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BIIC Part 2 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Exotoxins

A

Secreted by bacteria and can act locally or systemically.

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2
Q

Explain Membrane-Active Exotoxins

A

Mostly pore forming. They can mess with ion concentrations and let other unwanted substances into the cell.

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3
Q

What are Hydrolytic Enzymes?

A

They cleave different cellular proteins.

They can also convert plasminogen to plasmin

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4
Q

Explain the make up of Exotoxins

A

A and B units

A unit helps with toxic activity
B unit helps mediate adherence, and aids with entrance into the cell.

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5
Q

Endotoxins

A

Associated with the LPS on the bacterial membrane of gram-negative bacteria.

Will lead to hypotension, hemorrhages, disseminated intravascular coagulation. By release of IL-1 and TNF-a.

LPS acts on lipid A portion:
-Causes fever.

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6
Q

Bacillus Anthracis

A 
Gram Positive
Nonmotile
Aerobic
Facultative anaerobic: can live as without O2
Spore-forming rod

Etiological agent of anthrax

Plasmids encode the virulence factors:

  • Toxin production
  • Capsule formation: decrease Macrophage efficiency

Toxins:

  • Protective Antigen (PA)
  • Lethal Factor (LF)
  • Edema Factor (EF)
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7
Q

Bordetella Pertussis

A

Gram-negative
Aerobic
Coccobacillus

Cause whooping cough

Toxin:

  • pertussis toxin (PT): Hydrolyze cellular NAD and transfers the released ADP-ribose to alpha subunit of heterotrimeric G-proteins
  • Adenylate Cyclase Toxin (ACT): pore-forming repeat in toxin hemolysis domain
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8
Q

Corynebacterium Diptheriae

A

Gram-Positive
Rod

Grow on mucous membranes of UR tract to cause Diptheria

Toxin:
-Diphtheria toxin: encoded in lysogenic, temperate (virus in a) bacteriophage. ***availability of inorganic iron limits bacterial growth rate. The toxin inhibits peptide chain elongation factor EF-2 (important for DNA)

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9
Q

Clostridium Tetani

A

Gram Positive
Rod
Anaerobic

Found in the environment and causes tetanus by contaminate wounds. Spores germinate in the anaerobic environment of devitalized tissue

Toxin: Tetanospasmin

  • Binds to receptors on presynaptic membranes of motor neurons. Stops transport system to the cell bodies in the spinal cord and brainstem.
  • Toxin diffuses to terminals of inhibitory cells
  • Degrades synaptobrevin- required for docking of neurotransmitter vesicles on the presynaptic membrane.

Symptoms:
-Spastic Paralysis. Small amounts of toxin are lethal to humans

Prevention: Immunization with tetanus toxoid.

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10
Q

Clostridium Botulinum

A

Gram positive
Anaerobic
Spore-forming

Found in soil, water, and may grow in foods.

Toxin: Botulinum Toxin- most potent toxin

  • heat label
  • similar to tetanus toxin
  • absorbed from the gut. Binds to receptors of presynaptic membranes of motor neurons of the peripheral nervous system and cranial nerves.
  • Botulinum toxin results in proteolysis of target proteins in the neurons which inhibits release of ACh at the synapse. Results in flaccid paralysis
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11
Q

Clostridium Perfringens

A

Gram-positive
Anaerobic
Spore-forming

Spores introduced into wounds by soil or feces

Toxins are necrotizing and hemolytic. Can cause gas gangrene by distending the tissue.

Toxins:

  • Alpha (CPA): Lecithinase: damages cell membranes by splitting lecithin to phosphorylcholine and diglyceride. Causes Gas Gangrene
  • Beta (CPB): Necrotizing enteritis and enterotoxemia in neonatal individuals
  • Enterotoxin (CPE): Human food-poisoning

Also has collagenases and DNAses

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12
Q

Staphylococcus Aureus

A

Gram-positive
Non-motile cocci

30% of people have it

Skin and soft tissue pathology: impetigo, Scalded skin, folliculitis

Invasive infections: endocarditis, bone and joint infections, bacteremia, and TSS. GI infections cause outbreaks of food poisoning.

