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Mycobacterium tuberculosis
- causes tuberculosis (TB)
- -obligates aerobes
- acid-fast (neither gram neg or pos)
- cell wall made up of long chain of fatty acids (mycolic acid)- waxy, resistant to acid and bases, impermeable, resistant to dehydration
- spread by aerosol, lung infection, easily spread in close communities
- causes most death/year worldwide
- 1/3 of pop infected, 90% infected asymptomatic
- symptoms: fever, malaise, lung degeneration, chronic cough, septicemia, multiple organ failure, weightloss despite apetite/consumption
- virulence: waxy cell wall, no exotoxins, no LPS, major factor is ability to invade and survive within macrophages "exported repetitive protein" prevents phagosomes from joinign with lysosomez so bacteria are not exposed to degradative aspects of lysosome
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Disease progression:
bacterium inhaled into lungs, ingested by lung macrophages, reside and kills macrophage
inflammation- more phagocytes travel to site "exudative lesion"
ends up with a mass of live and dead bacteria- live and dead phagocytes surrounded by outer layer of macrophage "granuloma"- which then surrounded by fibrin and calcifies = tubercle- can be seen by xray, infection may stop at this point (latent) no symptoms
liquifaction: tubercle break through lung into blood vessels and travels throughout body (50% mortality rate)
tubercle can be coughed up and swallowed- becoming systemic via GI
can be reactivated
- Diagnosis: chest xray, tuberculin skin test (Mantoux test) - where purified protein derviatives, part of cell walls injected underskin, measure welts, cell mediated hypersensitivity rxn (type4) if Tc cells recognize teh PPD, positive rxn means your been exposed to the organism, could have active infection, been infected but asymptomatic, or have been immunized
- vaccine: BCG (bacilli calmete guerin)- made to stimualte cell mediated response, uses live attenuated M.bovis which causes TB in cows, most effective in children in endemic regions, some cases human contracts M.bovis from vaccine and unpasterized milk
- treatment: isoniazid (INH) most specific targets formation of cell wall, work on actively growing bacteria
- -also given rifampin and pyrazinamide (protein synthesis inhibitor) which work well on dormant bacteria and prevents reactivation
- -treatment daily for 6-9 months does to slow growth of bacteria and risk of reactiviation
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Mycobacterium leprae:
- cuases leprosy
- 10-12 million cases, africa and asia
- prolonged incubation (5yrs)
- humans natural host, also armadillos, optimum growth 30 degrees C in toes, fingers, nose
- trasmitted by prolonged exposure to nasal secretion and skin lesion
- NOT CONTAGIOUS
- replicates intracellularly -causing inflammation and localized cell death, can become systemic
- symptoms: tuberculoid- similar to TB- granulomas form, pneumonia like symptoms
- lepramatous: slow onset, nodules on skin, loss of feeling in extremeties leads to truama that are unnoticed, bone degeneration at extremities
- treatment: dapsone, suplonamides in combination of rifmapin for 2 yrs
- two vaccines used: heat killed M.laprae and attenuated M. avium
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Mycoplasma pneumoniae
- causes "walking pneumonia" -10% of all pneumonia
- transmitted by aerosols
- has no peptidoglycan, no cell wall inhibiting effect of antibiotics
- lysozyme has no effect
- virulence: bacteria attaches to mucosal cell vai and adhesin and enzymes degrade surface
- inflammation, edema causing pneumonia
- self-resolving
- treatment: erythromycin, or tetracycline
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Treponema pallidum
- causes SYPHILIS (STD)
- spirochete
- transmitted by direct contact with open lesions, can cross placenta
- cannot be cultivated, must detect serologically (look for Ab)
- NO KNOWN VIRULENCE FACTOR- difficult to study
- immune complex formations- acquired autoimmunity- thoguht to accound for symptoms in latter stages
- DISEASE PROGRESSION: primary stage- watery lesion (chancre) at inoculate site, highly infectious, microbes burrow into tissues, lesion disappear in 1-2 weeks, bacteria enters blood stream, may be asymptomatic
- secondary stage-weeks to months later, rash, pustules on palms and soles, watery lesions on skin and mucous membranes, minor fever, malaise, headache, non-specific symptoms, may be asymptomatic, symptoms subside
