spore coat proteins on outside for stability. Below that is the peptidoglycan cortex. Below that is the spore protoplast (core)--consists of DPA, SASPs, cytosol, DNA). DPA (dipicolinic acid) binds Calcium at high levels and assist in heat resistance. SASPs (small acid soluble proteins) bind DNA to protect it.
Dormant spores have a thick coat, active (germinating spores) have a thin coating.
Germination: when spore releases growing cell when food/water become available.
Diseases: botulism (Clostridium botulism), gas gangrene (C. perfringes), Tetanus (C. tetani), Anthrax (Bacillus anthracis).
Some gram - produce myxospores--not as strong as endospores.
Bacillus anthracis
Gram + rods (bacilli means rod). Seen in chains or pairs.
Facultative aerobes (distinguishes Bacillus from Clostridium)
Virulence factors: Spores. Antiphagocytic capsules. Edema Toxin--affects adenylate cyclase activity--leads to fluid accumulation. Lethal Factor--a zinc metalloprotease--stimulates cytokine release from macrophages.
Spores present in 2-3 day old cultures--usually not found in clinical specimens?
Disease: Cutaneous Anthrax--red skin and papule develops on skin--can rupture and enter blood/lymph. 20% mortality. GI anthrax--rare, but fatal. Inhalation Anthrax--terrorist weapon--Can get processing goat wool--longer latent period--gives fever, cough headache at first stage--then massive enlargement of lymph nodes at second stage--95% mortality if not treated--due to shock--usually have meningitis with it as well.
Treatment: susceptible to ciprofloxacin--usually penicillin and doxycycline gets it too, but resistance reported. Vaccines available
Eradication unlikely--since lives in soil.
Two others of genus: Bacillus cereus, can grow on food and cause food poisoning via exotoxin. Bacillus stearothermophilus--used to monitor autoclaves.
Corynebacterium (Corynbacterium diptheriae)
General Info: Aerobic, Gram +, Non-sporulating, non-motile. HIgh lipid & wax content, but not acid fast. (dye not removed by acid)
Part of normal flora--Respiratory, GI, Urogenital tracts, skin.
Virulence factors: Diptheria toxin--an A-B toxin (two parts) that inhibits translation--B subunit binds, A subunit enters cell to cause damage--B binds heart and nerve cells mostly--Caused by phage conversion...endoded by tox gene by lysogenic bacteriophages (not transduction).
Disease: Diptheria--spread by skin contact/droplets. Humans only reservoir, but asymptomatic carriers, so can't eradicate. Mostly in kids. Gray/White exudate. Spots turn to pseudomembranous lesions. Can be respiratory (exudative pharyngitis), or cutaneous diptheria. The disease is caused by the toxin--which can spread and damage whole body.
Treatment: A diptheria anti-toxin given. Penicillin/erythromycin given. The DPT vaccine uses toxoids.
3 standard bacterial vaccines given in US
Diptheria, pertussis (whooping cough), tetanus bacterial vaccines routinely given to children in USA. Booster shots recommended.
Actinomyces
Gram +, anaerobic or facultative, rods, non sporulating, form branched hyphae.
Commonly in oral cavity--normal flora. In gingival crevice and tonsillar crypts.
Infections often follow dental procedures where mucosa broken.
Disease: Actinomycosis often misdiagnosed as neoplasm. Characterized by purulent exudates--described as sulfur granules--creamy yellowish granules. A tangled mass of actinomyces filaments with club like extensions.
Associate with branching, filaments. (same for Nocardia)
Nocardia
Gram +, strict aerobes, branched filamentous hyphae.
Closely related to Mycobacteria: have mycolic acids in cell wall--though shorter chains. Only weakly acid fast.
Opportunistic pathogen--on the rise due to HIV, etc.
Disease: Bronchopulmonary disease, Cutaneous infections
Mycobacterium
General Info: Can be considered gram + (though atypical structure--stain weakly). Acid fast because of mycolic acids (lipids) in inner leaflet. Known for lipids and waxes in cell wall making hydrophobic and resistant to destruction by immune system, disinfectants, acids/bases.. Nonmotile, aerobic, rods.
