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FMS 3 > Microbiology: Intracellular bacteria, mycobacteria, and spirochetes > Flashcards

Microbiology: Intracellular bacteria, mycobacteria, and spirochetes Flashcards

1
Q

Intracellular bacteria

A
  • Includes Rickettsiae, Chlamydiae, and Mycobacteria
  • These cannot reproduce outside of their host cells
  • Can be acquired directly from blood (rickettsia), mucosa (M tuberculosis), and enterally
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2
Q

Rickettsiae

A
  • Small GN coccobacilli (obligate intracellular) that do not stain w/ gram stain but do stain w/ giemsa
  • Energy parasites that have ATP transport system to use host ATP supplies
  • Transmitted by arthropod vectors (ticks, mites, fleas, lice)
  • Cause rocky mountain spotted fever
  • Targets endothelial cells
  • Separated into groups based on Ag composition: spotted fever group, typhus group, and scrub typhus group
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3
Q

Pathogenesis of Rickettsiae

A
  • Inoculated into dermis of skin by a tick bite or an open wound
  • Bacteria spread through blood stream and infect epithelia, causing destruction of the endothelial cells due to replicating bacteria
  • The bacteria attach to the cells, are phagocytosed, and then replicate (binary fission) in cytoplasm
  • Can move within the endothelial cells via F actin
  • Release and spread as filopodia
  • Leakage of fluid from brain can lead to encephalitis
  • Immune cells produce INF-g and TNF-a activate killing of the bacteria by autophagosome and subsequent lysosome fusion
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4
Q

Rocky mountain spotted fever

A
  • Caused by rickettsia rickettsii
  • Fever 4-10 days after tick bite, along w/ muscle pain, headache, lymphadenopathy (swollen lymph nodes)
  • Rash from extremities to trunk (sometimes on palms and soles)
  • Dx by culture (requires BSL-3 condition), also microimmunofluorescence (MIF) against outer membrane proteins and LPS (followed by western/PCR to confirm)
  • Rx is doxycycline
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5
Q

Epidemic Typhus

A
  • From louse-borne rickettsia prowazeckii (closest relative to mitos)
  • Contains microcapsule and slime layer, life cycle requires lice (reservoirs: humans, flying squirrels)
  • Bacteria enter blood from scratching caused by the lice, allowing them to infect endothelial cells
  • Usually occurs in crowded, unsanitary places
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6
Q

Pathogenesis of epidemic typhus

A
  • Bacteria can multiply within endothelial cells, causing vasculitis and thrombosis
  • 1 week after infection there is fever, severe headache, and myalgia (muscle pain). 5 days later there is petechial rash under arms which radiates outward to entire body
  • Dx is clinical presentation + potential conditions for lice, detection of Abs to rickettsial Ags in serum, isolation from culture
  • Prevention: delousing, vaccination, Rx w/ choloramphenicol or tetracycline
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7
Q

Chlamydiae

A
  • Small intracellular obligate rods with a specific form of LPS, no peptidoglycan (GN, susceptible to osmosis), and are ATP parasites
  • 2 main genera: chlamydia and chlamydophila
  • They form metabolically inactive infectious elementary bodies (EB, to enter cells) and metabolically active but noninfectious reticulate bodies (RB, to replicate within the cells)
  • EBs are resistant to harsh conditions like spores
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8
Q

Chlamydia trachomitis

A
  • Growth: EB binds to receptors on susceptible (nonciliated) epithelial cells and are internalized by endo/phagocytosis
  • EBs become RBs in endosome, bacteria prevents fusion of endosome w/ lysosome to avoid degradation
  • RBs replicate by binary fission in endosome and become EBs again, and are eventually released by lysis or extrusion
  • Immune system does not produce lasting immunity
  • Causes UTI, trachoma (roughening of inner surface of eyelids), conjunctivitis (pink eye), pneumonia, an lymphogranuloma venereum (LGV, swollen ilial lymph nodes)
  • Divided into 3 biological variants (biovars): trachoma, LGV, mouse neumonitis
  • Human biovars divided into serovars (serological variants) based on their outer membrane protein
  • Dx by molecular amplification, Rx by doxycycline or erythromycin
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9
Q

Mycobacteria

A
  • Obligate intracellular aerobic rods that are non-motile, non-spore forming
  • Complex lipid-rich cell wall (very hydrophobic), containing mycolic acids (responsible for acid fast stain)
  • Composition of cells wall responsible for acid fastness, slow growth, resistance to detergents and antibios, and antigenicity
  • On top of the mycolic acids in cell wall it also has arabinogalactan, and mannose-capped lipoarabinomannan
  • Can survive and replicate within phagocytes, making them inaccessible to circulating Abs (requires cellular)
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10
Q

Mycobacterium Tuberculosis

A
  • Weakly GP acid fast rods
  • Capable of intracellular growth in alveolar macrophages
  • Disease primarily host response to infection
  • IC, alcohol/drug patients are most likely to acquire
  • Humans are only reservoir, spread by infectious aerosols
  • Disease usually isolated to pulmonary infection
  • Dx by skin test, microscopy, culture, and PCR
  • Rx is long to prevent drug-resistant strains. Used Isoniazid (INH), ethambutol, pyrazinamide, and rifampin for 2 months. Followed by 2 months of INH+rifampin (used in prophylaxis as well)
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11
Q