Diseases: TSS, SSSS, necrotizing pneumonia, deep-seated skin infections

Toxins:

  • Enterotoxins: food not properly refrigerated like dairy and meat
  • Staphylococcal enterotoxin: absorbed in gut and stimulates vagus nerve receptors to induce vomiting center
  • Pore-forming toxins
  • exfoliating toxins
  • superantigens
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13
Q

What are the virulence factors of Staph Aureus?

A

Panton-Valentine Leukociding (PVL)
- causes lysis of human WBC

Alpha-Hemolysin (alpha toxin)
-Forms pores leading to cell lysis

Phenol-soluble modulins (PSMs)
-small amp hip attic protein that lose human cells like neutrophils and RBC

Arginine catabolic mobile element (ACME)

agr regulatory locus
-[that controls the expression of toxins

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14
Q

Explain the Pore-forming toxins of Staph aureus

A

Hemolysis-a
-Pore formation causing cell lysis, altes cell signaling pathways

Hemolysis-B: Cytotoxic to human keratinocytes, monocytes and T-cells

Leukotoxins: Panton-Valentine Leukocidin, y-hemolysin, leukotoxin ED and AB/GH

Phenol-soluble modulins (PSM)
-Attaches to the cytoplasmic membrane in a non-specific way, which in turn, can lead to membrane disintegration

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15
Q

What are exfoliating toxins of staph Aureus

A

Epidermolytic toxins, induces skin peeling and blister formation using pro teases that Hydrolyze desmosine cadherins

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16
Q

What causes TSS T-1

A

Superantigens of staph aureus

Toxic shock syndrome lots of IL-2, IFN-y and TNF-a.

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17
Q

Streptococcal Toxins

A

Gram-positive
Cocci

Group A B-hemolytic streptococci

Makes a sort of soft tissue infection like TSS

Makes superantigens:

  • Pyrogenic exotoxins A, C, G-M
  • Streptococcal superantigens
  • Streptococcal mitogenic exotoxin Z
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18
Q

Explain Streptolysin S and O

And streptococcal pyrogenic exotxoin B (SpeB)

A

S
-Targets primarily RBC, platelets, subcellular organelles and leukocytes

O

  • Cholesterol-dependent cytolysin
  • Targets macrophages, neutrophils, epithelial cells, and endothelial cells.
  • contributes to impaired phagocytosis clearance

SpeB
-Cysteine protease, cleaves IgG into Fc and Fab. Degrades the other Ab

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19
Q

What are examples of Strep enterotoxins?

A

Bacillus cereus

Vibrio cholera
-Increase cAMP, and increases secretion of electrolytes into the small bowel. Lose Cl, Na, and bicarbonate

Salmonella

Shigella

Escherichia

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20
Q

What are the common features of viral hemorrhagic fevers?

A

Affect many organs
Damage the blood vessels
Affect body’s ability to regulate itself.

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21
Q

Arenaviridae

Bunyaviridae

Filoviridae

Flaviviridae

A

Lassa fever, Junin and Machupo

Crimean-Conga haemorrhagic fever, Rift Valley fever, Hantaan haemorrhagic

Ebola and Marburg

Yellow Fever, Dengue, Omsk Haemorrhagic Fever, Kyasanur Forest disease.

22
Q

Arenaviridae

A

RNA genome, enveloped

Associated with rodent-transmitted diseases.

Tacaribe complex: new world rats and mice
LCM/Lassa Complex: Old world rats and mice.

Viruses shed by urine or droppings. Human infections by ingestion of contamination, direct contact by broken skin, inhalation of rodent urine

Lassa Fever Virus

Acute viral haermorrhagic illness: 2-21 days usually occurs in West Africa.

Transmission: Contact with food or household items, or person to person infections.

Endemic in Benin, Ghana, Guinea, Liberia, Mali, Sierra Leone, and Nigeria

Treatment: Early Supportive care with rehydration and symptomatic treatment.

23
Q

Bunyaviridae

A

Single-strand RNA
Enveloped

Transmitted by Arthropods and Rodents

Occasionally infect humans.

Rift Valley Fever (transmitted by mosquitoes). Sub-Saharan Africa. Mostly infects animals.

  • Incubation 2-6 days.
  • Prevented by program of animal vaccination

Crimean-Congo Hemorrhagic Fever: In Crimean peninsula, transmitted by tick and then human to human transmission.