Disease: Cause granulomatous lesions in infected tissues. Usually cause lung lesions, also can spread to kidney.
Other Disease: Miliary TB--Disseminated TB, spreads via bloodstream--causing smaller lesions than original one. Mycobacterium leprae: causes leprosy--similar to TB. Mycobacterium avium complex: includes MAI--not really a problem unless get HIV.
Pulmonary TB: associated with granulomas. Primary TB is the early phase of infection. Ghon focus is a lesion at site of primary pulmonary infection. See giant cells, caseating necrosis associated with nodes of neck. Lesions do not produce bloody sputum. Secondary TB--develops long after primary infection--still associated with lungs, but can spread.
Do NOT produce either exotoxins or endotoxins.
Acid fast: treat with Zihl Neelson stain, followed by acid. Most bac lose stain with acid, not these. Structure of mycolic acids and basic fuchsin dye used in acid fast stain. Dye binds mycolic acids.
Very Difficult to Kill: mycolic acids prevent uptake of Abx. Clustering in Ghon complexes further inhibits access of Abx. Can be intracellular. Slow growth--makes less prone to Abx.
Treatment: Takes 6-12 months. Rifampin targets transcription. Isoniazid growth factor analog inhibits cell wall synthesis. There is a mycobacterium vaccine (BCG)--an attenuated mycobac--not used in US. Works best if given to kids--can't give to HIV, etc.
TB test: 1/3 of world has it--most don't know. Test--inject protein, watch for type 4 sensitivity.
Neisseria sp.
-General Info: Gram -, cocci, often in pairs (like 2 kidney beans--diplococci), strict aerobes.
-Some are part of normal flora.
-Humans only natural hosts
-Not very tough, so spread primarily by sexual contact.
-Neisseria meningitidis: Often in normal flora, spreads from oral pharynx to cause meningitis mosly in kids under 5. Spread by aeresol. Distinguished from N. gonorrhoeae because can utilize maltose as well as glucose. One of most common causes of meningitis along with strep pneumonia. Kills if untreated. Virulence Factors include: Pili, capsule, LP, IgAase.
-Neisseria gonorrhoeae: causes gonorrhea--2nd STD only to chlamydia. Commonly affects urethra, cervix, vagina--also throat, rectum, conjunctiva. Can disseminate and cause arthritis. 50% females have no symptoms--reservoirs. Can get in babies eyes at birth. Men get symptoms in 2-7 days--urinating pain, pus. Virulence factors: affinity for mucous membranes, pili attaches, opa protein for penetration, IgA protease, Beta lactamase.
Enterobacteriaceae family
Escherichia coli
Salmonella sp.
Yersinia
Klebsilla
Proteus
-Ability to become resistant key in hospital infections
-Commonly infect CNS, lower respiratory tract, blood, GI, urinary tract.
Eschericia coli
-General info: Gram -, rods, flagellated.
-Disease: most common cause of infected bladder, female UTI's, and gram - sepsis meningitis. Also causes 'travelers diarrhea' in US from food or water containing 'coliforms.' (killed people at Jack in the Box).
-Commonly found in GI tract--but when get a different strain, causes problems?
-Virulence:
EHEC: (Enterohemorrhagic E coli)--Express shiga toxins via lysogenic bacteriophages (phage conversion). Those toxins inhibit protein synthesis. Cause bloody diahrea.
ETEC: (erotoxigenic E. coli)--produce heat labile enterotoxins, which activate adenylate cyclase in enterocyte. Increased cAMP upsets ion balance, causes water to leave cell, causing 'travelers diahrea.'
Salmonella typhi.
-General Info: Gram -, facultative anaerobes, rods.
-NOT part of normal flora--boards (salmonella never are)
-Comes from animal products. Transmitted orally. (eggs/poultry).