Mycobacterium leprae

A
  • Weakly GP acid fast rods
  • Cannot be cultured on artificial media
  • Contains capsule for intracellular growth
  • Disease mostly from host response
  • Lepromatous, but not tuberculoid, disease is highly infectious
  • Spread by direct contact or inhalation of infected aerosols
  • Can cause tuberculoid form of leprosy or lepromatous form
  • Dx from microscopy (only sensitive to lepromatous form), skin testing for tuberculoid leprosy
  • Rx for tuberculoid form: rifampficin and dapsone for 6 mo
  • Rx for lepromatous form: add clofazimine to tuberculoid Rx and extend Rx to 12 mo
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12
Q

Tuberculoid leprosy

A
  • Causes a strong cellular response but weak humoral response
  • Infected tissues have many lymphocytes and granulomas but few bacteria
  • Bacteria causes large production of IL2 and IFN-g resulting in activation of macrophages
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13
Q

Chronic delayed-type hypersensitivity granulomas

A
  • Host immune response to intracellular bacteria is cause of tissue injury and disease (bacteria resist dying in phagosomes)
  • As a result they can persist and cause chronic inflammation, causing granulomas surrounding the bacteria
  • This results in deposition of scar tissue (in TB much of the respiratory difficulty is caused by replacement of normal tissue w/ scar tissue
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14
Q

Tuberculin skin test

A
  • Extracted + purified outer cell wall Ags are injected to see exposure to M tuberculosis
  • Induration can be 5, 10 or 15 mm. The larger the induration the more difficult it is to pass the test (i.e. only ppl who fail w/ induration of 5 are IC, evidence from CXR)
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15
Q

Spirochetes

A
  • Thin, helical GN bacteria
  • Can swim via flagella
  • 2 main pathogenic families: Lyme borreliosis (lyme disease) and Leptospirosis
  • They call cause mulit-system inflammatory disorder
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16
Q

Borrelia Burgdorferi

A
  • Causes Lyme disease
  • GN but stain w/ aniline (giesma)
  • Genome contains linear chrom plus linear and circular plasmids
  • World-wide tick borne illness (usually in summer, most frequent tick-transmitted illness in US)
  • B burgdorferi found in US and Europe, other two strains (B garinii and B afzelii found in Europe and Asia)
  • Reported in 49 states, mostly in Northeast, Midwest, Pacific West and Southeast
  • Life cycle is: larva-> nymph-> adult (feeds on blood of deer and humans)
  • Lives in Ixodes ticks, which is the vector of transmission
  • Grows in Kelly’s medium
17
Q

Pathogenesis of lyme disease

A
  • Causes erythema chronic migrans (ECM) or erythema migrans (EM)
  • Characterized by flat reddened area w/ central clearing (usually develops 2-23 days after infection at site of tick bite)
  • This starts as a red macule that expands to become a ring-like lesion
  • Accompanying it are malaise, fatigue, headache, fever, chills, myalgias/arthralgias, arthritis, lymphadenopathy
  • Bacteremia occurs in untreated patients within days to weeks
  • Once sepsis occurs other symptoms may arise: cardiac dysfunction (myopericarditis, CHF), nephritis, and neurologic signs (facial palsy, meningitis, encephalitis)
  • Possible to develop late lyme disease consisting of arthritic (most common), neurologic, musculoskeletal and/or cardiac complications weeks-years after exposure due to deposition of Ag-Ab complexes
18
Q

Lyme disease Dx

A
  • CDC defines it as: EM + laboratory confirmation or one late manifestation
  • CDC criteria for Dx: isolation of bacteria, or demonstration of IgM/IgG levels to spirochetes, or increase in Ab btw acute/convalescent serum samples
  • Clinical manifestations often used for diagnosis, along w/ indirect immuno-fluorescnece assay (IFA, measures IgM) + western to confirm
  • Culturing is possible but low-yield (under dark field microscopy)
19
Q

Lyme disease Rx and prevention

A
  • Early administration of amoxicillin, doxycycline or ceftriaxone lessens likelihood and severity of late complications
  • Patients w/ recurrent arthritis or PNS diseases required prolonged IV antibios
  • 3 stages in infection: 1) skin lesions and flu symptoms, 2) arthritis with cardiac abnormalities, chronic meningitis, neuritis, and 3) dementia, nerve demyelination, destruction of bones + joints
  • Prevention: tight fitting clothes, avoid animals (no vaccine), use alcohol on skin
20
Q

Leptospirosis

A
  • Caused by leptospira interrogans
  • Fine, tightly coiled spirals, curved at ends to form hooks
  • Seen under dark field microscopy
  • Motile, obligate aerobe, is culturable
  • World wide zoonotic disease (sources are pets/livestock contamination of water)
  • Enters through skin abrasions or mucous membranes
  • Infects all tissues from blood
21
Q

Pathogenesis of leptospirosis

A
  • Can present as a sub-clinical mild flu and fever w/ myalgia and then remit
  • Or can progress to systemic infection (Weill’s disease) w/ fever, jaundice, renal and hepatic failure, vasculitis, myocarditis, hepatitis, meningitis and death
  • Once in blood from skin or mucosa, it progresses to liver, kidneys, CNS
  • Causes hemorrhage, necrosis, jaundice
  • Acute phase lasts 3-10 days, followed by afebrile period, followed by recurrence of fever and severe symptoms
22
Q

Dx, Rx, and prevention of leptospirosis

A
  • Culture of blood and/or CSF w/in 10 days of onset, use urine after 10 days
  • Seen w/ dark field microscopy or giemsa stain
  • Can use microscopic agglutination test (MAT) w/ serum
  • Rx is IV penicillin or doxycycline, tetracycline to treat renal infection
  • Prevented by vaccinating livestock, preventing contamination of water

FMS 3 (20 decks)

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