Infection overview Flashcards

1
Q

What elements must you consider when a patient presents with an infection?

A
  1. Host
  2. Environment
  3. Pathogen

always consider pathogen last

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2
Q

According to Dr. Ahmadi, what about the HOST is most important to consider?

A

Immune competent or immune compromised

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3
Q

According to Dr. Ahmadi, what about the ENVIRONMENT is most important to consider?

A

Port of entry, community or hospital acquired

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4
Q

According to Dr. Ahmadi, what about the PATHOGEN is most important to consider?

A

MOA, pathogenicity, virulence

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5
Q

Patient with liver disease presents for routine exam. According to Dr. A, what should you consider and why?

A

Possibility of occult infection. Research shows 2/3 of those w/chronic liver disease have an occult infection.

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6
Q

3 types of immune compromised states

A
  • Primary immune deficiency
  • Secondary or acquired immune deficiency
  • Autoimmune disease
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7
Q

Examples of primary immune deficiency

A

Neonate, elderly

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8
Q

Examples of secondary immune deficience

A

AIDS, chemotherapy, relative immune deficiency (DM, cancer, poor nutrition state)

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9
Q

Autoimmune disease Dr. A mentions in relation to immune deficiency

A

SLE

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10
Q

What is surprising about SLE in relation to immune deficiency?

A

Although they have hyperactive immune systems, they’re not good at offering protection

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11
Q

Image: what does the pathogen want to in the body?

A

Attach → proliferate → avoid phagocytes → damage host via either toxins or invasion

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12
Q

Image: what do abs do to attempt to stop the pathogen at the attachment level?

A

Attachment: abs attach to fimbriae, lipoteichoic acids, and some capsules

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13
Q

Image: what do abs do to attempt to stop the pathogen at proliferation level?

A

Proliferation: a) Abs trigger complement-mediated damage to gram neg outer lipid bilayers, b) Abs block transport mechanisms & receptors (e.g., iron chelating compounds)

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14
Q

Image: what do abs do to attempt to stop the pathogen at the phagocyte avoidance level?

A

Avoidance of phagocytes: a) Abs to M proteins and capsules give opsonization via Fc and C3 receptors, b) Abs neutralize immunorepellents

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15
Q

Image: what do abs do to attempt to stop the pathogen at the host damage level?

A

Toxins: Abs neutralize toxins

Invasion: Abs neutralize spreading factors, enzymes (e.g., hyaluronidase

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16
Q

What type of organisms are those with B Cell deficiencies at risk for?

A

Encapsulated organisms, e.g., Streptococcus pneumoniae, Hemophilus influenzae

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17
Q

What organism is the most common cause of community acquired pneumonia?

A

Streptococcus pneumoniae

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18
Q

What types of infections are people with B cell deficiencies prone to?

A

Pneumonia, Sepsis, Infections of Sinuses, Ears and GI tracts

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19
Q

What types of infections are people with T cell deficiencies prone to?

A

Fungal, viral, and intracellular bacterial infections – e.g., chronic mucocutaneous candidiasis alerts you to T cell deficiency

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20
Q

Classic intracellular organism frequently seen, even in immune competent

A

Mycoplasma – chain coughing w/no other presenting symptoms

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21
Q

Syndrome that commonly causes T Cell deficiency

A

DiGeorge Syndrome: partial or complete absence of T cell immunity; lack of thymus; region of the developing embryo that is affected controls the development of the face, parts of the brain, the thymus, the parathyroid glands, the heart and the aorta.

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22
Q

Syndrome that leads to combined T and B deficiency

A
  • Wiskott-Aldrich syndrome
    • Normal IgA and IgG but very low IgM (so ACUTE phase is most problemetic)
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23
Q

What type of infections are those with Wiskott-Aldrich syndrome prone to?

A

Prone to infections with Encapsulated Bacteria

  • Pseudomonas, Strep, H. Influ,
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24
Q

Conditions that leads to combined T and B cell deficiency

A
  • RAG-1 or RAG-2 deficiency
  • Bare lymphocyte deficiency
  • MHC class I and II deficiency
  • Wiskott-Aldrich syndrome
  • Ataxia-telangiectasia (AT)‏
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25
Q

RAG-1 or RAG-2 deficiency: what does RAG stand for?