-Disease: causes enteritis & systemic infections. Asymptomatic carriers a major hazard in typhoid fever (typhoid mary). All salmonella can cause bacteremia. S. paratyphoid causes paratyphoid fever--less severe form. S typhimurium causes enterocolitis--the one you get from undercooked chicken, etc.
-Treatment: Hydration and fluoroquinones. Resistance growing.
Virulence: Invade and replicate in M cells of Peyer's patches(lymph tissue in GALT). Prevent fusion of vacuole with lysosome--so can keep replicating in cell.
Shigella sp.
-Gram -, facultative anaerobes, rods.
-Spread fecal-oral route. Mostly in kids--often in day care centers.
-Disease: Commonly associated with bacillary dysentary (a form of gastroenteritis--watery diahrea. Can progress to abdominal cramps with or without bloody stool.
-S. sonnei--causes most shigellosis in US.
-S. flexneri--causes most in developing countries.
-Shiga toxins produced--exotoxin, disrupts protein synthesis. Expressed on large virulence plasmids.
-Can lyse vacuoles to prevent killing of phagolysosome? Mobilize cytoskeleton?
-Treatment: fluoroquinolones
Yersinia sp.
-Gram -, facultative anaerobes, rods.
-A zoonotic disease--infects animals and humans.
-Type 3 secretion system--molecular syringe--initiages apoptosis in bound macrophages.
-Y. pestis: causes bubonic plague--treated with streptomycin. Infections in squirrels, rabbits, field rats, etc.
-Y. enterocolitica and Y. pseudotuberculosis both usually self limiting.
Bordetella pertussis
-General Info: Small, gram -, cocci, strict aerobe, non-motile.
-spread by aeresols person to person.
-Disease: whooping cough
-Virulence factors: Pertussis toxin--an A-B toxin. Activates surface G proteins and turns on adenylate cyclase. Increased cAMP then increases secretions and mucus production--resulting in the famous cough.
Treatment: inactivated pertussis toxin used as vaccine--given along with diptheria and tetanus toxoids. Usually treat with macrolides.
Vibrio cholerae
-General Info: gram -, facultative, rods, halotolerant
-Infects GI tract only, spread by contaminated water or shellfish, not really from person to person.
-V cholerae O1 and O139 produce cholera toxin. Two biotypes of O1. Classical (old) and el tor (current) strains.
-Virulence Factors: Produce enterotoxins--exotoxins that act on small intestine. Cause diahrea. Another A-B toxin--B binds, A enters and activates adenylate cyclase. cAMP increased--causes ion flux, Na blocked out, Cl secreted.
Campylobacter sp.
-General Info: small, comma shaped rods, gram -.
-Disease: gastroenteritis & septicemia.
-C. jejuni = most common cause of bacterial gastroenteritis in US.
-C. coli also causes--not so much in US due to milk pasteurization.
Helicobacter pylori
-General Info: gram -, curved rods, very motile.
-Found in 70% of patients with gastritis, gastric ulcers. Peptic ulcers most commonly found in duodenum.
-Can live in stomach acid because produces lots of Urease.
Pseudomonas aeruginosa
-Gram -, rods, motile--polar flagella, obligate aerobes.
-Common nosocomial infections--resists disinfectants and Abx.
-Virulence factors: common in burn victims, cystic fibrosis patients. Exotoxin A inhibits protein synthesis. Elastases degrade elastase of ECM so can spread. Phospholipase C--heat labile, breaks down lipids and lecithin.
-Commonly infects pulmonary, skin, urinary, swimmer's ear, bacteremia.
Haemophilus influenza
-Multishaped (pleomorphic), gram -, facultative aerobes.
-Disease: 1. Pus forming Meningitis--usually unimmunized kids (2-3). 2. Pneumonia--usually adults.
-Vaccine: works for type B only. Made from capsule antigen. Now conjugated to protein so will work for infants too.
Legionella pneumophila
-Slender, pleomorphic, gram - rods, obligate aerobes, nutritionally fastidious.
-Can be intracellular parasites (prevent fusion of vacuole with phagosome) So immunity requires T cells to kill infected macrophages.
