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Basic Pathology > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

1
Q

Microbe Routes of Entry

A
  • Skin.
  • GI tract.
  • Respiratory tract.
  • Urogenital tract.
  • Vertical transmission.
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2
Q

Microbe Routes of Entry:
Skin:
- Main Defense Mechanisms

A

Epidermis:

  • Mechanical barrier (when intact).
  • Low pH.
  • Produces antimicrobial fatty acids.
  • Produced defensins (small peptides toxic to bacteria).
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3
Q

Microbe Routes of Entry:
Skin:
-How Defenses Breached and Common associated pathogen

A
  • Mechanical injury (e.g. puncture, burn, ulcer, IVC):
    • STAU
    • C. albicans
    • P. aeruginosa
  • Needle stick:
    • HIV
    • Hepatitis
  • Vector or animal bite:
    • Yellow fever
    • Malaria
    • Plague
    • Rabies
  • Direct penetration:
    • Schistosoma larvae (release enzymes which dissolve skin adhesion proteins).
    • Dermatophytes (superficial infections of intact skin, hair, nails).
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4
Q

Microbe Routes of Entry:
GI Tract:
- Main Defense Mechanisms

A
  • Acidic gastric secretions.
  • Mucus layer.
  • Pancreatic enzymes.
  • Bile detergents.
  • Epithelium - mechanical barrier.
  • Epithelium - produces antimicrobial defensins.
  • Mucosal lymphoid tissue (e.g. Peyers patches) - produces IgA.
  • Peristalsis.
  • Normal gut microbiota.
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5
Q

Microbe Routes of Entry:
GI Tract:
How Defenses Breached and Common associated Pathogen

A
  • Toxin production in food:
    • STAU (acute food poisoning).
  • Attachment and local proliferation:
    • Vibrio cholerae.
    • Giardia duodenalis.
  • Attachment and mucosal invasion^:
    • Shigella sp.
    • Salmonella enterica.
    • Campylobacter jejuni.
    • Entamoeba histolytica.
  • Uptake through M cells:
    • Poliovirus.
    • Salmonella sp.
    • Shigella sp.
  • Acid-resistant cysts and eggs:
    • Protozoa.
    • Helminths.
  • Obstruction, ileus, post surgical adhesions:
    • Mixed aerobic and anaerobic bacteria (E.coli, Bacteroides).
  • Resistant microbial external coats:
    • Hep A.
    • Rotavirus.
    • Norovirus.
  • Broad spectrum Abx use:
    • C. difficile.

^Mucosal invasion –> haemorrhage –> dysentery.

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6
Q

Microbe Routes of Entry:
Respiratory Tract:
-Main Defense Mechanisms

A
  • Mucociliary clearance (large microorg’s)
  • Alveolar macrophages (small microorg’s < 5 microns).
  • IgA.
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7
Q

Microbe Routes of Entry:
Respiratory Tract:
How Defenses Breached and Common associated Pathogen

A
  • Attachment, invasion and local proliferation:
    • Influenza (envelope protien - haemagglutinin)
  • Ciliary paralysis by toxins:
    • H. influenzae.
    • Mycoplasma pneumonia.
    • Bordatella pertussis.
  • Resistance to phagocyte killing:
    • TB.
  • Immunocompromised host:
    • Superseded bacterial infections.
  • Immunosuppressed host:
    • Pneumocystis jirovecii.
    • Aspergillus sp.
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8
Q

Microbe Routes of Entry:
Urogenital Tract:
-Main Defense Mechanisms

A
  • Regular urination.
  • Normal vaginal microbiota (lactobacilli) –> low pH environment.
  • Intact epidermal / epithelial barrier.
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9
Q

Microbe Routes of Entry:
Urogenital Tract:
How Defenses Breached and Common associated Pathogen

A
  • Obstruction of urinary flow or reflux of urine^:
    • E.coli.
  • Abx use (kills lactobacilli):
    • C. albicans.
  • Attachment and local proliferation:
    • N. gonorrhoeae.
  • Direct infection / local invasion:
    • Herpes.
    • Syphilis.
  • Local trauma:
    • STIs (e.g. HPV).

