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MS2 Unit 2 > Microbiology > Flashcards

Microbiology Flashcards

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1
Q

TLR4 effect

A

engagement of TLR4 leads to the release of proinflammatory mediators TNF-alpha, IL-1, and IL-6.

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2
Q

Factors leading to increased incidence of sepsis

A

increasingly aggressive chemo, corticosteroid use, increased immunosuppressive therapies for organ transplants, increased survival of groups predisposed to sepsis,increased use of invasive devices, increased antibiotic use.

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3
Q

Bacteremia

A

presence of viable bacteria in the liquid component of the blood
may be transient
can be primary (without an identifiable source of focus of infection) or secondary

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4
Q

SIRS

A 
systemic inflammatory response syndrome
two or more positive:
1)temp >100.4 or temp below 96.8
2)HR>90
3)RR>20 or PaCO2 below 32 mmHg
4)WBC above 12 or below 4, or greater than 10% bands
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5
Q

Sepsis

A

SIRS+ proof of bloodstream infection

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6
Q

Causes of SIRS

A 
Bloodstream infection
Trauma
Burns
Pancreatitis
Complication of Surgery
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7
Q

Severe Sepsis

A

Sepsis with organ disfunction

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8
Q

Septic Shock

A

Severe Sepsis with hypotension that will not respond to fluid resuscitation

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9
Q

Gram Negative shock can lead to

A

DIC, changes in vascular permeability, circulatory collapse, and hemorrhagic necrosis

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10
Q

number of acyl chains in lipid A

A

Lipid A with a reduced number of acyl chains can serve as an inhibitor of immune activation.
Bacteria can change the number of acyl chains in response to the environment.

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11
Q

DIC

A

Disseminated intravascular coagulation. Blood clots form throughout the body’s small blood vessels.

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12
Q

Protein C

A

inactive zymogen converted to activated protein C in the presence of thrombin and thrombomodulin

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13
Q

Activated protein C (APC)

A
  • Anti-inflammatory agent
  • inhibits the production of proinflammatory cytokines by LPS.
  • inhibits plasminogen activator inhibitor (decreases blood clots)
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14
Q

Plasminogen activator

A

serine protease that converts plasminogen to plasmin which promotes fibrinolysis (which prevents blood clots from growing)

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15
Q

Antithrombin

A

-“anti-clot”
inhibits thrombin production at multiple steps in the coagulation cascade as well as binding and inhibiting thrombin directly
-Naturally occuring regulator affected during sepsis.

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16
Q

Transient Bacteremia

A

from: Chewing, teeth brushing, manipulation of infected tissue, surgery involving non-sterile sites.

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17
Q

intermittent bacteremia

A

-most common pattern of bacteremia

  • usually from extravascular infection which provided a portal of entry for the bacteria (UTI, abscess)
  • seen in the early course of meningitis, pyogenic arthritis, and osteomyelitis
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18
Q

Continuous Bacteremia

A
  • Bacterial endocarditis and other endovascular infections

- Seen during the early stages of Typhoid fever, Brucellosis, Leptospirosis

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19
Q

Infective Endocarditis Pathogenesis

A

1) Damage to the cardiac endothelium
2) Deposition of platelets and fibrin
3) Organisms gain access to bloodstream and stick leading to colonization
4) Protective layer of fibrin and platlets matrix
5) Bacterial multiplication
6) Vegetation formation

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20
Q

Mycotic aneurysm

A
  • aneurysm arising from bacterial infection of the arterial wall.
  • Infection causes inflammatory damage and weakening of arterial wall.
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21
Q

Suppurative thrombophlebitis

A
  • Results from damage to the endothelial cells lining a vein

- Results in clot formation and seeding of the clot by organisms

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22
Q

CRBSI

A

Catheter-related Bloodstream Infection
Occurs in 8% of cathetered adults
-70% are due to S. aureus and coagulase negative Staphylococci