-Associated with cooling towers of air conditioning systems.
-Can survive chlorinatino by parasitizing amoebas.
-Disease: 2 forms. 1. Legionnaire's disease--severe form of pneumonia. 2. Pontiac fever--an influenza like illness.
Clostridium sp.
-Large rectangular gram +, form spores, mostly anaerobic
-4 most famous ones: 1. Clostridium perfringens 2. Clostridium tetani 3. Clostridium botulinum 4. Clostridium dificile
Clostridium perfringens
-Large gram +, rods, anaerobic, spore forming
-Disease: Cause gas gangrene (myonecrosis is another name). Occurs at wound sites--gas felt as crackly sensation when push on wound. Destroys tissue--necrosis from blood loss. Early symptoms--sweating, fever, anxiety, shock.
-Virulence Factors: 1.Lecithinase (phospholipase C or alpha toxin)--hyrdrolizes membranes of host cells. 2. Superantigen enterotoxin
-Diabetics commonly get in ischemic limbs.
Clostridium tetani
-Prevented with vaccine, boosters (DPT vaccine recommended for all kids (diptheria, pertussis, tetanus)
-Tetanus toxin is an A-B toxin.
-Enters through wounds--causes spastic paralysis and death. Toxin binds inhibitory neurons and prevents release of glycine (inhibitory neurotransmitter) onto motor neurons. Motor neurons constantly stimulated by acetylcholine.
Clostridium botulinum
-Gram +, anaerobic, rods
-Disease: 3 forms. 1. food poisoning (home canned veggies, cured pork/ham, smoked/raw fish) 2. wound botulism 3. Infant botulis (from eating honey 1st year).
-Botulism is an intoxication--not an infection (boards) doesn't even require presence of live organisms. Toxin blocks release of acetylcholine from pre-synaptic cleft--so can't stimulate muscles. Death when lungs fail--diaphrahm stops.
-Symptoms: 8-48 hours after ingestion. (staph toxin in 2-4 hours). Nausea, vomiting, dizziness, diplopia (double vision), dysphagia (difficulty in swallowing) muscle weakness, respiratory failure. NO FEVER (unless from wound infection).
-25% mortality from respiratory failure.
-Antitoxins slow further damage, but don't undo damage. Have to regrow axons to get better.
Clostridium difficile
-Spore forming obligate anaerobe.
-Part of normal flora. Wiping out normal flora with Clindomycin gives it the chance to thrive and cause Pseudomembrane colitis.
-Causes watery diarrhea/abdominal cramps. Yellow plaques lining colon.
-Can treat with vancomycin--or just fluid and discontinuing broad spec.
Actinomyces sp.
-Gram +, anaerobe or facultative, rods, non-sporulating. Form branched hyphae.
-Key in dentinal and root surface caries.
-A. israelii: causes actinomycosis. Part of normal flora. Infection arises with breach of mucosal tissue.
Actinomyces israelii
-Gram +, rod, facultative or anaerobic.
-Part of normal flora in healthy mouths.
-Disease: can cause Actinomycosis. An endogenous disease (normal flora). May follow surgical procedures. Accompanied by creamy yellowish granules called 'sulfur granules'--consisting of tangled filaments with club like extensions. Lesion often begins as hard, red, non-tender swelling abscess. Characterized by purulent exudate. Often mistaken for neoplasm--but infected tissue must be removed, and then treat with penicillin--so refer OS to be safe?
Lactobacillus sp
-Gram +, rods, aerotolerant anaerobes, acidogenic and acidouric--so cariogenic.
-Key in pit and fissure caries--along with S. mutans. These caries are most common.
-A secondary invader of caries (after strep mutans)
-Often found deep within carious lesion.
Bacteroides sp
-Gram -, rod, anaerobic, collagenase + (degrades collagen in chronic perio disease).
-Common colonizers (normal flora) of mouth and GI tract.
-Can cause disease as result of trauma getting it where shouldn't be.