^Facilitates microbial attachment and local proliferation.

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10
Q

Microbe Routes of Entry:
Vertical Transmission.

A
  • Placental - foetal:
    • e.g. Rubella in 1st trimester –> heart malformation, ID cataracts, deafness.
  • During vaginal birth:
    • e.g. gonococcal and chlamydia conjunctivitis.
  • Postnatal (through breastmilk):
    • e.g. CMV, HIV, Hep B.
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11
Q

Prokaryote

A
  • Lacks a nucleus.
  • DNA = single, ds, circular chromosome.
  • Transcription and translation can occur simultaneously.
  • Cell wall.^
  • Contain “plasmids” (carry extrachromosomal DNA).
  • Ribosome (70S) rich cytoplasm.

^Exception: mycoplasma.

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12
Q

Eukaryote

A
  • Has a nucleus with a nuclear membrane.
  • DNA = several chromosomes within nucleus.
  • Transcription and translation occur separately.
  • Membrane bound organelle rich cytoplasm.
  • 80S ribosomes.
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13
Q

Microbe Spread in Host

A
  • Lymph system: direct or within inflammatory cells.
  • Bloodstream: direct, within inflammatory cells, or via lymph system.
  • Nervous system.
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14
Q

Microbe Strategies to Evade Host Immune Defenses

A
  • Modulation of surface antigens to avoid recognition.
  • Inhibition of phagocytosis.
  • Inhibition of phagosome-lysosome fusion.
  • Escape from phagosome.
  • Modulate signal transduction.
  • Modulate gene expression.
  • Modulate cell death.
  • Production of viral cytokines or soluble receptor homologs.
  • Inhibition of antigen presentation.
  • Hide from immune surveillance (viral latency).
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15
Q

Microbe Strategies to Evade Host Immune Defenses:
Modulation of surface antigens:
-Mechanisms

A
  • High mutation rate:
    • HIV.
    • Influenza.
  • Genetic reassortment:
    • Influenza.
    • Rotavirus.
  • Genetic rearrangement (gene recombination / gene conversion / site-specific inversion):
    • Borrelia burgdorferi (Lyme disease).
    • Neisseria gonorrhoeae.
    • Trypanosoma brucei (African Sleeping Sickness).
    • Plasmodium falciparum.
  • Large diversity of serotypes:
    • Rhinovirus.
    • Streptococcus pneumoniae.
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16
Q

Microbe Strategies to Evade Host Immune Defenses:
Inhibition of Phagocytosis:
-Mechanisms

A
  • CHO capsule:
    • S. pneumoniae.
    • N. meningitidis.
    • H. influenzae.
  • Protein A expression –> binds Fc portion of abs –> prevents binding to phagocytes Fc receptors:
    • S. aureus.
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17
Q

Microbe Strategies to Evade Host Immune Defenses:
Inhibition of Phagosome-lysosome fusion:
-Example pathogen

A

Myobacteria.

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18
Q

Microbe Strategies to Evade Host Immune Defenses:
Escape from Phagosome:
-Example pathogen

A

Listeria monocytogenes.

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19
Q

Examples of Injury by Host Immunity

A

M. tuberculosis:
* Granulomatous inflammatory reaction –> tissue damage and fibrosis.

HBV / HCV:
* Hepatocyte damage secondary to host T and NK cells trying to clear infection.

Streptococci:
* Antibodies against Strep M antigen damages heart –> rheumatic heart disease.
* Strep ag-antistrep abs immune complexes deposit in glomeruli –> post strep GN.

Gut microbes:
* Inflammation and epithelial injury cycles –> IBD.

Viruses (HBP / HBC / HPV) / Bacteria (H.pylori):
* Cause chronic inflammation –> cancer.

