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ACEM Primary Written > Infectious diseases: Pathology - General principles of microbial activity > Flashcards

Infectious diseases: Pathology - General principles of microbial activity Flashcards

1
Q

What are prions?

A

Abnormal forms of host protein, normally found in neurons
Do not contain RNA/DNA

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2
Q

What is the pathophysiology of prion disease?

A

Prior protein undergoes conformational change that confers resistance to proteases and promotes conversion of normal protease-sensitive PrP to resistant form

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2
Q

What kinds of disease are caused by prions?

A

Spongiform encephalopathies (e.g. kuru, Creutzfeldt-Jakob, bovine spongiform encephalopathy)
Neurodegenerative diseases (e.g. fatal familial insomnia)

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3
Q

Describe the composition of viruses

A

Nucleic acid genome encased in (icosahedral or helical) protein capsid, with or without a lipid envelope

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4
Q

What size are viruses?

A

20-300nm

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5
Q

Give two examples of viruses which aggregate within cells to form larger inclusion bodies

A

CMV
HSV

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6
Q

What kind of organism are bacteria?

A

Prokaryotes (have cell membrane but lack membrane-bound nuclei and other membrane-enclosed organelles)

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7
Q

What is the difference between Gram positive and negative bacteria?

A

Gram positive: thick wall surrounding cell membrane which retains crystal-violet stain
Gram negative: thin wall sandwiched between two phospholipid bilayer membranes

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8
Q

Do Gram positive or negative bacteria have capsules?

A

Both can be encapsulated

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9
Q

Do Gram positive or negative bacteria express lipopolysaccharides?

A

Gram negative bacteria have LPS on their outer cell membranes

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10
Q

How are bacteria based on whether they replicate inside or outside host cells?

A

Extracellular
Facultative intracellular: can survive and replicate inside or outside host cells
Obligate intracellular: can only grow inside cells

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11
Q

Give three examples of obligate intracellular bacteria

A
  1. Chlamydia
  2. Rickettsiae
  3. Coxiella burnetti
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12
Q

Describe the replication of Chlamydia

A

Replicates inside membrane-bound vacuoles in epithelial cells
Cannot synthesise its own ATP (dependent on host cell)

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13
Q

Three types of infection caused by Chlamydia

A
  1. Genitourinary infections
  2. Conjunctivitis
  3. Respiratory infections
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14
Q

Describe the replication of Rickettsiae

A

Replicates inside membrane-bound vacuoles in endothelial cells
Cannot synthesise its own ATP (dependent on host cell)

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15
Q

What type of illness is caused by Rickettsiae?

A

Haemorrhagic vasculitis

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16
Q

How are Rickettsial infections spread? Give three examples

A

Via arthropods:
- Lice: epidemic typhus
- Ticks: Rocky Mountain spotted fever
- Mites: scrub typhus

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17
Q

How is Q fever spread?

A

Aerosol spread, often from domestic animals such as cattle

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18
Q

What organism causes Q fever?

A

Coxiella burnetti

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19
Q

Describe the structure of Mycoplasma

A

Unique extracellular bacteria that lacks a cell wall

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20
Q

What are bacteriophages and plasmids?

A

Mobile genetic elements that encode bacterial virulence factors (e.g. adhesins, toxins, antibiotic resistance)

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21
Q

What are fungi?

A

Eukaryotes with thick chitin-containing cell walls and ergosterol-containing cell membranes

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22
Q

Describe the two possible structural arrangements of fungi

A

Rounded yeast cells
Filamentous hyphae (may be septate or aseptate)

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23
Q

What is thermal dimorphism?

A

Refers to fungi that are in hyphal forms at room temperature but yeast form at body temperature

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24
Q

What are fungal species confined to the superficial layers of human skin called?

A

Dermatophytes

25
Q

What three types of infections are caused by fungi in otherwise healthy people?

A
  1. Superficial skin infections (e.g. tinea pedia)
  2. Abscesses (e.g. sporotrichosis)
  3. Granulomas (e.g. histoplasma)
26
Q

What types of infection are caused by fungi in immunodeficient populations? Give five examples of opportunistic fungal pathogens

A

In immunodeficiency patients, opportunistic fungal pathogens can cause life-threatening infection marked by tissue necrosis, haemorrhage, and vascular occlusion
E.g. Pneumocystis jirovecii, Candida, Aspergillus, Mucor, Cryptococcus

27
Q

What are protozoa?

A

Single-celled eukaryotes with a nucleus, pliable plasma membrane, and complex cytoplasmic organelles

28
Q

How do protozoa replicate?