-Also associated with chronic adult periodontitis--will see IgG antibodies in sulcus. Collagenase assists. Can cause trench mouth--Acute necrotizing ulcerative gingivitis thru polymicrobial infection.
-Treatment: clindamycin can be used here (for serious anaerobic infections)
-B fragilis: normal flora. Causes most anaerobic infections of peritoneal cavity.
-B melaninogenicus: higher concentrations in gingival crevice then on tongue or in plaque.
Other Gram - associated with disease of oral cavity.
-Porphyromonas gingivalis: can degrade collagen in periodontal disease via collagenase.
-Fusobacterium sp.: part of normal flora--implicated in perio disease. (F nucleatum and F polymorphum)
-Prevotella intermedia: associated with perio disease (P nigrescens isolated more from heatlhy gingiva)
-Prevotella and Porphyromonas sp referred to as black pigmented anaerobes.
-Veillonella sp: can metabolize lactic acid and reduce incidence of caries.
Spirochites
-Gram -, motile (flagella), tightly coiled (unique form)
-Dark-field microscopy useful for observing--light from side.
-2 main spirochetes: 1. Treponema pallidum: causes syphillis. 2. Borrelia burgdorferi: causes lyme disease.
Treponema pallidum
-A spirochete
-Gram -, coiled, motile
-Causes syphillis: 3rd most common STD.
-3 syphillis stages: 1. primary stage: non painful hard chancre at site of contact (can be oral)--occurs after 3-6 weeks. Infectious 2. secondary stage: highly infectious stage--6 weeks later. Maculopapular rash appears on skin and mucosa. 3. Tertiary stage: can occur in infected persons many years after treatment of secondary syphillis. Gumma typifies this stage--a non cancerous granuloma. Can cause neurological or heart problems, and can destroy any organ really.
-Congenital Syphillis: transmitted across placenta any time during pregnancy. Complications include hutchinson's teeth (widely spaced peg incisors) and mulberry molars, and saddle nose (sunken nasal bridge).
-Only affects humans. Wont grow in cell free medium. Use dark field to view.
-Treatment: PCN G
Borrelia burgdorferi
-Spirochete
-Gram -
-Disease: Lyme disease. Initial skin rash at site of tick bite. Untreated will progress to neurological and cardiac dysfunction, joint pain, arthritis.
-Leading vector born disease in US. Humans only reservoir.
-Treatment: Early symptoms treated with amoxicillin, doxycycline, ceftriaxone. Later with penicillin or ceftriaxone.
-Borrelia recurrentis: causes relapsing fever. Treat with tetracycline or erythromycin. Epidemic disease is louse born. Endemic is tick borne.
Mycoplasmas
-unusual for prokaryotes in that have no cell wall have sterols
-smallest free living bacteria
-can cause form of pneumoniae by colonizing respiratory tract
-can be diagnosed by serological tests or PCR
-erythromycin, tetracyclines and fluoroquinolones can treat
Rickettsia species
-gram -, cocci, very small
-Obligate intracellular parasites--once thought to be viruses for that reason (and b/c so small)
-Cannot be grown on media
-Diseases obtained via arthropods
-Mainly infect endothelial cells of capillaries and other small vessels.
-Causes swollen and necrotic vessels--and ruptured vessels.
-Symptoms: headache and fever followed by rash.
-Degrade phagosomes to avoid phagocytosis.
-Cause Typhus, Rocky Mountain Spotted Fever, Reckettsialpox (mild form of previous), Q fever (unique for airborne transmission--resembles influenza, no rash, etc)
Rickettsia prowazekii
-Gram -, cocci, very small obligate intracellular parasite
-Disease: Cause Typhus. An epidemic disease transmitted by louse. Bac introduced thru the bite, and they replicate in cells lining vessels.
Symptoms: fever, headache, fatigue, and eventually rash on whole body except face and palms.
Rickettsia rickettsii
-Gram -, cocci, very small obligate intracellular parasites.
-Named where discovered--actually more common in southeast.
