Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/26

Click to flip

26 Cards in this Set

  • Front
  • Back
Anthrax:

characteristics or bacteria and disease (animal and human)

Treatment:
Bacillus anthracis = G+, spore forming rod

Primarily disease of animals -> causes frequently fatal systemic infection

Human infections
- often life-threatening unless treated with appropriate antibiotics
- some of pathology caused by exotoxins
- Protective Antigen: allows exotoxins to enter mammalian cells *Abs to this Ag prevent disease
- poor prognosis indicated by systemic spread with bacteremia

Vaccine: crude yet effective and safe, consists of B. anthracis proteins, for at-risk populations (vets, troops threatened w/ bio warfare)
Anthrax:

3 pathways for human infection
*A zoonotic infection, very rare human to human transmission*

1) Cutaneous Anthrax: *most common and least serious
- from spore contamination of existing skin lesion
- Bacteria grows and forms a painless vesicle with surrounding edema -> lesion turns into an Eschar (black scab)
- Untreated cutaneous lesion may lead to fatal bacteremia

2) Intestinal Anthrax: *rare
- from ingestion of spores in meat

3) Inhalation Anthrax:
- 3rd world countries -> occupational disease assoc with wool or animal hides (was also seen in America before near elimination)
- pulmonary macrophages phagocytose inhaled spores -> spores germinate and produce exotoxins
- Early sign is enlarged mediastinal (between lungs) lymph nodes
- rapidly fatal and difficult to treat because diagnosis often delayed
Spirochetes:

Characteristics -

Multiplication -
-G- type structure with *no known spore stages*
-elongated, flexible, motile
-helicoid (twist spirally on their long axis)
-flagellar structure spirally wound around cell and anchored through hook-like base at each pole (Axial filament or Internal flagellum)

- Binary fission
Spirochetes:

3 major groups -
1) Genus Treponema:
- causes syphilis, yaws and pinta
- non pathogenic organisms in oral cavity, intestine and genitalia (humans and other mammals)

2) Genus Borrelia:
- causes relapsing fever and Lyme Disease (named after french microbiologist Borrel)

3) Genus Leptospira:
- cause of leptospirosis
Treponema pallidum:

characteristics -

survival in lab -
- G-, to small to be gram stained
- agent of syphilis
- 5-15 micrometers long, 0.2 micrometers wide *less than resolving power than light microscope*
- made visible by "Darkfield microscopy", immunofluorescence, silver salt deposition, electron microscopy

- Live organisms can't be grown in culture, but can be kept motile in anaerobic, very rich media (albumin and serum)
- survives in whole blood only for ~24hrs, tissue specimens for several days (*won't survive in blood stored for days as in blood bank)
- Easily killed by: heat, drying, soap, water
- Can survive for years at -80 degrees celcius, then revived
- Perpetuate in lab by injection into rabbit testicular tissue
Treponema pallidum:

Mode of Transmission -
- usually by direct genitalia or mucous membrane contact
- generally not transmissible in late stages (~4yrs post infection)
- Congenital syphilis: from mother to fetus, preventable by early treatment of mother, can cause still birth, abortion, symptoms similar to secondary syphilis at birth
- Tranfusion syphilis: to a recipient of freshly obtained blood or rarely to health care workers through cuts
Treponema pallidum:

Pathogenesis -
Incubation
Primary lesion
Secondary lesions
Tertiary lesions
2-6 wks, clinical evidence absent, but bacterial rep at entry site active

=chancre, appears 1-4wks post infection, on genitalia with focal lymphadenopathy, heals spontaneously 1-5 wks later

occurs b/c of disseminated organism, general skin rash or mucosal lesions (*HIGHLY infectious*) 2-20wks post primary lesion appearance
Phase = "secondary syphilis" may -> arthritis, renal dysfunction, other

Many years post infection in CNS, aortic heart valve, other
Consistency = "gumma", rubbery
Generally no organisms seen, damage due to hypersensitivity
Treponema pallidum:

Diagnosis -
history of exposure

Organisms in lesion - darkfield of exudate from lesion

Serological tests -
Early:
1) Wasserman Ab reacts with specific lipid diphasphatidylglycerol/"cardiolipin" -> add lecithin and cholesterol -> measure degree of complement fixation
2) Later modified as flocculation tests, usually named for modifier
3) Origin of Ag that Ab's are made against is unknown

