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MS2 Unit 2 > Microbiology > Flashcards

Microbiology Flashcards

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
Q

Procalcitonin

A
  • 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
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26
Q

Malaria Cases and Deaths

A

50 million new cases/year

1-3 million deaths/year

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27
Q

Malaria species

A

single-celled protozoan species:

P. falciparum, P. vivax, P. ovale, and P. malaria

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28
Q

P. falciparum

A
  • 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
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29
Q

P. vivax

A

Most common strain worldwide and most common strain in the US, not much in sub-Saharan Africa.

30
Q

Anopheles

A

mosquito species that are capable of carrying and transmitting malaria parasites

31
Q

Malaria in the US

A
  • used to be very common in the 19th century

- 1 million cases of malaria during the civil war

32
Q

P. malariae

A

All malarious areas, but spotty

33
Q

P. ovale

A

Tropical areas of western Africa; occasionally, western Pacific and Southeast Asia

34
Q

Genetic protection from malaria

A
  • hereditary elliptocytosis (Leach phenotype-glycophorin C deficiency)
  • hemoglobin S or HbC
  • Thalassaemia
  • glucose-6-phosphate dehydrogenase deficieny
35
Q

Duffy antigen

A

erythrocyte receptor for P. vivax merozoite invasion.

Low incidence of vivax malaria in West African because many people are missing the duffy antigen.

36
Q

pathology of malaria

A

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
Q

Malaria Symptoms

A

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
Q

Recrudescence

A

parasitemia falls below detectable levels and then later increases to a detectable parasitemia.

39
Q

Relapse

A
  • 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
Q

PfEMP-1

A

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
Q

Symptoms of P. falciparum infection

A

Hypoglycemia
Anemia
Non-caridogenic Pulmonary Edema
Metabolic Acidosis

42
Q

Cerebral Malaria

A

sequestration of parasites in the cerebral microvasculature stimulates the production of cytokines

43
Q

Malaria of pregnancy

A

mature parasites accumulate on the placent. involving interaction with syncytiotrophoblastic chondroitin sulfate A (CSA), hyaluronic acid, and immunoglobulins.

44
Q

paraquinine

A

-eliminates the liver stage for P ovale and P vivax

45
Q

Trypanosomiasis

A
  • Reduvid bug
  • romaha sign=bite usually around the eye
  • can cause: cardiomyopathy, mega-colon, mega-esophagus
46
Q

Leishmaniasis

A
  • 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
Q

Toxoplasmosis

A
  • 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
Q

congenital Toxoplasmosis

A
  • 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
Q

Toxoplasma in immunosupressed patients

A
  • 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
Q

Toxoplasma Ocular Infection

A

-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
Q

Rickettsia virulence factors

A

1) OmpA&B: adhesion
2) Type 4 secretion system: entry
3) Phospholipase A2: escape from endosome
4) ActA: actin-based cell-cell spread

52
Q

characteristic rash that begins on the extremities and moves towards the trunk suggests:

A

Rocky Mountain Spotted Fever

53
Q

characteristic rash that begins on the trunk and moves towards the extremities suggests:

A

Epidemic Typhus

54
Q

virulence factors for Group A streptococci

A 
Strucural: Pili
Toxins: Streptokinase
Streptodornase
Hyaluronidase
Pyrogenic toxin
Erythrogenic toxin
55
Q

Group A strep are sensitive to:

A

penicillin, erythromycin, and cephalosporins

56
Q

Group A streptococci bacteriology

A

Gram pos
Catalase Neg
Beta hemolytic
Bacitracin suseptable

57
Q

Rheumatic Fever

A

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
Q

Aschoff body

A

Granulomatous structures consisting of fibrinoid change, lymphocytic infiltration, occasional plasma cells, and characteristically abnormal macrophages surrounding necrotic centres. Indicative of Rheumatic Fever.

59
Q

Viridans streptococci bacteriology

A

Alpha hemolytic. Optochin resistant.

60
Q

Viridans stroptococci pathology

A

produce high molecular weight carbohydrates that form biofilms on tooth surfaces. Then they break down sugars to form acid.

61
Q

Treatment of Viridans streptococci

A

caries: removal of caries

62
Q

Corynebacterium diptheria

A
  • Gram pos, club shaped rods
  • Causes local and cardiac necrosis
  • There is just toxin in the blood not diptheriae
63
Q

Diptheria culture

A
  • 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
Q

Diptheria treatment

A

Antitoxin (Equine)
Penicillin/ erythromycin helps resolution
Mechanical ventilation as needed

65
Q

Causes of bacterial endocarditis

A

Viridans and Group A streptococci

66
Q

S. aureus bacteriology

A

Gram pos, catalase pos, coagulase pos

67
Q

Treatment of staphylococci

A
  1. Mupirocin ointment
  2. Penicillinase–resistant beta lactam (Nafcillin / oxacillin) or Cephalosporins
  3. Depending on sensitivity test: Clindamycin, Methicillin, Vancomycin, Linezolid
68
Q

Staphylocoocus epidermidis bacteriology

A

Gram pos, catalse pos, Coagulase Negative

69
Q

Scabies diagnosis and treatment

A 
diagnosed clinically (no lab tests)
Treatment: Topical steroids, topical or systemic permethrin/ malathion
70
Q

Impetigo Mild case treatment

A

mupirocin ointment

71
Q

Impetigo serve case treatment

A

Penicillin-resistant penicillins (Nafcillin or Oxacillin, or Amoxicillin with a penicllinase inhibitor, or cephalosporins

72
Q

Scabies treatment

A

topical steroids for itching, Permethrin to kill mites

MS2 Unit 2 (1 decks)

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