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20
Q

Examples of Infections in Immunodeficiencies

A

Antibody deficiencies (e.g. X-linked agammaglobulinaemia):

  • Extracellular bacterial infections (S. pneumoniae, HMIN, STAU).
  • Viruses (Rotavirus, enterovirus).

Complement defects:

  • Encapsulated bacterial infections (S. pneumoniae).
  • Neisseria spp. (C5 - C9 / MAC deficiencies).

Neutrophil Fn defects (e.g. Chronic granulomatous disease):

  • STAU infections.
  • GNB infections.
  • Fungal infections.

Toll-like receptor signalling pathway defects:

  • MyD88 or IRAK4 mutations - pyogenic bacterial infections (S. pneumoniae).
  • Impaired TLR3 - HSV encephalitis.

T-cell defects:

  • Intracellular pathogens (viruses, some parasites).
  • IL-12, IFN-gamma, STAT1 mutations –> impaired T-helper 1 (Th1) generation –> atypical mycobacterial infections.
  • STAT3 mutations –> impaired Th3 generation –> chronic mucocutaneous candidiasis.
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21
Q

Examples of Infection Causing Immunodeficiency

A
  • HIV.
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22
Q

Examples of Infections in Acquired Immunodeficiencies

A

Opportunistic pathogens:
* Aspergillus spp.
* Pseudomonas spp.

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23
Q

Common Infections in Non-Immune diseases / injuries

A

CF:

  • Pseudomonas aeruginosa.
  • Burkholderia cepacia.

Sickle cell disease:

  • S. pneumoniae (due to loss of splenic macrophages).

Burns:

  • P. auruginosa.
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24
Q

Viral Tropism

A
  • A viruses preference of cell to infect.
  • Major determinant = viral receptors on cell surface.
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25
Q

Leptospirosis:
-Key facts

A
  • Caused by bacterial spirochete Leptospira.
  • Spread by infected animal urine and body fluids.
  • Temperate and tropical climates mostly affected.
  • Flood and hurricanes = biggest source of outbreaks.
  • Symptoms vary from non-specific illness (fever, myalgia, vomiting, diarrhoea) to renal / liver failure, or meningitis.
  • Treat with doxycycline PO or peniciilin IV.
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26
Q

Leptospira

A
  • Spirochete (GN spiral bacteria).
  • Long.
  • Thin.
  • Motile.
  • Causes Leptospirosis.
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27
Q

Leptospirosis:
-Source

A
  • Urine of infected animals (Cows, pigs, horses, dogs, rodents, wild animals).
  • Soil and water contaminated with infected urine.^
  • Infected animals can excrete bacteria sporadically or continuously for months to years.
  • Occurs worldwide, but most common in temperate and tropical climates.

^Can live in soil / water for weeks to months.

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28
Q

Leptospirosis:
-Transmission to humans

A
  • Through contact with infected animals urine or bodily fluids (NOT saliva) directly or through contaminated water / soil / food.
  • Enters through skin, or mucous membranes especially if skin damaged, or through drinking contaminated water.
  • Person to person transmission RARE.
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29
Q

Leptospirosis:
-Outbreaks

A
  • Floods.
  • Hurricanes.

i.e. exposure to contaminated water.

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30
Q

Leptospirosis:
-Incubation period

A
  • 2 days to 4 weeks.
  • Commonly between 5 to 14 days.
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31
Q

Leptospirosis:
-Symptoms

A
  • May be asymptomatic.
  • Symptoms begin abruptly with high fever +/- other sx.
  • Can present in 2 phases:
    1. Fever, chills, headache, myalgia, diarrhoea. May have recovery period then redevelop illness.
    2. Kidney or liver failure, meningitis, respiratory distress, or haemorrhage. 2nd phase more severe.
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32
Q

Leptospirosis:
-Length of disease

A

Few days to >=3 weeks.
Untreated, can last months.

