streptococcus: gram, catalase, breathing
gram positive, catalase negative, aerotolerant
streptococcus: how are they classified?, describe
hemolysis and lancefield (alpha = translucent, beta = transparent, gamma = none), (a-u depending on carbohydrate antigen in the cell wall)
what streptococcus are beta hemolytic?
group a (most pathogenic; pyrogenes) and group b (aglaciae
what strep are alpha hemolytic
strep pneumonia and virians strep
what strep are gamma?
group a strep: shape/size/color, hemolytic size/type, what is essential to its virulence?
small, round, 0.5-1mm, white, beta hemolytic large around colony, m protein (80 serological types)
what determines group a strep pathogenicity?
antiphagocytic crap, hydrolytic enzyme, exotoxin
where are group a strep present in flora/ what's the percentage
what diseases are caused by group a strep
pharyngitis, middle ear, sinusitis
scarlet fever, rheumatic fever, puerperal, cellulitis, erysipelas, pyoderma,
TSS, necrotizing fasciitis, glomerulonephritis
rheumatic fever: cause, symptoms, after implications
antibodies confuse heart antigens with group a strep,
carditis, arthritis, skin nodules
what was the #1 infectious disease in children in the 1900s
group a strep scarlet and rheumatic fever
identification of group a strep, treatment, prevention
taxo a (bactricin), immunology with antibodies, gram positive diplococci in skin lesions
penicillin, erythromycin if allergic
ANTIBODIES: m protein of s pyogenes, can't get immunity bc 80 m protein strains, no vaccine b/c so many AND can infect heart
what diseases does s galactiae cause? normal age of victim? percentages? treatment/prevention?
pneumonia/septicemia/meningitis, neonate, 3/1000 is life threatening, 60% get infected, 25% get neuro damage, 5% die
penicillin G, prophylactic to mom or imminization
what diseases to strep viridians cause?
caries (mutans), dental abscess (mixed with anaerobic), infective endocarditis (osler nodes, embolism, splinter hemorrhage, heart attack, stroke)
where does strep pneumoniae colonize in flora/percentage? what infections does it cause
pneumonia, otitis media, sinusitis, meningitis, endocarditis
who are victims of strep pneumoniae
virulence factors of strep pneumoniae
phosphorocoline: induce phagocytosis
polysac capsule (93 of them)
iGa protease: covers/protects mucous membranes, destroyed, the complex is swept up to the throat and swallowed
pneumolysin: lyses ciliated cells and disrupts lysozymes
- how many get hospitalized/ who are usual victims
- aspiration of pneumoniae into lungs
- difficult breathing, fluid in alveoli/inflammation, chills, fever, sputum
- 60% hospitalized, usually old/young people AFTER a viral infection
what's the most common cause of sinusitis?
viral, but s pneumoniae is common for bacterial (usually secondary after viral
what's the most common cause of otitis media? how long does it last?
s pneumoniae, self-limiting 4-6 weeks
what bacteria causes meningitis and endocarditis when it gets in blood?
what's the most common cause of meningitis in the US? how many per year?
- s pneumoniae (life threatening)
how do you diagnose s pneumoniae? treat? prevent?
- observe gram + diplococci in sputum or CSF
- penicillin (but 40% resistant)
- vaccines: 13 strains for 2 months of age, 23 strains for >65 years
what were enterococcus once classified as? what type of diseases? victims?
group d pneumoniae
- opportunistic infection, old/compromised
treatment of enterococcus
- most resistant to all antibiotics but vancomysin, 30% resistant to that and can't be killed w any antibiotic
- can transmit to MRSA on plasmids
- ubiquitous in feces, resist desiccation, hard to avoid in hospitals
bacillus: gram, breath, how many species, which are pathogens
gram +, aerobic/facultative anaerobe, 70 species, b cerus and anthracis are pathogen
virulence features of b anthracis
-anthrax toxin: lethal/protective/edema chain
- pyrogenic toxin
how do humans get b anthracis
- food (most common for animals)
- contact (most common for humans)
how many anthrax cases
15 in the last 30 yrs
mortality rate/symptoms of gastrointestinal anthrax
- 75-100% mortality
- diarrhea, hemorrhage, perotinitis
cutaneous anthrax symptoms, how does it effect the body as it continues
papule in 12-36 hours, pustule (black) after that with scab (eschar) on top
- 80% is self limiting, 20% go to lymph and cause fatal septicemia
inhalation anthrax: mortality/symptoms
- flu symptoms, the pneumonia/shock/death
- 75-100% mortality with treatment, bio warfare
treatment b anthracis
- penicillin resistant normally
b cereus: virulence
- 2 toxins: one heat stable/vomit, another like cholera/diarrhea
where are b cereus commonly found (food)
- beans/rice, asian/mexican restaurants
diagnose b cereus/treat/prevent
- 10^5 per gram food
- self limiting = no treatment
- prevent: proper temperature storage of food
virulence of c perfringens
- 11 exotoxins
where are c perfringens found usually
- gi tract, soil/water
mortality rate of gas gangrene
-40% with treatment
diagnose c perfringens
- food: 10^5 food, 10^6 feces
- gas gangrene: symptoms
treat c perfringens
- food: self limit
- gas gangrene: penicillin, NO vaccine, amputation, hyperbaric chamber
virulence of c difficile
- 2 exotoxins, kill mucous epithelial cells/hemorrhagic lesions
how many infections of c difficile per year? deaths? percent of hospital and non hospital? death rate over 65? cost for hospitals?