-Transmitted by ticks
-Grow in nucleus as well as cytosol of cells (most rickettsii only cytosol)
-Symptoms: same as typhus, except could also have diahreah and vomiting.. Fever, headache, body rash all over.
-Rickettsialpox: a mild form of rocky mountain spotted fever that causes oral legions.

-Treatment: tetracycline, chloramphenicol.
Chlamydia sp.
-Similar to rickettsia in that they're obligate intracellular parasites. Have little metabolic activity. Also once thought to be viruses due to size and intracellular dependance.
-Presence of DNA and RNA differ from viruses. Viruses have one or other.
-Chlamydia trachomatis: leading cause of STD in USA. Many asymptomatic carriers. Often co-infection with gonorrhea. Cause inflammation of urethra--young women can have infected falopian tubes.
-Same bug above also causes Trachoma. eye disease causing vascularization and scarring of cornea.
-C. pneumoniae: causes pneumonia like symptoms.
-Life Cycle: 1. Elementary body(EB)--resistant to drying makes more spreadable, an airborne invader of respiratory system. 2. Reticulate body (RB): these are vegetative cells, divide by binary fission.
True or False:
Viral Genomes can be either DNA or RNA. Single stranded or double stranded.
True
True or False:
Viruses can affect animals and bacteria, but not plants.
False
Affect all 3.
Bacteriophages
-Viruses that infect bacteria
-genomes can be circular, linear or segmented
-resistance to bacteriophages provided by restriction endonucleases (enzymes)
-infection of bacteria leads to either lysis or lysogeny
-bacteriophages kill host cells through lysis whereas animal viruses can kill cells through either lysis or budding
Virion
A complete virus particle with its DNA or RNA core and protein coat (capsid) as it exists outside the cell. Also called a viral particle. No metabolic processes going on.
Nucleocapsid
-nucleic acid + protein and are symmetrical structures
-The nucleocapsids of viruses contain symmetry.
-Two kinds of symmetry are found in nucleocapsids;
1. Helical symmetry-in rod-shaped viruses and
2. Icosahedral symmetry-in spherical viruses
T or F
Naked capsid viruses are more environmentally resistant.
True
-more resistant to acid (of stomach), proteases, disinfectants, drying
-naked capsid viruses released from cell through lysis
-humoral immune response may be sufficient to clear
Enveloped Viruses
-protein containing membrane surrounds nucleocapsid
-released by budding (slow) or lysis
-more sensitive to environmental insults; acid, drying, heat, disinfectants & detergents
-must stay hydrated when spread; airborne droplets, secretions, sexual transmission
-cell mediated immune response often required to clear
Steps of viral infection
1-Attachment (also called adsorption)
2-Penetration- of virus into cells
for animal viruses, virion typically endocytosed
3-Synthesis of nucleic acid and protein
4-Assembly-of structural units and packaging of nucleic acid
5-Release-of mature virions into the cell
What is the most critical process determining host specificity of viruses?
Attachment
-Cell surface Receptors- facilitate specific attachment to components of virus.
-Receptors can be glycoproteins, glycolipids, lipids, or combinations of these.
-Cells can acquire resistance to viruses by not expressing the viral receptors, yet often the receptors are vital to the host.
-A cell that allows multiplication of a virus to take place is said to be permissive for that virus.
One step growth curve for viruses:
Name four steps
-Eclipse period- after virus has entered cells, nucleic acid is separated from protein--presence of infectious virus “eclipsed” if cells lysed open at this time
-Latent period period of time when no infectious virons are present extracellularly.
-Maturation phase is entered when nucleic acid are assembled with viral proteins to form infectious viral particles. The infectivity of the viruses increases dramatically during the maturation phase.
-Release of mature infectious viruses-occurs by cell lysis or by budding from cells and secretion.
What are the early viral proteins?
-Early proteins-synthesized soon after infection, usually in smaller amounts.
-Early proteins often required for expression and/or replication of genome
What are the late viral proteins?
-Late proteins- synthesized late in the infection are proteins that make up the virus coat, made in abundance.