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33
Q

Leptospirosis:
-Treatment

A

Mild disease:
* PO doxycyline 100mg BD.
* Alternate options: azithromycin, ampicillin, amoxicillin.

Severe disease:
* IV penicillin.
* Alternate option: ceftriaxone.

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34
Q

Leptospirosis:
-Pet symptoms

A
  • Fever.
  • Vomiting.
  • Abdominal pain.
  • Diarrhoea.
  • Refusal to eat.
  • Severe weakness and depression.
  • Stiffness.
  • Severe muscle pain.
  • Inability to have puppies.
  • May be asymptomatic.

NB. Pets can be vaccinated against Leptospirosis.

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35
Q

Sporothrix

A
  • Fungus
  • Found in soil and on plant matter (sphagnum moss, rose bushes, hay, wood).
  • Also from infected Brazilian cats.
  • Causes sporotrichosis (Rose-gardener’s disease).

Image: https://www.cdc.gov/fungal/diseases/sporotrichosis/

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36
Q

Sporotrichosis:
-Types and Human transmission

A

Cutaneous:

  • Most common.
  • From broken skin touching infected plant matter or from infected Brazilian cat scratches / bites.

Pulmonary:

  • Rare.
  • Breathing in fungal spores.

Disseminated:

  • Immunocompromised / immunosuppressed patients.

NB.: No person to person spread.

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37
Q

Sporotrichosis:
-Symptoms

A

Cutaneous:

  • Small, painless lump –> large, open sore / ulcer.
  • Slow to heal.
  • Can have multiple lumps.

Pulmonary:

  • Cough.
  • SOB.
  • Chest pain.
  • Fever.

Disseminated:

  • Joint pain.
  • Concentration difficulties.
  • Headaches.
  • Seizures.
38
Q

Sporotrichosis:
-Incubation period

A

1 to 12 weeks.

39
Q

Sporotrichosis:
-Treatment

A

Cutaneous:

  • Itraconazole PO for 3 - 6 months.
  • Supersaturated potassium iodide.
  • Above not suitable in pregnancy.

Pulmonary or Disseminated:

  • IV amphotericin B followed by PO itraconazole for 12 months total.
  • Pulmonary may require surgical resection.
40
Q

Sporotrichosis:
-What is Sporothrix brasiliensis, what region of the world is it found, and how is it transmitted to humans

A
  • Fungus found in cats in Brazil and South America.
  • Spread from plants to cats / rodents / humans AND animals to animals AND animals to humans.
  • Infected cats are identified by lesions.
  • Spread to humans through cat scratch / bites or from touching infected cat and then touching ones eyes.
41
Q

Urethritis

A
  • Inflammation of the urethra.
  • Causes: infectious and non-infectious.
  • Primarily from an STI.
42
Q

Urethritis in men:
-Diagnosis

A
  • Mucopurulent or purulent urethral discharge.
  • Urethral smear gram stain:
    • > 5 polymorphonucelar (PMN) cells per high power field.
    • Most sensitive and specific for non-specific urethritis and gonorrhoea in asymptomatic men.
  • First pass urine:
    • > 10 PMN cells per high power field.
    • Low sensitivity.
43
Q

Urethritis in men:
-Classification

A
  • Gonococcal.
  • Non-gonococcal (other pathogens or non-infective causes)^.
  • Persistent or Recurrent (10-20% of non-gonococcal urethritis).

^ More common than Gonococcal.

44
Q

Urethritis in men:
-Non-gonococcal causes

A
  • Chlamydia trachomatis.^
  • Mycoplasma genitalium.^
  • Pathogen negative (older males without sx).
  • Trichomonas vaginalis (men > 30 yrs).
  • Ureaplasma urealyticum (5-10%).
  • ?UTI (6.4%).
  • Adenovirus (2-4%; associated conjunctivitis).
  • HSV 1 and 2 (2-3%).
  • EBV.
  • N. meningitidis.
  • Haemophilus spp..
  • Candida spp..
  • Urethral stricture.
  • Foreign bodies.