A

Recombinant activating gene

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26
Q

RAG-1 or RAG-2 deficiency: signs and symptoms

A
  • No symptoms are detected during pregnancy, birth and within the first few weeks of life.
  • The clinical signs are characterized by chronic respiratory disease, recurrent acute pneumonia, therapy-resistant mucocutaneous candidiasis, eczematous dermatitis and systemic bacterial infections.
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27
Q

Effect of recurrent infections and chronic enteritis of RAG-1 and RAG-2 deficiencies

A
  • a therapy-resistant growth failure. Intracellular parasites (Listeria, Legionella), viruses (EBV) and cytomegaloviruses (CMV) cause lethal complications.
  • All SCID children die within few months if they are not provided with haematopoietic stem cells.
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28
Q

Physical Exam of RAG deficient patient reveals…

A

unusual infections and a characteristic absence of lymphatic organs. In most cases cervical lymph nodes and tonsils are undetectable.

29
Q

What type of person does listeria tend to infect?

A

Those at extremes of age. Classic intracellular organism

30
Q

Types of complement deficiency

A
  • C3 deficiency
  • Mannose-binding lectin (MBL) deficiency
  • Properdin deficiency – terminal part of pathway
  • Factor I and factor H deficiency
  • C9 deficiency – terminal part of pathway
31
Q

What type of infection do phagocyte deficiencies tend to lead to?

A

Gram positive infections

32
Q

What is Chédiak-Higashi syndrome?

A
  • Defect in Cytoplasmic Granules (microtubule polymerization)
  • Associated With Oculocutaneous albinism
33
Q

Clinical signs of Chédiak-Higashi syndrome?

A

Mild coagulopathy, Hepatosplenomegaly
Recurrent Gram Positive infections Skin and Respiratory tract

34
Q

Diagnosis of of Chédiak-Higashi syndrome?

A

Neutrophils with giant lysosomes,
Pancytopenia

35
Q

Treatment of of Chédiak-Higashi syndrome?

A

Daily Bactrim, Daily ascorbic acid

36
Q

Seen in Severe congenital neutropenia

A

Cyclic neutropenia

37
Q

What is myeloperoxidase deficiency ?

A

NADPH Oxidase Deficiency

38
Q

myeloperoxidase deficiency and candidiasis

A

Only DM patients get Candidiasis

39
Q

What is Chronic granulomatous disease?

A

Mutation in NADPH complex, can not produce H2O2

40
Q

Clinical characteristics of chronic granulomatous disease

A

Severe Pneumonias, Tumor like granuloma in the lungs, skin, bones

41
Q

Treatments For Immune Deficiencies

A
  • Gamma-globulin therapy
  • Transplantation or transfusion
  • Treatment with soluble immune mediators
  • Gene therapy
42
Q

Normal microbiome

A
  • symbiotic relationship between humans and microorganisms
  • skin, mouth, GI tract, respiratory tract, genital tract
43
Q

Explain symbiotic relationship with the microbiome in the gut

A
  • normal bacterial microbiome of human gut is provided w/nutrients from ingested food & in exchange
  • produce enzymes that facilitate digestion of complex molecules
  • produce antibacterial factors (baceriocins, colicins) to prevent colonization by pathogens
  • produce usable metabolites metabolites (e.g., vit K, B)
44
Q

True pathogens vs opportunistic microorganisms

A
  • Opportunistic microorganisms cause disease only in immune compromised state
  • True pathogens find a way to circumvent individual’s defences (usually d/t # of organisms, not immune competence)
45
Q

How is homeostasis maintained w/normal microbiome?

A
  • Physical integrity of skin/gut (breach –> local infections, sepsis, etc)
  • Immune & inflammatory systems (compromised immune –> opportunistic infections)
  • BUT this relationship can be breached by injury. Leave normal site and go cause infection
46
Q

Stages of infection (pathogen perspective)

A
  • Colonization
  • Invasion
  • Multiplication
  • Spread
47
Q

How does colonization work?