Modern Tests:
1) Nonspecific tests: very sensitive and generally done first
- Widely used screening tests: Venereal Disease Research Lab tests (VDRL), Flocculation test with cardiolipin (clumping on a slide)
- Newer version:
Rapid plasma reagin (RPR)- Ag absorbed to carbon particles, makes clumping easier to detect
Treponema pallidum:

Serological diagnosis
Early:
1) Wasserman Ab reacts with specific lipid diphasphatidylglycerol/"cardiolipin" -> add lecithin and cholesterol -> measure degree of complement fixation
2) Later modified as flocculation tests, usually named for modifier
3) Origin of Ag that Ab's are made against is unknown

Modern Tests:
1) Nonspecific tests: very sensitive and generally done first
- Widely used screening tests: Venereal Disease Research Lab tests (VDRL), Flocculation test with cardiolipin (clumping on a slide)
- Newer version:
Rapid plasma reagin (RPR)- Ag absorbed to carbon particles, makes clumping easier to detect

Specific Tests: to confirm results of non-specific tests
1) Fluorescent treponemal antibody - absorption test (FTA-ABS): patient's serum absorbed with non-pathogenic treponemes to remove non-specific antibodies -> serum added to a slide with T-Pallidum (commercial product), washed -> made visible by adding a second fluorescent Ab
2) Microhemagglutinin test: involves red cells coated with T. pallidum Ag -> mix with pt serum
3) Treponema pallidum immobilization test (TPI): Ab from pt reacts directly with T. pallidum in presence of complement -> organism loses motility *difficult test, important in suspected false positive

False + and -'s:
May be false + if -> Malaria, mono, or absence of disease
Incidence of false + or - is higher in VDRL and RPR tests than FTA-ABS
Treponema pallidum:

Antibiotic treatment -

Vaccine -
Very sensitive to penicillin
No resistance found
Therapy duration depends on stage
Therapy must be enough to completely eliminate infection

Alternative Antibiotics = tetracyclin, erythromycin


No effective vaccines
Because T. pallidum can't be cultured in vitro and is difficult to study

*Genomic sequencing may provide clues about surface molecules to target
Yaws:

aka
Cause
Transmission
Affects who
ID tests
Sequelae
Treatment
framesia, pian, boubas, parangi

T. pertenue

Open sores on skin, no transplacental

often children

"mother yaw"/primary lesion resembles rasberry
late lesions may appear in bones and disfigure face

Show positive syphilis test

Highly sensitive to penicillin
Bejel:

cause
Who?
transmission
treatment
T. pallidum (subspecies endemicum)

common among children in Syria

similar to yaws, non venereal

Penicillin
Pinta:

aka
Cause
Where
Sequelae
Treatment
carate, mal de los pintos, azul

T. carateum

Central and South America

Rarely serious, flat, ulcerating skin lesions on hands, feet and scalp - heal spontaneously, leave depigmented areas

Penicillin
Borrelia:
1) Relapsing fever
most notable causes:
ID:

For both species -
Where?
Transmission
- notably by B. recurrentis, B. hernsii
- can stain and view by light microscopy, grow well in chick embryo, not artificial medium
B. hernsii:
- Endemic to western US
- Ticks -> rodents -> human
(wild rodents = natural reservoir)
B. recirrentis:
- epidemic, not in US
- human -> body louse -> human
Borrelia:
1) Relapsing Fever:

- Course of disease:
what causes relapse?
- Diagnosis:
- Treatments:
4-5d fever -> afebrile 7-10d -> fever recurrs with 3-10 relapses before recovery -> relapse caused by surface protein Ag variation (encoded on a linear plasmid)

- clinical symptoms, Borrelia in stained blood smears (Wright's stain) or dark field microsc, inject blood into mouse then examine for Borrelia

Penicillin, tetracycline
Borrelia:
2) Lyme disease:

- cause:
- Location:
- Reservoirs:
- Genetics:
- B. burdorferi

- east coast and pacific NW

- white tailed deer and white footed mouse

- virulent strain carries 7 linear and 2 circular plasmids
Borrelia:
2) Lyme disease:

- Pathogenesis:
1st stage:
papule with expanding erythema, 3-14d pose bite, fever, headache, stiff neck, malaise

2nd:
neurologic and cardiac symptoms

3rd:
migrating arthritis episodes weeks to months, maybe years post bite
Borrelia:
2) Lyme disease:

- Diagnosis:
- Late manifestations:
- Treatment:
- Vaccine:
- Unique Iron characteristic:
Symptoms and expanding bright red rash
Difficult to isolate organism
ELISA to detect circulating Abs is available

without treatment:
Chronic arthritis - 3-5 yrs (also in HLA-DR4 straing, don't respond well to tetracyclin)

Tetracyclin, or ampicillin as safe alternative for children

Contains outer surface protein A = OspA
For people with high risk of exposure (forest workers)

NO requirement for iron, may require manganese for enzymes (usually, iron required for bio processes and signaling for virulence gene regulation)
Leptospira:

- transmission:
- Manifestations:
- At risk populations:
uncommon human disease

By rats, dogs and others usually from infected urine -> skin or upper alimentary mucosa

Nephritis, jaundice, meningitis

sewage workers, slaughter house workers, ppl in rat infested areas
Leptospira:

- Pathogenesis:
- Symptoms:
- Weil's disease:
- Diagnosis
- Treatment
- Vaccine
enter blood -> invade tissues and organs (esp Kidney, liver, conjunctiva, meninges)

Muscular pain, headache, photophobia, fever, chills, lasts a few weeks

infectious jaundice caused by one serovariation -> renal failure, hepatic injury, fatality rate up to 25%

Grown and ID serologically

Penicillin, erythromycin, tetracyclin

No vaccine for humans
Mycoplasma:

- Characteristics
- # of type
- Reproduction
*Not fungus

- pleomorphic, poor staining (can't be ID'd by Gram), NO cell walls, *cytop memb contains cholesterol* obtained from host cell(the only bacteria that does!) -> causes osmotic rigidity

- over 70 types

- No spores, smallest organism to grow and reproduce autonomously, colonies are small and grow slowly, have "fried egg" appearance, must have sterols in growth med
Mycoplasma pneumoniae:

Characteristics:
- size
- Specific differences from other mycos
- causes what disease
- epidemics
*only proven human pathogen* (others suspected)

- very small, originally thought to be a virus

- Antigenically different from other human mycos
- Protein P1 complex = specialized terminal structure, promotes host cell attachment
- Ferments glucose (unlike hominis, orale, and salivarium)

- causes primary atypical pneumonia (primarily in young adults): spotty points of infection on XRay, not lobar
- also caused by coxiella, chlamydia, legionella, resp viruses

- usually of summer pneumonias every 4-8 years
Mycoplasma pneumoniae:

- usual course of disease:
- symptoms:
- Sputum gram stain ->
- serotypes
- Immunity:
- transmitted by resp droplets -> only small percent of infections cause pneumonia, usually mild resp infection

- fever, weakness, cough, headache, diffuse changes in chest X ray, slow onset, rare fatalities, sometimes CNS involvement

- only one known

- not lifelong - maybe 5-10yrs


- shows PMNs, no organism
Mycoplasma pneumoniae:

- serum in early stages shows:
- Pathogenesis:
- "cold hemagglutinins": agglut type O RBC
- + complement fixation test
- DNA probes: useful due to extremely slow growth

-Gliding motility: through resp secretions, between cilia -> epithelial surface
- Attachment: to epith surface via P1 protein complex at tip
- Ciliotosis: elaboration of H2O2 and superoxide resulting in host cell memb and DNA damage, altered metabolism
- Inflammation - increase severity of disease with inc age = prior immunity and inflamm are factors
- Immune evasion - bact cell surface has variable lipoproteins (VLPs) - structure variation to avoid prior immunity and stabilize bact memb
Mycoplasma Pneumoniae:

Epidemiology -
Treatment -
Vaccine -
- spread via close contact or family

- Chemotherapy: erythromycin or tetracyclin *Mycoplasma have no cell wall, so don't treat with something that inhibits cell wall synth*

- no vaccine
Other Mycoplasmas:

M. hominis:

M. arthritidis:

Ureaplasma urealyticum:

M. genitalium:

M. fermentans, M. incognitus:
- commonly in female genital tract
- role in upper female gen tract infections (PID, endometritis, low birth wt, postpartum fever)
- erythromycin resistant, tetracyclin sensitive

- produces super Ag, may cause serious arthritis
- super Ags may factor in rheumatoid arthritis

- a mycoplasma that is common genital tract inhabitant
- causes 20% non-gonococcal urethritis (NGU)
- assoc with male infertility (treat with doxycyclin)
- hydrolyzes urea

- suggested link to NGU in males

- may be HIV infection cofactors