^30 - 80% cases. Usually younger patients with discharge / dysuria.

45
Q

Urethritis in men:
-Recurrent or Persistent causes

A
  • No identifiable cause.
  • Mycoplasma genitalum (20 - 40%).
  • Ureaplasma urealyticum (tetracycline R).
  • Trichomonas vaginalis.
46
Q

Urethritis in men:
-Symptoms

A
  • Asymptomatic (90-95% with gonococcal; 50% with chlamydia).
  • Mucopurulent or purulent urethral discharge +/- blood.
  • Urethral pruritis.
  • Dysuria.
  • Penile discomfort.
  • Skin lesions (if HSV cause).
  • Systemic symptoms (conjunctivitis, arthritis).
  • Haematuria.
  • Lymphadenopathy.
47
Q

Urethritis in men:
-Investigations

A
  • First pass urine for Chlamydia / gonorrhoea PCR.
  • Urethral swab MC+S and chlamydia / gonorrhoea PCR.
  • +/- Pharyngeal +/- rectal swab.
  • Urine MC+S.
  • Consider: HIV, Hepatitis and syphilis testing.
48
Q

Urethritis in men:
-DDx

A
  • Candidal balanitis.
  • Epididymo-orchitis.
  • Cystitis.
  • Acute prostatitis.
  • Urethral malignancy.
49
Q

Urethritis in men:
-Treatment

A

Non-gonococcal urethritis:
* Doxycyline 100mg BD for seven days.
* Azithromycin 1g stat.
* If M. genitalium positive- azithromycin 500mg stat then 250mg daily for 4 days.

Gonococcal urethritis:
* Uncomplicated- ceftriaxone 1g IM stat.

NB. Need contact tracing^, treat partner, and advise no sexual activity (including oral) for 14 days post rx (if azithromycin), or on completion of doxycycline, or sx resolved and partner also completed treatment.

NB. Review post treatment with proof of cure for gonorrhoea.

^NGU- 4 weeks prior to dx (or 6 months if asymptomatic).
Gonococcal- 2 weeks prior.

50
Q

Urethritis in men:
-Complications

A
  • Epididymitis and/or orchitis.
  • Prostatis.
  • Systemic dissemination of gonorrhoea (conjunctivitis, arthritis, skin lesions).
  • Reactive arthritis.
  • PID.
  • HIV.
51
Q

Anaerobic Gram Positives

A

Susceptible to beta lactams

52
Q

Anaerobic Gram Negatives

A

Produce beta-lactamases.
Treat with Metronidazole.

53
Q

Why are Chronic Granulomatous Disease patients susceptible to catalase-positive organisms?

A
  • Chronic granulomatous disease = deficiency of NADPH oxidase.
  • NADPH oxidase required for oxidation of NADPH to NADP in neutrophils.
  • Oxidation of NADPH –> production of ROS.
  • ROS –> killing of microorganisms.
  • No NADPH oxidase –> No oxidation of NADPH –> no ROS –> unable to kill microorganism.
54
Q

How are virulence factors acquired and what are some examples?

A

Via:

  • Plasmids
  • Bacteriophages^ (e.g. Corynebacteria diphtheria acquire virulence factor from virus).

Examples:

  • Biofilms (ability for communities of bacteria to live in viscous polysaccharide –> persistance of infection particularly on surfaces and devices, and increases abx resistance).
  • Adhesion properties.
  • Invasive properties.

^ Bacteriophages = viruses which transfer virulance factors to bacteria.

55
Q

Syphilis:
What bacteria causes Syphilis, what are the stages of syphillis, and what are the manifestations at each stage?

Highly examinable

A

Bacteria:

  • Treponema pallidum (spirochete).