T/F
Viruses use a wide variety of replication schemes
True
-Genome of virus dictates mechanism used
-DNA viruses utilizing host RNA polymerase & DNA polymerase must translocate to the nucleus
-single stranded DNA virus will require DNA synthesis step prior to transcribing viral genes (class II)
RNA viruses require unusual replication mechanisms.
-RNA dependent RNA polymerase
-Reverse Transcriptase
-these strictly viral enzymes make great anti-viral therapeutic targets
-single stranded RNA viruses can be classified as + or - based on orientation of genome to mRNA used in host cell--theoretically, exact same molecule of RNA could be + or -
-some can transcribe proteins directly off genome, but most viruses must first make mRNA
-yet all RNA viruses will require synthesis of more RNA genomes
-virus with SS RNA genome same orientation as mRNA is positive-strand RNA virus
-virus with SS RNA genome complementary to mRNA is negative-strand RNA virus.
-all negative strand RNA viruses enveloped also are double-stranded RNA viruses
-Retroviruses; RNA molecules that precede through DNA intermediate -require enzyme Reverse Transcriptase. SS RNA genome does NOT function as either + or - sense molecule--instead, SS RNA acts as template for production of viral DNA. ability of viral DNA to integrate into host genome can lead to alterations in host transcription leading to tumors
T/F
virus with SS RNA genome same orientation as mRNA is negative-strand RNA virus
False
Positive
T/F
virus with SS RNA genome complementary to mRNA is negative-strand RNA virus.
True
Nucleoside Analougues
-Antiviral
- Do have side effects--but affects RNA dependent RNA polymerases and reverse transcriptases more--since don't proofread. Also affects rapidly dividing viral infected cells more.
-These promote faulty base pairing or prevent chain elongation (a 3' hydroxyl group on analog does this).
-Base analogs resemble normal dNTP's used in DNA synthesis.
-Many viruses encode thymidine kinase to phosphorylate nucleosides and analogs (resistance?)
Base Analogs
-Antivirals
-2 types:
1. Base Analogs: resemble normal dNTP's used in DNA synthesis but have faulty base pairing properties. Produce mutations when replicate.
Protease Cocktail
-Treats HIV
-HIV cycle requires a protease to cleave a large polypeptide into active proteins.
-HIV protease--a dimer of identical subunits.
-HIV protease inhibitors dramatically increased life span and quality for HIV patients.
-Crixivan specifically inhibits HIV protease
Syncytium
-Formed between cells--permits virus to spread between cells without being exposed to antibodies.
-HIV and measles both use them.
Interferon and other Antiviral Immune Responses
-Helps distinguish viral from bac infection.
-Double stranded RNA recognizes viral infection, secretes interferons (IFN).
-Protects un-infected cells by inhibiting translation of that cell, and interfering with trascription of viral DNA and assembly.
-IFN alpha: secreted by leukocytes.
-IFN beta: secreted by fibroblasts
-IFN gamma: secreted by T and NK cells--these have more systemic effects--activate immune system.
-We can use IFN's to treat viral infections.
-Other viral responses: antibodies can be useful to prevent spread and attachment--but wont help latent infections, and can't access if passed between cells via a syncytium. CD8 T cells kill cells that are producing foreign stuff (presented on MHC 1). Th1 (CD4's) activate celular immunity. Th2 (CD4's) stimulate B cells to make Ab. NK cells kill cells that have downregulated MHC1's.
T/F
Encephalitis most often caused by bacterial infection
False
Viral
-an uncommon inflammation of the brain, usually caused by infections
-viremia can permit travel of virus to the brain
-white blood cells invade brain tissue while trying to fight off infection
-brain tissue swells (cerebral edema) processes can cause;
-destruction of nerve cells, bleeding within the brain (intracerebral hemorrhage)
-symptoms include- photophobia, fever, headache, vomiting and stiff neck and back
What tests are used to check for HIV?
-ELISA used initially--but gives many false positives.
-Western blot used to confirm. More specific.