- tertiary stage-no lesions, no longer contagious, bacteria penetrated organs, nervous tissues and bones, blindness, deaf, personality change (insanity) , crippling and organ failure
- treatment: beta lactam very effective in primary and secondary stage, nothing works for tertiary stage
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Borerelia burgdorferi
- causes LYME DISEASE
- spirochete
- transmitted by a specific type of tick (Ixodes spp)- during ticks 2nd year of life cycle, it takes three blood meals (larvae feed on mice and deer, nymphs feed on mice and humans- during the summer, adults feed on deer and humans- fall)
- disease named after first major outbreak in New Lyme Conneticut- large number of juvenile arthritis
- -endemic in eastern NA and progressively migrating west
- detected by presence of Ab in serum or PCR
- VIRULENCE FACTOR UNKNOWN
- does express a number of surface proteins which are likely important in attachment
- not typical Koch's postulate
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Disease progression: primary stage- painless bull's eye rash around bite, flu-like symptom or asymptomatic, rash and symptoms disappear
secondary stage- weeks to months later, fever, flu-like symptoms, microbe has penetrated into nervous and cardiac systems, facial paralysis, heart damage, meningitis, symptoms disappear (latent phase occurs)
3rd stage: months to years later, symptoms depends on where microbes has localized, crippling arthiristis, mood/personality change, organ failure
- treatment: beta lactams works well for 1 and 2 stage, 3rd stage hard for antibiotic to reach microbe
- vaccine: release in 1998 vaccine called LYMErixstopped in 2002, made up on OspA, not effective as it B.burgdorferi only produces OspA in ticks
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Obligate Intracellular pathogens:
Chlamydia spp.
- c. psittaci- spread inhalation of dried feces from infected tropical birds- causes lung infection, pneumonia
- c. trachomatis- humans, trachoma (eye infection and STD), direct contact
- c. pneumoniae- humans, aerosol transmission, cuases pneumonia
- ALL CHLAMYDIAS HAVE UNSUAL REPLICATION CYCLE
- -extracellular, non-metabolizing ELEMENTARY BODY (EB) enters host cell by phagocytosis
- -germinates into RETICULATE BODY, replicated in INCLUSION BODIES (vacuoles) to form more EB
- usually detected by presence of inclusion bodies, primarily infect epithelial and mucosal cells,
- NO VIRULENCE FACTOR, NO PEPTIDOGLYCAN
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Chlamydia trachomatis
- 15 different types based on surface protein Ag
- types A, B, and C most associated with conjunctivitis, trachoma and can lead to blindness
- types D-K cause genital tract infections (most common): non gonnococcal urethritis
- 70-80% of females infected are asymptomatic, 20-50% men are asymptomatic
- neonatal conjunctivitis, neonatal npneumonia (inhaled by new born from birth canal)
- PID
- treatment: tetracycline or erythromycin
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Rickettsiae: intracellular parasite
- spread by insect vectors
- common symptom: rash caused by damaged blood vessels
- little is known about virulence factor
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Rickettsiae rickettsii
- causes Rocky Mountain Spotted Fever
- spread by tick bite
- symptoms: rash, fever, headache, coma, CNS damage
- accounts for 95% of all rickettsial diseases
- fatal if untreated
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Coxiella burnetii
- causes Q fever (Q for query)
- spread by aerosol - pneumonia
- reservoirs- cattle, sheeps and goats
- killed by pasteurized milks
- ppl who work with live stocks are at risk
- vaccine of killed bacteria very effective
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R typhi and R prowazekii
- cuases Endemic (typhi) and Epidemic (prowazekii) Typhus
- grows in gut of louse and excreted in fecal mater, eventually kills louse
- spread by rat fleas, human lice - systemic when theres a breakage in skin due to scratch
- called camp fever, jail fever -can spread easily in close area
- symptoms resemble Typhoid Fever- headache, fever, flu-like symptoms can escalate to coma and death
- treatment: tetracycline, chloramphenicol
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