Bacteroides & Abscesses Flashcards
(20 cards)
Bacteroids
Gram - rods energy source complex carbs strict anaerobes but can tolerate short exposures intestinal flora
Why is B. fragilis the predominant species in intra-abdominal abscesses
- evades phagocytosis
- tolerates the initial oxygenated environment of peritoneal cavity
- thrives once the environment becomes anaerobic
SOD
Superoxide dismutase
02- + 2H—-> 02 + H202
Bacteremia
presence of bacteria in the blood, with or without the presence of illness
Sepsis
severe systemic illness characterized by hemodynamic derangement and multiple organ malfunction, brought on by interaction of microbial products and macrophages
Hemodynamic Derangement
Circ. Sys. going ape: High cardiac output, low bp, inadequate perfusion of organs
Mediators of Sepsis
IL-1 TNF-a from macrophages
host own molecules cause most of damage
LPS(gram -) peptidoglycan (gram +)
Effects of IL-1 TNF-a
Vasodilation: decrease BP
vascular leakage
Intravascular coagulation–> blood clots
increased expression of neutrophil adhesion molecule–> causes tissue damage
Treatment for sepsis
Administer 02, IV fluids, adrenegic drugs
Antibiotics must be used, but dead bacteria release future harmful molecules
Spirochetes
Helical
Visualized by darkfield microscopy, SEM
Cause few diseases in humans
periplasmic flagella
Treponema pallidum
Causes syphilis
- lack of animal model
- cant grow in lab setting
Diagnosis involves detecting antibodies against bacterium
Primary Syphillis
chancre forms from immunoresponse
-increases risk of HIV infection
painless, heal on own—> already systemic
Secondary Syphillis
3-6 weeks after primary
Bacterium replicates in lymph nodes, liver, joints, muscle , skin, and mucous membrane
Many variable symptoms
Lesions on one or more surfaces
**Penicillin therapy can result in fever and shock (Jarisch-Herxheimer reaction)
Symptoms resolve w/ or w/o treatment
In 2/3 of cases bacterium goes latent for decades
Tertiary Syphillis
Destruction of tissues due to pressence of treponemal antigens chronic inflammation and vasculitis lesions loss of motor function and dementia death
Borrelia burgdorferi
Causes lyme’s disease
- dormant in midgut of ticks
- -feed on mammal blood–> migrates to tick salivary glands
** spread facilitated by ability to bind to human plasminogen and convert to plasmin—> promotes tissue invasion
Lyme’s Stage 1
Localized infection —>lesion (erythema migrans)
Lyme’s Stage 2
Disseminated infection
CNS, skin, musculoskeletal affected
pain, 2o lesions, meningitis, eye and neuro abnormalities
IL-1 TNF-a cause damage
Lyme’s Stage 3
Months to years after initial infection
Arthritis
memory, mood, sleep
skin lesions that lead to atrophy of skin (acrodermatitis chronica atrophicans
Lyme’s diagnosis
detecting antibodies against bacterium
Lyme’s Treatment
Penicillin not effective