Dr. Igboin Study Guide 2 Flashcards
Bacteroides
Gram-negative, Rod-shaped, Complex carbs, that are Strict anaerobes
How are Bacteroides able to tolerate short exposure to Oxygen
Secrete SOD and catalase (enzymes) that detoxify and breakdown reactive oxygen species
The peritoneal cavity
Fluid filled space between the organs contained in the abdomen
Susceptible to contamination more than any other bodily area
How can the peritoneal cavity become infected?
Spillage of intestinal material (from ruptured bowl, ruptured kidney, or abdominal surgery) can be catastrophic because that material contains billions of bacterial cells form 100s of different species
Characteristics of infections of the Peritoneal cavity
Biphasic - acute inflammation the leads to a localized abscess
Few species predominate in these abscesses, although hundreds are introduced into the PC
Why does B. fragilis predominate in intraperitoneal abscesses?
The spillage mobilizes phagocytes - B. fragilis has anti-phagocytic capsule
The Peritoneal cavity is well oxygenated - it can tolerate oxygen, but thrives once all of that oxygen is used up
How are abscess harmful to a host?
Serve as a reservoir for bacteria to enter the blood, leading to secondary infections, sepsis
Can extend to nearby sites and lead to tissue necrosis
Diagnosis of abscesses
CAT scan
Culture fluid drained from the abscess under anaerobe conditions
Treatment of Abscesses
Combined surgical and medical approach - drain the abscess and combine an antibiotic therapy
Sepsis
Sever systemic illness characterized by hemodynamic derangement and multiple organ malfunction, brought on by an interaction of microbial products with host macrophages
Hemodynamic derangement
High cardiac output, yet low blood pressure and inadequate perfusion of organs
What microbial components can trigger sepsis?
In Gram- : LPS
In Gram+ : Peptidoglycan
What are the primary cytokine mediators of sepsis?
Pro-inflammatory cytokines: IL-1 and TNF-a
Effects of IL-1 and TNF-a on the vasculature
Vasodilation, which decreases BP
Vascular leakage: edema
Intravascular coagulation, which impedes blood flow, and consumes clotting factors, which increases bleeding
Increase expression of neutrophil adhesion molecules, which causes degranulation in tissues and tissue damage
Treatment for sepsis
Ventilator
IV fluids
Adrenic drugs
General characteristics of Treponemes
Helical shape
Corkscrew-like movements mediated by periplasmic flagella
Modes of T. pallidum transmission
Sexual - through mucous membranes and minute skin abrasions that occur during sex
Transplantal
Stages of Transmitted Sypillis
Primary
Secondary
Tertiary
Primary Syphillis
WBCs battle replicating spirochetes at location of initial inoculation, forming a lesion called a syphilitic chancre
They’re painless and heal spontaneously, but the infection is already systemic
Where does bacterium replicate during Secondary Syphillis?
Lymph nodes, liver, joints, muscles, skin, and mucous membranes
Symptoms of Secondary Syphillis
Many Variable symptoms - including lesions
Where can lesions occur on the body during secondary syphillis?
One or more places, even on the palms and soles of feet
Jarish-Herxheimer reaction
Shock brought on by secondary syphillis
Latency of Secondary Syphillis
in 1/3 of people, bacterium are no longer present
In the other 2/3, bacterium become latent for up to decades and then develop into the tertiary stage
What mediates the tertiary stage of Syphillis?
Treponemal antigens
Tertiary syphillis
The destruction of host tissues in response to treponemal antigens
Gummas
Lesions that appear in tertiary syphillis that destroy soft tissue and bone
CNS symptoms of Tertiary Syphillis
Staggering (ataxic gait)
Demetia
General paresis
Eventually can cause death
How is syphillis detected
It involves antibodies against the bacterium
How is syphillis treated
Penicillin at all stages
Mode of B. burgdorferi transmission
Ticks that normally feed on deer and mice have it in their gut. Inject it into the skin of mammals (while they’re feeding) from their salivatory glands
Potential importance of Plasminogen/Plasmin to B. burgdorferi
B. burgdorferi binds to plasminogen, converting it to plasmin. Plasmin is a protease that may promote tissue invasion
Stage 1 Lyme disease
Involves a localized infection due to bacterial multiplication at the bite site - forming a lesion called erythema migrans
Stage 2 Lyme disease
Infection has disseminated and has spread throughout the body
Mechanism of damage in Stage 2 Lyme disease
Host reaction to the presence of bacteria. This reaction is mediated by pro-inflammatory cytokines IL-1 and TNFa
Stage 3 Lyme disease symptoms
Arthritis
CNS effects - memory, mood, sleep
Skin effects - lesions that lead to atrophy (Acrodermatitis chronica atrophicans)
Lyme disease diagnosis
Detecting antibodies against bacterium
Lyme disease treatment
Penicillin is not effective
Doxycycline
Amoxicillin
Cephalosporin - if neurologic issues