A

Intracellularly within a variety of cells (e.g. Plasmodium within RBCs, Leishmania in macrophages)
Extracellularly in genitourinary system, intestine or blood

29
Q

How are bloodborne protozoa spread? How are intestinal protozoa spread?

A

Bloodborne: insect vectors
Intestinal: ingestion of cysts in contaminated food/water

30
Q

Give three examples of protozoa and explain how each is transmitted

A
  1. Trichomonas vaginalis: sexually transmitted, colonises vagina and male urethra
  2. Entamoeba histolytica, Giardia lambia: inform of mobile trophozoites that attach to intestinal wall, or immobile stomach acid-resistant cysts
  3. Toxoplasma gondii: from cats
31
Q

What are helminths?

A

Highly differentiated multicellular organisms with complex life cycles

32
Q

Describe the life cycles of helminths

A

Alternate between sexual reproduction in the definitive host and asexual multiplication in the intermediary host

33
Q

What are ectoparasites?

A

Insects or arachnoids that attach to or live on skin
E.g. lice, ticks, mites, bedbugs

34
Q

Five immune factors that form part of the host barrier to infection

A

Innate immunity:
1. Physical barriers (e.g. skin epithelium)
2. Phagocytes and natural killer cells
3. Plasma proteins (complement, cytokines, collectins, acute phase proteins)

Adaptive immunity (stimulated by exposure to microbes, and increase in magnitude, speed, and effectiveness with successive exposures):
1. B lymphocytes
2. T lymphocytes

35
Q

Three skin factors that form part of the host barrier to infection

A
  1. Physical barrier (dense keratinised epithelium)
  2. Low pH 5.5*
  3. Presence of fatty acids*
  • prevents growth of microorganisms other than normal flora
36
Q

Six GIT factors that form part of the host barrier to infection

A
  1. Acidic gastric secretions
  2. Viscous mucus layer covering intestinal epithelium
  3. Lytic pancreatic enzymes and bile detergents
  4. Defensins (mucosal antimicrobial peptides)
  5. Normal flora
  6. IgA antibodies (secreted by B cells in mucosa-associated lymphoid tissue, MALT)
37
Q

Two respiratory tract factors that form part of the host barrier to infection

A
  1. Mucociliary action:
    - Mucus secreted by goblet cells is transported by ciliary action to the back of the throat, where it’s swallowed and cleared
  2. Alveolar macrophages and neutrophils
38
Q

Three genitourinary system factors that form part of the host barrier to infection

A
  1. Regular flushing of urethra with urine
  2. Lactobacilli in vagina maintain low pH
  3. Anatomy (e.g. longer urethra in men protective against UTI)
39
Q

Give four examples of bacteria which impair mucociliary activity

A
  1. H. influenzae
  2. B. pertussis
  3. P. aeruginosa
  4. M. pneumoniae
40
Q

What is tropism?

A

Describes the predilection of viruses to infect certain cell types

41
Q

Outline four factors which determine viral tropism, giving an example of each

A
  1. Expression of host cell receptors for virus (e.g. HIV glycoprotein gp120 binds CD4, CXCR4, CCR5)
  2. Presence of cellular transcription factors that recognise viral enhancer and promoter sequences (e.g. JC virus limited to oligodendrocytes for this reason)
  3. Anatomic barriers (e.g. enteroviruses replicate in GIT due to inherent resistance to acids, bile, digestive enzymes)
  4. Local temperature, pH and host defences (e.g. rhinoviruses replicate optimally in lower temperatures of the upper respiratory tract)
42
Q

What are the three mechanisms by which viruses damage host cells? Give examples where relevant

A
  1. Direct cytopathic effects:
    - Prevent synthesis of host DNA, RNA and proteins (e.g. poliovirus)
    - Produce degradative enzymes (e.g. HSV)
    - Induce apoptosis (e.g. HIV)
  2. Antiviral immune responses (especially cytotoxic T lymphocytes)
  3. Transformation of infected cells into benign or malignant tumour cells
43
Q

Describe three factors which determine bacteria’s ability to damage host cells

A
  1. Adherence to host cells
  2. Invasion of cells and tissues
  3. Toxin production
44
Q

How do bacteria adhere to cells? Give an example

A

Via adhesins (including filamentous bacterial surface proteins called pili)
E.g. protein F and tecichoic acid on Streptococcus pyogenes bind to fibronectin

45
Q

Give two examples of bacteria which have pili

A

E. coli
N. gonorrhoeae

46
Q

Give three examples of mechanisms by which bacteria invade cells and tissues

A
  1. Opsonisation (e.g. M tuberculosis activates the alternative complement pathway)
  2. Gram negative bacteria have a complex secretion system which involves creating pores in host cell membranes to gain entry
  3. Direct cell-to-cell entry via manipulation of the cytoskeleton (e.g. Listeria)
47
Q

Define endotoxin vs exotoxin

A

Endotoxin: lipopolysaccharide (LPS) from outer cell membrane of Gram negative bacteria
Exotoxin: secreted bacterial proteins

48
Q

What is the mechanism of action of endotoxin?