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23
Q

Adult Blood cultures

A
  • Can have less than 1 organism per ml

- Yield is increased by 3.2% for each mL of blood cultured

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24
Q

Child blood cultures

A

Bacteric load is 10 to 100 times higher than adults

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25
Procalcitonin
- PCT is stimuated by bcterial products and cytokines - Indicative of Bacterial pnemonia and bacterial Sepsis (increased PCT seen in 3 to 6 hours) - Increased levels-->poorer prognosis - can be tracked for evaluation of effectiveness of treatment
26
Malaria Cases and Deaths
50 million new cases/year | 1-3 million deaths/year
27
Malaria species
single-celled protozoan species: | P. falciparum, P. vivax, P. ovale, and P. malaria
28
P. falciparum
- most lethal malaria strain - Predominates in sub-Saharan Africa, but also occurs in Southeast Asia, South America - has ability to sequester in the deep venous microvasculature
29
P. vivax
Most common strain worldwide and most common strain in the US, not much in sub-Saharan Africa.
30
Anopheles
mosquito species that are capable of carrying and transmitting malaria parasites
31
Malaria in the US
- used to be very common in the 19th century | - 1 million cases of malaria during the civil war
32
P. malariae
All malarious areas, but spotty
33
P. ovale
Tropical areas of western Africa; occasionally, western Pacific and Southeast Asia
34
Genetic protection from malaria
- hereditary elliptocytosis (Leach phenotype-glycophorin C deficiency) - hemoglobin S or HbC - Thalassaemia - glucose-6-phosphate dehydrogenase deficieny
35
Duffy antigen
erythrocyte receptor for P. vivax merozoite invasion. | Low incidence of vivax malaria in West African because many people are missing the duffy antigen.
36
pathology of malaria
consists of hemolytic anemia (rupture of parasitized erythrocytes, removal of parasitized and unparasitized erythrocytes by the spleen, capillary sequestration and bone marrow dyserythropoiesis), and an impaired microcirculation.
37
Malaria Symptoms
Incubation period depends on the hepatic phase, and can last from 7 days to 8 months. Signs: 1st-Cold Stage (15-60 minutes), Lysis of RBCs 2nd- Hot stage (2-6 hours), burning skin, throbbing headache 3rd- Sweating stage (2-4 hours) profuse sweating, declining temperature, sleep
38
Recrudescence
parasitemia falls below detectable levels and then later increases to a detectable parasitemia.
39
Relapse
- the sporozoites invade hepatocytes, in which they develop into schizonts and may not be observed in the circulation and the individual may be asymptomatic. - After a period of time the hepatocyte ruptures. -Each infected hepatocyte that ruptures liberates 10,000 to 30,000 merozoites that invade circulating erythrocytes. - Growth and development of the parasites in red cells result in subsequent waves of merozoite invasion
40
PfEMP-1
P. falciparum erythrocyte membrane protein-1 - 60 different var genes are present - produce the antigenic variation in P. falciparum populations during the course of an infection. - CD36 is the major receptor for PfEMP-1
41
Symptoms of P. falciparum infection
Hypoglycemia Anemia Non-caridogenic Pulmonary Edema Metabolic Acidosis
42
Cerebral Malaria
sequestration of parasites in the cerebral microvasculature stimulates the production of cytokines
43
Malaria of pregnancy
mature parasites accumulate on the placent. involving interaction with syncytiotrophoblastic chondroitin sulfate A (CSA), hyaluronic acid, and immunoglobulins.
44
paraquinine
-eliminates the liver stage for P ovale and P vivax
45
Trypanosomiasis
- Reduvid bug - romaha sign=bite usually around the eye - can cause: cardiomyopathy, mega-colon, mega-esophagus
46
Leishmaniasis
- transmitted by the sand fly - multiplication occurs in histocytes - cutaneous lesihmaniasis--> chronic skin ulcers - mucocutaneous leishmaniasis--> metastatic spread of primary lesions to the mouth, nose pharynx where destruction of the mucosa occurs - visceral lesihmaniasis-->there is often fever, weight loss, anorexia, splenomegaly and hepatomegaly
47
Toxoplasmosis