- 337,000 infections per year
- 25% hospital, 75% not
- 90% death over 65
- 1 billion dollars for hospitals
how is c difficile spread?
- hand contact
c botulinum virulence
- neurotoxin, 7 strains (a-g) abe are for humans
- deadliest toxins
how does c botulinum work
- neuromuscular junction = paralysis
3 forms of botulism
- food borne
what foods does food botulism infect
- meat, fish, honey, veggies
symptoms of botulism (food and wound), what causes death
- blurred vision, bad speech/swallow, constipation, weakness, paralysis
- diaphragm paralysis = death
how many cases of food botulism per year
- 25 cases
what age is the cutoff for infant botulism, why
- 9 months (normal flora not established)
how many infant botulism cases? percentage of mortality? symptoms? what is the most common cause
- 100 per year, 3% mortality
- crying, weakness/paralysis, constipation
- honey most common cause
cases of wound botulism per year?
- 10 per year
mortality rate of botulism if not treated? how is it treated? mortality if it IS treated?
- antitoxin (NOT antibiotics... antibiotics/flushing system can be used to prevent further infection)
^ this changes the mortality to 10%
- sterilize canned food
- refrigerate/ use nitrite/ acidify to 4.5ph
- heat canned food before eating
- don't eat spoiled food, idiot
- don't give honey to bebes
commercial uses of botulinum
- botulism toxin a is used to stop muscle contractions
- botox (1.3 billion dollars per year)
clostridium tetani virulence features
- tetanus toxin (neurotoxin with 1 antigen and 2 polypeptide chains)... ON PLASMID
- terminal endospores
how does tetanus work
- moves to motor neurons, inhibits relaxation (lockjaw)
mortality of tetanus if treated/if not? deaths per year? who affected?
- 50% treated, 100% if not
- 1,000,000 deaths per year, babies in undeveloped countries
treatment of tetanus
- antitoxin, use antibiotics ONLY to prevent further production
- remove wounds
- tetanus toxoid vaccine (dpt)
- booster every 7-10 years
s aureus pneumonia: who gets it, mortality rate, leading cause of what type of pneumonia
- 50% mortality
- leading cause of ventilator pneumonia : 24%
- cystic fibrosis, ventilator, measles (young), flue (old)
treatment of staph
-methicillin (95% penicillin resistant, 40% meth resistant, in which case use vancomycin)
- surgical drain abscess
- hand antisepsis
does listeria monocytogenes make spores? what type of infection do they cause?
- chronic intracellular infection: stillborn, meningitis, abortion
L monocytogenes virulence features
- NO toxins or enzymes
- produce an adhesin, invasin, listerolycin O (avoids phagosomes), induce microfilaments to transfer them to new bacteria
how do people usually get L monocytogenes
- cheese, meat, undercooked poultry
- newborns get it from birth canal if mother has it/ placenta
what are the symtpoms of L monocytogenes?
- flu-like symptoms, diarrhea
mortality rate of L monocytogenes in immunosuppressed/infants? how many cases per year?
- 20% mortality
- 800 cases per year
- presence of bacteria in CSF (rare because not many bacteria are needed for infection)
- cold enrichment (4 degrees C) is slow but effective because few other bacteria grow at this temperature
- tumbling motility
- DNA tests
prevention of L monocytogenes
- pasteurize food/ cook
- many food recalls... LM CANTELOUPES killed people in 2011... AHH!
corynebacteria: shape, where does it colonize?