A

Induces cytokines, chemokines and costimulatory molecules for T cell activation
Plays a role in shock, DIC and ARDS due to excess cytokine production (particularly TNF-a, IL-1 and IL-12)

49
Q

Which receptor does endotoxin bind?

A

Complexes with CD14 and then binds TLR4

50
Q

What are the four types of bacterial exotoxins? Give an example of each

A
  1. Enzymes (e.g. proteases secreted by S. aureus)
  2. Toxins altering intracellular signalling and regulatory pathways: have B (Binding) subunits and A (enzymatically Active) subunits (e.g. Vibrio cholerae, Bacillus anthracis, some E. coli strains)
  3. Neurotoxins (e.g. Clostridium botulinum and tetani produce toxins which impair neurotransmitter release and cause paralysis)
  4. Superantigens: stimulate very large numbers of T cell lymphocytes (e.g. S. aureus and S. pyogenes cause toxic shock syndrome)
51
Q

Describe four mechanisms by which microbes evade the host immune system

A
  1. Growth in niches inaccessible to host immune system
  2. Antigenic variation
  3. Resistance to innate immune defences
  4. Impairment of T cell response
52
Q

Give four examples of ways in which microbes grow in niches inaccessible to the host immune system, to evade the immune response

A
  1. Propagate in intestinal lumen (e.g. Clostridium difficile) or gallbladder (e.g. S. typhi)
  2. Rapid invasion of hostel cell before effective humoral response is mounted (e.g. malaria sporozoites entering hepatocytes)
  3. Forming cysts with dense capsule (e.g. tapeworm larvae)
  4. Viral latency
53
Q

Give two examples of mechanisms of antigenic variation

A
  1. Inherent genomic instability (e.g. HIV, influenza)
  2. Variable expression of surface proteins (e.g. Trypanosoma, pneumococcus)
54
Q

Give four examples of ways in which microbes exhibit resistance to innate immune defences

A
  1. Produce capsule which shields bacterial antigens from phagocytosis (e.g. pneumococcus, meningococcus)
  2. Secrete proteases that degrade antibodies (e.g. Neisseria, Haemophilus, Streptococcus)
  3. Replicate inside phagocytes (e.g. mycobacteria, Listeria, Legionella, Cryptococcus, toxoplasmosis)
  4. Produce proteins that block complement activation (e.g. many viruses including HIV)
55
Q

Give two examples of ways in which microbes may impair T cell responses

A
  1. Binding or altering expression of MHC class I (e.g. HSV, CMV, EBV)
  2. Direct infection of lymphocytes (e.g. HIV, EBV)
56
Q

What are the five histological patterns of tissue reaction seen in infection? What types of microbes typically produce each?

A
  1. Suppurative/purulent: pyogenic bacteria (mostly extracellular Gram positive cocci and Gram negative rods)
  2. Mononuclear/granulomatous: viruses, intracellular bacteria, spirochetes, intracellular parasites, helminths
  3. Cytopathic-cytoproliferative: viruses
  4. Tissue necrosis: Clostridium perfringens, E. histolytica
  5. Chronic inflammation: chronic HBV, schistosomiasis
57
Q

Describe the histological features of suppurative infection

A

Increased vascular permeability
Leukocyte infiltration (predominantly neutrophils)
Liquefactive necrosis -> pus

58
Q

Describe the histological features of mononuclear infection

A

Diffuse mononuclear interstitial infiltrate
Mononuclear cell type dependent on host response
Granulomas stimulated by M. tuberculosis, Histoplasma (characterised by epithelioid/giant cells +/- caseous necrosis)

59
Q

Describe the histological features of cytopathic-cytoproliferative infection

A

Cell necrosis or proliferation, usually with sparse inflammatory cells
Inclusion bodies, polykarons, benign/malignant masses

60
Q

Describe the histological features of tissue necrosis infection

A

Gangrenous necrosis
Few inflammatory cells -> resemble infarcts

ACEM Primary Written (160 decks)

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