(stages of infection)

A
  • Microorganism finds its way from reservoir to individual
  • After deposition, stabilizes adherence to tissue through specific surface receptors (thus difficult to removal by mechanical factors, e.g. by coughing)
  • Specificity of adherence limits infection locations – e.g., cold virus to respiratory tract
  • Adherence often through pili on bacteria (rod-like projections), but many other methods – complement receptors, AA sequence in fibronectin, etc.
48
Q

Biofilm

A

Consist of mixed species of microorganisms, e.g., bacteria, fungi, viruses – often grow together to increase chance of survival. Play a role in recurrent and persistent infections

49
Q

Colonization: types of reservoirs

A
  • Animal reservoirs
  • contaminated materials (direct exposure)
  • Human
    • Horizontal transmission
    • Vertical transmission
50
Q

Colonization: animal reservoirs

A
  • Direct contact (e.g., rabies bite)
  • Vectors (insects)
    • Mechanical vectors (passive: housefly)
    • Biologic vectors (bites/stings: fleas, lice, mosquitos)
51
Q

Colonization: direct exposure to contaminated materials

A
  • Fecal-oral (salmonella, cholera, hep A, polio, rotavirus)
  • Soil (tetanus)
52
Q

Colonization: human-human horizontal transmission

A
  • Droplets (respiratory – common cold, flu, strep throat, bact meningitis)
  • Physical contact (sex, blood, wounds – STIs, hep B, CMV, HSV, warts)
  • Airborne transmission (rare – SARS, TB, norovirus, smallpox)
53
Q

Colonization: human-human vertical transmission

A
  • Mother-child placenta (treponoma pallidum, listeria monocytogenes, CMV, toxoplasma gondii)
  • Mother-child birth canal (GBS, E coli, chlamydia, gonorrhoeae, hep B, HIV, C. albicans)
  • Mother-child breast milk (S. aureus)
54
Q

How does invasion work?

(stages of infection)

A

After colonization, find way to penetrate tissues & evade nonspecific and specific defenses (inflammation & immunity)

55
Q

How does multiplication work?

(stages of infection)

A
  • Human tissue is warm & nutrient filled = most microorganisms can rapidly multiply
  • Viruses: replicate w/in cells
  • Bacteria: some intracellular and replicate in macrophages and other cells
  • Immune response takes 3-5 days. If can divide faster, more effective and fatal (cholera, some group A strep, GBS)
56
Q

How does spread work?

(stages of infection)

A
  • Relies on virulence factors (e.g., adhesion molecules, toxins, protection against inflammatory & immune systems)
  • localized w/o spread to other regions (cholera)
  • Or highly invasive – lymphatics, blood, internal organs
57
Q

Stages of infection (individual perspective)

A
  • Incubation period
  • Prodromal stage
  • Invasion period
  • Convalescence (or, less commonly fatal or latent)
58
Q

Mechanism of action

A

How organism damages tissue

59
Q

Infectivity

A

Ability of pathogen to invade & multiply in host

60
Q

Pathogenicity

A

Organisms potential to cause disease

61
Q

Virulence

A

Capacity of pathogen to cause severe disease

62
Q

Immunogenicity

A
  • Capacity of pathogen to cause significant immune reaction
  • e.g. Staph aureus, while waiting for echo, you can get rheumatoid factor (if no RA). Sensitive not specific.
63
Q

Toxigenicity

A
  • Toxin production capacity, influences virulence
  • e.g., 2 strains of e coli w/differing toxigenicity. One releases toxins, the other not
64
Q

Endemic classification

A

Relatively high, but constant, rates of infection in a particular population

65
Q

Epidemic classification

A

Number of new infections in a particular population greatly exceed number usually observed

66
Q

Pandemic

A

Epidemic that spreads over a large area, such as continent or worldwide

67
Q

Pathogen defense mechanisms

A
  • Surface coats
  • Antigenic variation
68
Q

Examples of antigenic variation

A
  • Mutation
    • Antigenic drift
  • Recombination
    • Antigenic shift
  • Gene switching
    • “hypermutable gene”
69
Q

Gene switching: which is the most concerning hypermutable gene?

A

Pseudomonas