- pleomorphic, irregular
- humans, animals, soil/plants because of G+C content
+++ skin, respiratory, GI, genital/urinary
how does corynebacteria divide?
- snapping division, makes 2 daughter cells attached together into Y V or palisade shapes
how does corynebacteria cause disease?
- diptheria toxin
- opportunistic infections
composition of diptheria toxin
- A strand ADP ribosylates proteins and inactivates them
- B strand binds to surface antigens
how does corynebacteria get the diptheria gene? how many antigenic types?
- lysogenic prophage
- 1 antigenic type
how does diptheria cause disease?
- when there is iron deficiency in patients
- inactivates protein synthesis
where does C diptheria colonize?
who gets diptheria?
- young kids (don't have natural immunity yet)
if you get C diptheria on the skin, what happens? throat?
- skin = natural immunity
- throat = diptheria
symptoms of diptheria
- bulged neck, pseudomembranous growth, prostration, dyspnea
where can the diptheria toxin infect?
- heart (arrhythmias, most common cause of death)
*** THE TOXIN DOES THIS, THE CELL ITSELF CANNOT SPREAD
C diptheria symptoms in immunized patients
- asymptomatic or mild flu-like symptoms
cutaneous diptheria: how is it caused, symptoms
- caused when wound is infected
- oozing, pseudomembrane, unable to heal
- antibiotics don't work against toxin, can be used to kill CELLS
- tracheostomy if airway is blocked by pseudomembrane
how is diptheria prevented
- dpt vaccine: ages 2, 4, 6, 15, 65, and a booster in adults every 10 years
what bacteria causes acne?
what is cystic acne? how many people get it per year/age group?
- serious acne, usually scars
- 350,000 teens per year
- usually just soap
- serious cases need accutane
accutane side effects
- birth defects, stomach bleeding, lowered flora (opportunistic infections)
nocardia: breath, shape, where are they found
- branching filaments, break into rods or coccus
what type of infection does nocardia cause?
what are the important species of nocardia
- asteroides (lung disease, common in US)
- brasilienes (tropical... warmth beaches summer happy)
where does nocardia cause infections
- lungs, then can spread to BRAIN, kidneys, skin
cutaneous nocardia: how is it caused? what conditions are caused by it? what geographic area is it usually found in?
- soil into a wound
- madura/mycetoma: painless lesions
actinomyces: breath, shape
- branching filaments
what is actinomyosis? where does it infect?
- chronic, suppurative, granuloma
- usually head and neck, can also be pelvis/thorax
where is actinomyces found?
- mouth, GI, genitourinary tract
how does actinomyces infect
- not very invasive
- occurs when mucous membrane is injured
what strains of actinomyces cause actinomyosis normally
- mostly israelii
- also vicsosis, naeslundii, propionica
what are the physical characteristics of cervicofacial actinomyosis?
- minor pain
- hard/pus filled nodule around head/neck
- *** one or more draining sinuses
- ** suppurative inflammation
- ** sulfur granules
- drain lesions
- antimicrobials for 4-12 weeks
mycobacteria: breath, shape, special characteristics (2)
- mycolic acid AND acid fast
mycolic acid: what percentage of cell wall weight? characteristics of mycobacteria because of it
- slow growth
- protects from phagocyte killing/can grow in phagocytes
- detergents/stains don't work
- forms matted colonies
what mycobacteria species are overt pathogens and what disease do they cause
- m tuberculosis/ m bovis: both cause tuberculosis
- m leprae: leprosy
what mycobacteria is in the normal flora of human skin?
- m smegmatis
mycobacteria opportunistic species, and what diseases are caused
- m ulcerans , m fortuitum-chelonae, marinum: WOUNDS/SKIN ABRASIONS infections
- m avium-intracellulare/ m kansasii: tuberculosis-like disease, GI infection
- m scrofulaceum: lymph node/bone infections in children/ AIDs patient (ESPECIALLY cervical lymph nodes
virulence features of m tuberculosis
- NO toxins or enzymes
- induces harmful host immune responses
- replicates in macrophages
cord factor: what is it?
what bacteria has it?
what does it do?
- in mycobacteria tuberculosis
- attaches cells together in a serpentine fashion, also causes inflammation (causes inflammatory cytokine activation)
what are sulfitides?
- mycosides that inhibit lysosome/phagosome fusion = m tuberculosis can survive in cell
what is wax d?
- mycoside that causes delayed hypersensitivity (causes most damage in host)
what does m boviis cause? (disease)
tb in cattle
how much of the population in the world has tb? in the US?