Hantaviruses
-Sin Nombre Virus. In American southwest in 1993

24
Q

Filoviridae

A

Single-stranded Negative sense RNA
Enveloped

Cause Severe Hemorrhagic Fever in humans and nonhuman primates.

Virions may appear in several shapes
-Long, sometimes branche filaments

25
Q

Marburg Virus

A

Filoviridae

Recognized in 1967

Severe, often fatal illness in humans, severe viral hemorrhagic fever
Transmitted to people from fruit bats
-spreads among humans from human to human.

MVD fatality rate is 50%. Early supportive care improves survival

26
Q

Ebola Virus

A

Filoviridae

Identified in 1976 in Zaire and Sudan

Highly lethal.

Spread initially from direct contact with blood, body fluids of a sick or deceased person with EVD

Survivors: Side effects- tiredness, muscle aches, eye and vision problems, and stomach pain.

health workers without proper infection control are at the highest risk. Ebola poses little risk to travelers or the public who have not cared for or been in contact (within 3 feet) with someone sick with Ebola.

Persistence: Can remain in areas of the body that are immunologically privileged. In body fluids, the virus can survive up to several days at room temp.

Investigational Treatments. REGN-EB3 mAb114

Vaccine: Ervebo: live virus that has small portion of Ebola virus.

Infects monocytes and dendritic cells that cause a cytokines storm

27
Q

Flaviviridae

A

Positive single strand
Enveloped
RNA viruses

Found in arthropods and occasionally infect humans.

Mosquito-transmitted: yellow fever, dengue fever, Japanese encephalitis, west Nile, Zika

Tick-transmitted: Encephalitis, Omsk Hemorrhagic fever

28
Q

Yellow Fever Virus

A

Flavivirideae

Found in tropical areas of Africa and South America and transmitted through infected mosquito bite.

Disease: fever with aches and pains to severe liver disease with bleeding, organ failure, and jaundice with 30-60% fatality rate.
-Initial symptoms are fever, chills, myalgia, headache. Most people have no symptoms.

Diagnosis: laboratory testing, symptoms, travel history

Treatment: no specific treatment

Prevention: Insect repellent, long-sleeved shirts, long pants, and vaccination.

Vaccine is single dose and provides lifelong protection.
-Attenuated vaccine. Recommended for people 9 months and older who are traveling and it may even be required to enter certain countries.

Transmission cycles:

  • Jungle (sylvatic): transmission between non-human primates and mosquito in the forest canopy.
  • Intermediate (savannah): transmission from mosquitoes to humans living in the jungle
  • Urban cycle: Transmission between humans and urban mosquitoes primarily Aedes Aegypti.
29
Q

Engine Virus

A

Flavivirideae

Four serotypes: DENV1, 2, 3, 4. Immune system doesn’t cover every one. 2nd infection is worst.

Female Mosquito-borne Aedes aegypti viral infection. Global incidence is increasing. Found in tropical and mostly urban areas.

Severe dengue: Leads to serious illness and death amount Asian and Latin countries.

Get severe flu-like symptoms

Critical Phase 3-7 days after illness onset. severe bleeding, organ impairment and/or plasma leakage, respiratory distress.

Diagnosis: High fever (104) with two of the following: headache, pain behind eyes, muscle and joint pain, nausea, vomiting, swollen glands, rash. Symptoms last 2-7 days

No specific Treatment. But NSAIDS should be avoided!!! With fluids, severe dengue death goes from 20% to less than 1%

Live attenuated Dengue Vaccine CYD-TDV

  • efficacious and safe in seropositive people.
  • Carries increased risk of severe dengue in those who experience their first natural dengue infection after vaccination.
  • Only vaccinate those who have had past dengue using Ab test.*****
30
Q

What are defects in adaptive and innate immunity?

A

Adaptive: Ab deficiency and combined immunodeficiences

Innate: Phagocytes, Toll-like receptors, and complement

31
Q

How do you screen for SCID?

A

You look for TREC (T-cell receptor excision circles in a healthy infant’s blood.). Without this they have SCID.

