Dr. Igboin Study Guide 2

Question 1

Bacteroides

Answer 1

Gram-negative, Rod-shaped, Complex carbs, that are Strict anaerobes

Question 2

How are Bacteroides able to tolerate short exposure to Oxygen

Answer 2

Secrete SOD and catalase (enzymes) that detoxify and breakdown reactive oxygen species

Question 3

The peritoneal cavity

Answer 3

Fluid filled space between the organs contained in the abdomen
Susceptible to contamination more than any other bodily area

Question 4

How can the peritoneal cavity become infected?

Answer 4

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

Question 5

Characteristics of infections of the Peritoneal cavity

Answer 5

Biphasic - acute inflammation the leads to a localized abscess
Few species predominate in these abscesses, although hundreds are introduced into the PC

Question 6

Why does B. fragilis predominate in intraperitoneal abscesses?

Answer 6

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

Question 7

How are abscess harmful to a host?

Answer 7

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

Question 8

Diagnosis of abscesses

Answer 8

CAT scan

Culture fluid drained from the abscess under anaerobe conditions

Question 9

Treatment of Abscesses

Answer 9

Combined surgical and medical approach - drain the abscess and combine an antibiotic therapy

Question 10

Sepsis

Answer 10

Sever systemic illness characterized by hemodynamic derangement and multiple organ malfunction, brought on by an interaction of microbial products with host macrophages

Question 11

Hemodynamic derangement

Answer 11

High cardiac output, yet low blood pressure and inadequate perfusion of organs

Question 12

What microbial components can trigger sepsis?

Answer 12

In Gram- : LPS

In Gram+ : Peptidoglycan

Question 13

What are the primary cytokine mediators of sepsis?

Answer 13

Pro-inflammatory cytokines: IL-1 and TNF-a

Question 14

Effects of IL-1 and TNF-a on the vasculature

Answer 14

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

Question 15

Treatment for sepsis

Answer 15

Ventilator
IV fluids
Adrenic drugs

Question 16

General characteristics of Treponemes

Answer 16

Helical shape

Corkscrew-like movements mediated by periplasmic flagella

Question 17

Modes of T. pallidum transmission

Answer 17

Sexual - through mucous membranes and minute skin abrasions that occur during sex
Transplantal

Question 18

Stages of Transmitted Sypillis

Answer 18

Primary
Secondary
Tertiary

Question 19

Primary Syphillis

Answer 19

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

Question 20

Where does bacterium replicate during Secondary Syphillis?

Answer 20

Lymph nodes, liver, joints, muscles, skin, and mucous membranes

Question 21

Symptoms of Secondary Syphillis

Answer 21

Many Variable symptoms - including lesions

Question 22

Where can lesions occur on the body during secondary syphillis?

Answer 22

One or more places, even on the palms and soles of feet

Question 23

Jarish-Herxheimer reaction

Answer 23

Shock brought on by secondary syphillis

Question 24

Latency of Secondary Syphillis

Answer 24

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

Question 25

What mediates the tertiary stage of Syphillis?

Answer 25

Treponemal antigens

Question 26

Tertiary syphillis

Answer 26

The destruction of host tissues in response to treponemal antigens

Question 27

Gummas

Answer 27

Lesions that appear in tertiary syphillis that destroy soft tissue and bone

Question 28

CNS symptoms of Tertiary Syphillis

Answer 28

Staggering (ataxic gait)
Demetia
General paresis
Eventually can cause death

Question 29

How is syphillis detected

Answer 29

It involves antibodies against the bacterium

Question 30

How is syphillis treated

Answer 30

Penicillin at all stages

Question 31

Mode of B. burgdorferi transmission

Answer 31

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

Question 32

Potential importance of Plasminogen/Plasmin to B. burgdorferi

Answer 32

B. burgdorferi binds to plasminogen, converting it to plasmin. Plasmin is a protease that may promote tissue invasion

Question 33

Stage 1 Lyme disease

Answer 33

Involves a localized infection due to bacterial multiplication at the bite site - forming a lesion called erythema migrans

Question 34

Stage 2 Lyme disease

Answer 34

Infection has disseminated and has spread throughout the body

Question 35

Mechanism of damage in Stage 2 Lyme disease

Answer 35

Host reaction to the presence of bacteria. This reaction is mediated by pro-inflammatory cytokines IL-1 and TNFa

Question 36

Stage 3 Lyme disease symptoms

Answer 36

Arthritis
CNS effects - memory, mood, sleep
Skin effects - lesions that lead to atrophy (Acrodermatitis chronica atrophicans)

Question 37

Lyme disease diagnosis

Answer 37

Detecting antibodies against bacterium

Question 38

Lyme disease treatment

Answer 38

Penicillin is not effective
Doxycycline
Amoxicillin
Cephalosporin - if neurologic issues