Stages:

  • Primary (3 - 90 days, ave 21 days post infection).
  • Secondary (Weeks - months post primary).
  • Tertiary.
  • Latent.
  • Congenital.

Manifestations - Primary:

  • Chancre (painless skin lesion on pharynx, penis, vagina, anus)

Manifestations - Secondary:

  • Systemic illness - fever, weight loss, night sweats, adenopathy, rash, alopecia, hepatitis.

Manifestations - Tertiary:

  • CV disease.
  • Gummatous disease (granulomatous disease of skin, subcut tissues, bone, viscera)

Manifestations - Latent:

  • Asymptomatic.

Manifestations - Congenital:

  • Asymptomatic (60 - 90%).
  • Hepatomegaly.
  • Jaundice.
  • Nasal discharge.
  • Rash.
56
Q

By which mechanism do Candida evade antifungal therapy?

A

Formation of a biofilm.

57
Q

What is Staph aureus’s distinctive inflammatory feature?

A

Local destruction of host tissue.

58
Q

In sepsis, what does the release of endotoxins from GNBs cause?

A

Endothelial cell injury –> DIC.

Lab results:
* Prolonged PT and aPTT.
* Low platelets.
* High D-dimer.

59
Q

Which bacteria have no cell wall

A
  • Mycoplasma.
  • Ureaplasma.
  • Chlamydiaceae.
  • Coxiella burnetti.
  • Rickettsia.
60
Q

What stain is used for Mycobacteria and why.

A

Stain:
Zeihl-Neelsen.

Why:
Different cell wall with mycolic acid causing them to be Acid-fast.

61
Q

What are the structural features of Gram-positive bacteria.

A

Cell membrane:

  • Only one.
  • Inner location, under cell wall.
  • Bi-phospholipid layer.

Cell wall:

  • Thick.
  • Rich in peptidoglycan.
  • Gives strength.
  • Opposes osmotic pressure.

Capsule:

  • Only in some (e.g. SPPN).
  • Essential for immune evasion.

Porins:

  • Located in Cell membrane.
  • Allow substrates in and toxins out.

Flagella:

  • Only in some.
  • Extends from cell membrane.
  • Gives motility.

Fimbriae / pilli:

  • Hair-like extension.
  • Extends from cell membrane.
  • For adhesion.

Inside cell:

  • Cytoplasm.
  • Nucleoid.
  • Plasmids.
  • Storage granules.

Endospores:

  • Only in some (e.g. Clostridium).
  • Formed as a result of environmental stress.
62
Q

What are the structural features of Gram-negative bacteria.

A

Cell membrane:

  • Two.
  • Inner and outer, surrounding cell wall.
  • Creates periplasmic space.
  • Important for concentration of beta-lactamases and cells processes.

Cell wall:

  • Thin.
  • Little peptidoglycan.

Capsule:

  • Only in some (K. pneumo).
  • For immune evasion.

Porin:

  • Found in inner and outer membranes.
  • Allows substrates in, toxins out.

Flagella:

  • Only in some.
  • Extends from inner cell membrane.
  • For motility.

Fimbriae / pilli:

  • Hair-like extensions.
  • Extends from inner cell membrane.
  • For adhesion.

Inside cell:

  • Cytoplasm.
  • Nucleoid.
  • Plasmids.
  • Storage granules.
63
Q

What are the dsDNA viruses

A
  • Herpes family (HSV1, HSV2, CMV, EBV, VZV, EBV, HHV6, HHV8)
  • Adenovirus.
  • Hepatitis B.
  • Parvovirus.
  • Papilloma virus.
  • Molluscum virus.
  • JC virus.
64
Q

What are the ssRNA viruses

A
  • Echovirus.
  • Rhinovirus.
  • Coxsackie virus.
  • Coronavirus.
  • Influenzae A and B.
  • Paraflu 1 - 4.
  • Hepatitis A, C, D, E.
  • Measles.
  • Rubella.
  • HIV 1 and 2.
  • HTLV 1 and 2.
  • Dengue and other arboviruses.
  • RSV.
  • Mumps virus.
65
Q

What are the dsRNA viruses

A

Rotavirus

66
Q

Describe yeasts and give examples.