- 1/3 of the world aka 2 billion
- 15,000,000 US (5%)
how long can m tuberculosis survive in the air?
- dried droplets = ***8 months!
how is m tuberculosis transmitted? m bovis?
- m tuberculosis is usually caused by inhalation, but can be from food
- m bovis is opposite: usually gotten from food, but can be from inhalation
what is the #1 cause of death from a single microbe?
how many new cases of tuberculosis per year in the world? in the US? how many US deaths?
- 8,000,000 globally
- 12-15,000 US
- 1,000 deaths
who gets most of the tb infections? what is the biggest risk factor?
- people who already had it (reactivation)
- HIV patients
- immunosuppressed is the worst thing for it
what disease has primary, secondary, disseminated (miliary) and ingestion infections?
primary TB: where does it cause infection? how does it progress?
- 95% get arrested infections
5% get progressive primary**
what percentage of people get reactivated tb? how long does it usually take?
- 2 years after primary infection
how many cells are required for a tb infection?
- 10 cells
how does tuberculosis cause disease in the body?
- infects macrophages in lungs, which are taken to lymph nodes, which causes TH1 lymphocytes to be activated and form a *tubercule aka * granuloma around the cells and causes *delayed hypersensitivty
if you have a BCG vaccine or a tb infection, what will occur for the rest of your life?
a positive tuberclin skin test
where does tb disseminate to where
- lymph nodes
- joints/bones/muscle (**hunchback)
what disease causes caseous necrosis
what disease gets a ghon complex? how many people get it (%)? what is it?
- it's an immpenetrable mass on x rays from the granulomas
what is the only sign that someone has had a primary infection (after it has passed) of tb?
tuberculin skin test
what does progressive primary tb progress into?
- miliary tb (disseminated in blood)
who usually gets progressive primary tb?
- AIDs patients, kids under 5, old people
why does reactivation of tb happen? who usually gets it?
- viable tb come out of the granuloma
- elderly people/AIDs/anything immunosuppressed
- since they're immunosuppressed, it's fatal without drugs
secondary tb: effects when acute? chronic? is acute or chronic more common? what percentage gets lesions at other places
- acute: pneumonia/miliary
- chronic: MORE COMMON, destroys lung tissue slowly
- 70% get lesions elsewhere
are people with secondary tb infectious? why?
- the bacilli are replicating in bronchioles = very easy respiratory transmission
what are the symptoms of chronic secondary tb?
- fever, night sweat
- weight loss
miliary tb: how does it spread? what does it look like? what does it cause? how many people get it (%)
- macrophages take it throughout the bloodstream to other organs
- small tubercles all over organs
- 30 % get it
- causes wasting**
how long does it take for a sample of tb to be cultured
- 3-6 weeks
what tests are used to detect tb?
- acid fast is ineffective
- rna/dna analysis are used
what does a positive tb test entail
red, has an induration: 1cm or less in size
treatment of tb
- drug cocktail, 12-18 months long with isoniazid and rifampin
how do you know if a patient is taking the drug cocktail for tb?
- rifampin causes orange pee
side effects of treatment for tb
delayed hypersensitivity and liver disease
what issue is occuring with treating tb?
- isoniazid and rifampin resistant strains are being made
how can tb be prevented?
- US doesn't use it because it causes a positive skin test, even if you haven't had the disease
who should get tested for tb regularly?
what bacteria effects macrophages and peripheral nerves?
why is m leprae not well understood?
can't be grown artificially.... just in humans and armadillos (random...? lolz)
how many stages of leprosy are there
what tissues does m leprae grow on (body regions)? why>
- skin, superficial nerves, throat, superficial areas
- superficial areas because optimal growth is at 30 degrees celsius
what are the most important types of leprosy? what are they characterized by?
tuberculoid: skin lesions, loss of feeling in peripherals, few visible cells in samples, strong immune response and positive lepromin test***
lepromatous: loss of feeling, many cells in samples, small immune response, negative lepromin test, lepromas**** aka thick nodules on face/hands
why is leprosy hard to diagnose?
long incubation period: 3-10 years
how is leprosy treated?
- drug cocktails: dapsone and rifampin, as well as clofazimine
are lepers confined to colonies as in history?
- no, prevention is effective through drugs/bcg vaccine
what is the 3rd leading cause of death in AIDs patients?
mycobacteria: opportunistic infections
which mycobacteria is the most common cause of opportunistic infection in AIDs patients? how is it transmitted?
- m avium-intracellulare
- food/water, affects peyers patches in intestines