- accidental consumption of feline fecal material, through food or water with fecal contamination, through the consumption of undercooked meat containing infective cysts, through transplantation, or transplacentally from mother to fetus. - healthy people don't show symptoms--> parasite goes in an inactive state, hat can be reactivated later
48
congenital Toxoplasmosis
- Results from an acute primary infection acquired by the mother during pregnancy - symptoms:chorioretinitis, hydrocephalus, and intracranial calcifications - most babies affected during pregnancy show no symptoms at birth but can develop hearing, visual and learning disabilities later in life.
49
Toxoplasma in immunosupressed patients
- Toxoplasmosis is the leading cause of focal central nervous system (CNS) disease in AIDS. - A person who is HIV-infected and who has reactivated Toxoplasma infection can have symptoms that include fever, confusion, headache, seizures, nausea, and poor coordination.
50
Toxoplasma Ocular Infection
-retinochoroiditis from congenital infection or infection after birth - acute inflammatory lesion of the retina, which resolves leaving retinochoroidal scarring -symptoms: eye pain sensitivity to light, tearing, blurred vision -The eye disease can reactivate months or years later, each time causing more damage to the retina
51
Rickettsia virulence factors
1) OmpA&B: adhesion 2) Type 4 secretion system: entry 3) Phospholipase A2: escape from endosome 4) ActA: actin-based cell-cell spread
52
characteristic rash that begins on the extremities and moves towards the trunk suggests:
Rocky Mountain Spotted Fever
53
characteristic rash that begins on the trunk and moves towards the extremities suggests:
Epidemic Typhus
54
virulence factors for Group A streptococci
``` Strucural: Pili Toxins: Streptokinase Streptodornase Hyaluronidase Pyrogenic toxin Erythrogenic toxin ```
55
Group A strep are sensitive to:
penicillin, erythromycin, and cephalosporins
56
Group A streptococci bacteriology
Gram pos Catalase Neg Beta hemolytic Bacitracin suseptable
57
Rheumatic Fever
Post Streptococcal infection that occurs in 0.3% of cases. No active infection. Autoimmune response with fever, arthritis and endocarditis (usually leading to permanent valve distortion). Reocccurances are common. Treatment:anti-inflammatory drugs, prophylactic antibiotics for oral surgery
58
Aschoff body
Granulomatous structures consisting of fibrinoid change, lymphocytic infiltration, occasional plasma cells, and characteristically abnormal macrophages surrounding necrotic centres. Indicative of Rheumatic Fever.
59
Viridans streptococci bacteriology
Alpha hemolytic. Optochin resistant.
60
Viridans stroptococci pathology
produce high molecular weight carbohydrates that form biofilms on tooth surfaces. Then they break down sugars to form acid.
61
Treatment of Viridans streptococci
caries: removal of caries
62
Corynebacterium diptheria
- Gram pos, club shaped rods - Causes local and cardiac necrosis - There is just toxin in the blood not diptheriae
63
Diptheria culture
- Culture requires tellurite media, look for gram pos rods with clubbed ends and internal beads. (NOTE: smear is not useful because of existance of nonpathogenic corynebacteria - Lab cultures are confirmed to produce toxin by antibody tests or to have the toxin gene by PCR
64
Diptheria treatment
Antitoxin (Equine) Penicillin/ erythromycin helps resolution Mechanical ventilation as needed
65
Causes of bacterial endocarditis
Viridans and Group A streptococci
66
S. aureus bacteriology
Gram pos, catalase pos, coagulase pos
67
Treatment of staphylococci
1. Mupirocin ointment 2. Penicillinase–resistant beta lactam (Nafcillin / oxacillin) or Cephalosporins 3. Depending on sensitivity test: Clindamycin, Methicillin, Vancomycin, Linezolid
68
Staphylocoocus epidermidis bacteriology
Gram pos, catalse pos, Coagulase Negative
69
Scabies diagnosis and treatment
``` diagnosed clinically (no lab tests) Treatment: Topical steroids, topical or systemic permethrin/ malathion ```
70
Impetigo Mild case treatment
mupirocin ointment
71
Impetigo serve case treatment
Penicillin-resistant penicillins (Nafcillin or Oxacillin, or Amoxicillin with a penicllinase inhibitor, or cephalosporins
72
Scabies treatment
topical steroids for itching, Permethrin to kill mites

MS2 Unit 2 (1 decks)

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