A

Description:

  • Single cell.
  • Moist, creamy-opaque colonies.

Examples:

  • Candida.
  • Cryptococcus.
67
Q

Describe moulds and give examples.

A

Description:

  • Filamentous fungi.
  • Fluffy, cottony, wooly, or powdery colonies.

Example:

  • Aspergillus sp.
  • Mucour sp.
68
Q

What are some intracellular protozoa

A
  • Trypanosoma cruzi.
  • Leishmania sp.
  • Toxoplasma gondii.
69
Q

What are the bloodstream protozoa

A
  • Plasmodium sp.
  • Babesia sp.
  • Trypanosoma sp.
70
Q

What are the luminal / epithelial protozoa

A
  • Entamoeba histolytica.
  • Giardia lamblia.
  • Cryptosporidium sp.
  • Trichomonas vaginalis.
  • Blastocystic hominis.
  • Dientamoeba fragilis.
71
Q

What are the free living protozoa

A
  • Naegleria floweri (causes meningoencephalitis).
  • Acantomoeba (causes meningoencephalitis or keratitis).
  • Balamuthia.
72
Q

What are the Nematodes (round worms)

A
  • Enterobius vermicularis.
  • Ascaris lumbricoides.
  • Strongyloides stercoralis.
  • Trichuris trichuira
  • Hookworms (Ancylostoma duodenale and Necator americanus).
73
Q

What are the Filarial Nematodes

A

Onchocera volvulus.

74
Q

What are the Trematodes (Flukes)

A
  • Schistosomiasis sp.
  • Paragonimus sp.
  • Fasciola sp.
  • Opisthorchis sp.
75
Q

What are the Cestodes (flatworms)

A
  • Taenia sp. (Taenia saginatum, T. solium).
  • Diphyllobothrium latum (fish tapeworm).
  • Echinococcus granulosis.
76
Q

What is Gram-negative Endotoxin, what does is consist of, and what does it do

A

What it is:

  • Toxin which is part of the bacteria outer cell membrane.
  • Released when bacteria lysed.

Consists of:

  • Lipid (conserved) molecule.
  • Polysaccharide (variable) molecule (e.g. O-antigen).

Function:

  • Binds TLRs –> induces innate immune response.
  • Stimulates alternative complement pathway.
  • Causes endothelial damage –> tissue factor release –> initiation of coagulation –> DIC.
77
Q

What is Exotoxin, what are the types, what does each type do, and what are some examples.

A

What it is:

  • Toxins produced by microbes.
  • Excreted into the environment.
  • Named via target tissue (e.g. neurotoxin, enterotoxin)

Types:

  • Superantigens.
  • Enzymes.

Superantigen functions and example:

  • Fn - Bind large groups of T cells via conserved domains in TCR.
  • E.g. - Toxic shock syndrome toxin.

Enzyme functions and examples:

  • Fn - degrade keratinocyte adhesion molecule (e.g. exfoliatin).
  • Fn - alters intracellular signalling
78
Q

How does Aspergillus cause disease

A

Invades blood vessels –> haemorrhage and infarction superimposed on necrosis.

79
Q

How does mucour species (mould) cause disease

A
  • Local tissues necrosis.
  • Invades arterial walls.
  • Penetrates periorbital tissue and cranial vault.
80
Q

How does PJP cause disease

A
  • Fills alveolar spaces –> foamy, amorphous material, cellular debris and organisms.
  • Interstitial inflammatory reaction.
  • Widening of septa.
  • Protein and fibrin exudation.
  • Pneumocyte proliferation.
  • Escape of RBCs.
  • Formation of hyaline membranes.
81
Q

Echiococcus granulosus:
-What is it, what is the life cycle, what does it cause, and how is it diagnosed

A

What it is:

  • Tissue cestode (flatworm).

Life cycle:

  1. Adult worm in intestine of definitive host (dogs).
  2. Embryonated eggs in faeces (infective stage).
  3. Ingested by intermediate host (sheep, goat, swine) OR ingestion by humans.
  4. Egg hatches in small bowel and releases oncosphere.
  5. Oncosphere penetrates intestinal wall and migrates via circulation to other organs.
  6. Hydatid cyst formed in liver, lung (diagnostic stage).
  7. Definitive host ingests infected organs of intermediate host.
  8. Protoscolex released from cyst.
  9. Attaches to intestinal wall and matures (into scolex then adult).

Causes:

  • Hydatid cysts in liver, lung, other organs.

Diagnosis:

  • Radiology.
  • Serology.
  • +/- microscopy of cyst.
82
Q

Entamoeba histolytica:
-What is it, how is it transmitted, what is the life cycle, what does it cause, and how is it diagnosed

A

What it is:

  • Intestinal protozoa.
  • 12 - 60 microm diameter.

Transmitted:

  • Faecal - oral route.

Life cycle:

  1. Trophozoite (free living) and cyst passed in faeces.
  2. Cyst matures.
  3. Mature cyst ingested.
  4. Develops into trophozoite and more cysts.
  5. Trophozoite causes extensive tissue distruction via phagocytosis and cytopathic effect from humoral and cell mediated immune responses.

Causes:

  • Amoebic colitis.
  • Extraintestinal abscess (liver, colon).

Diagnosis:

  • Faecal or liver aspirate PCR.
  • Serology.
  • Faecal OCP (difficult to distinguish from non-pathogenic Entamoeba).
83
Q

Pneumocystis jirovecii
-What is it, what are the three forms and their approximate sizes, what does it cause, who is at risk, how is it transmitted, what are the microscopy features, and what is the treatment

Previously known as P. carinii

A

What it is:

  • Yeast-like fungus.

Forms and sizes:

  • Trophozoite (1 - 4 microm).
  • Sporocyte (5 - 6 microm).
  • Cysts (5 - 8 microm).

Causes:

  • Opportunistic infections.
  • Rapidly progressive, bilateral pneumonia.

Who it affects:

  • Immunocompromised (HIV / AIDS).
  • Immunosuppressed.

Transmission:

  • Airborne.

Microscopy:

  • Wright-Giemsa stains - can see nucleus and mitochondria.
  • Methenamine silver stain - can see cysts (stain black).
  • Histopathology - alveolar interstital thickening, eosinophilic honeycombed / foamy exudate in lumen of lung.

Treatment:

  • Cotrimoxazole.
84
Q

What is the infective agent in hookworm disease and how do they infect hosts

A

Infective agent:

  • Filariform larvae.

How:

  1. Larvae penetrate skin.
  2. Migrate through circulation to lungs, ascend bronchial tree to pharynx and are swallowed.
  3. Mature in intestine.
  4. Adult worms “hook” into intestine –> blood loss and Fe deficiency.
  5. Eggs passed in faeces.
  6. Rhabditiform larvae hatches in envronment.
  7. Develop into filariform larvae in environment.
85
Q

E. coli is a major causative agent of which diseases

A
  • Haemorrhagic colitis.
  • Peritonitis.
  • Osteomyelitis in IV drug users.
86
Q

Vitamin D is responsible for inducing the expression of what peptide in macrophages and what is this needed to kill?

A

Molecule:
Cathelicidin.

Needed to kill:
TB.

87
Q

What cell usually kills HMIN

A

Neutrophils.

88
Q

What cell usually kills SPPN

A

Neutrophils.

89
Q

How is RSV destroyed by the immune system

A

Destroyed by cell mediated response.

90
Q

How does the body destroy PJP

A
  • Activated macrophages.
  • CD4.

Basic Pathology (14 decks)

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