32
Q

Adenosine Deaminase Deficiency

A

ADA

Enzyme that converts adenosine to inside. Without ADA it causes apoptosis of lymphoid precursors in marrow and thymus

Autosomal recessive. 10-15% of SCID

33
Q

X-linked SCID

A

X-linked

40% of SCID

IL2RG common gamma chain defect. Impacts IL-7 receptors (kills thymocytes), IL-15 (kills NK cells)

If you have JAK3 defect it manifests the same way.

34
Q

Recombinant-activating gene 1 and 2

A

RAG1/RAG2 defects. Stops T and B cells from maturing in 20% of cases.

The NK cells are normal.

35
Q

CD40L deficiency

A

Hyper IgM Syndrome

Can’t class switch and also CD40L promotes DC maturation and IL-12 secretion which will cause even more problems

X-Linked

36
Q

X-Linked agammaglobinemia (Bruton’s)

A

No signaling through pre-BCR

There is no Briton tyrosine kinase and it leads to a block at the pro-B and pre-B stage of bone marrow differentiation that leads to absence of circulating B lymphocytes.

85% of early onset agammaglobulinemia.

37
Q

Common Variable Immunodeficiency

A

CVID

Most common clinically significant primary immunodeficiency.

Reduced levels of one or more ig isotypes AND impaired Ab production in response to infection and immunization.

Still have normal number of B-cells

Recurrent infections with common bacteria mostly starting in adulthood.

Also has tendency for autoimmune manifestations (granulomatous lesion, lymphoid hyperplasia and tumors

15% have TACI defects

38
Q

IgA deficiency

Specific Ab deficiency

A

1 in 700 affected individuals with 2/3 expressing no symptoms.

Remaining can experience recurrent infections and autoimmunity.

Specific Ab Deficiency: Can’t make Ab to one specific bug. Numbers of B-cells and total Ab is normal.

39
Q

Phagocytic Cell Defects

A

Defend against bacteria and fungi

3 kinds: Neutropenias (not enough)
Chronic granulomatous disease
Leukocyte adhesion deficiency (LAD) impaired trafficking

40
Q

Neutropenia

A

Problem mostly with Neutrophil elastase.

Primary Neutropenia from autosomal dominant defect. Less than 500/microliter.

Can also see Cyclic Neutropenia:
-ELA2 (elastase) defect that leads to shorter to normal lifespans. Causes nadir every 21 days. Periodicity of infections.

41
Q

Chronic Granulomatous Disease

A

Defects in NADPH in phagosome.

75% X-linked, 25% AR

Prone to unusual infections: Nocardia, Aspergillus

Phagocytes can’t make hydrogen peroxides or radicals and so they can’t kill the bugs. Also can cause sustained inflammatory response in hollow organs.

42
Q

Leukocyte Adhesion Deficiency

A

Impaired Trafficking

LAD1: defect in CD18 which leads to adhesion between leukocytes via integrins to allow trans endothelial passage

LAD2: impaired rolling due to (E-selectin) problem.

Present in early life with severe infections and no pus formation. Elevated white count.

Delayed separation of umbilical cord (mean 10 days)**

43
Q

Defects in TLRs

A

Mediates recognition of pathogen-associated molecular patterns (PAMPs) LPS, glycolipids, RNA

Autosomal Recessive.

Get invasive pyogenic infections early in life, becoming less of a problem later in life.

44
Q

Complement Defects

A

Problems with early classical pathway C1, C2, or C3 cause autoimmune manifestations lead to similar systemic lupus problems.

C2 and C3 Deficiency can also lead to increased tendency for encapsulated bacteria

Defects in late components (C5-C9) MAC associated with neisserial infections.

45
Q

Wiskott-Aldrich Syndrome WAS

A

X-linked triad of eczema, few/small platelets, and immunodeficiency. (Autoimmunity and malignancy)
-only expressed by hematopoietic cells and key role in actin cytoskeleton

46
Q

Ataxia-telangiectasia

A

AR

Triad with ataxia, ocular telangiectasias, and infections. ATM gene defect, involved in DNA repair. Poor T-cell numbers and function and hypogammaglobulinemia.

47
Q

Hyper-IgE syndrome

A

Triad of eczema, high IgE and infections

STAT 3 deficiency in AD version

DOCK 8 mutations in AR version

48
Q

Chediak-Higashi syndrome (CHS)

A

AR triad of gray hair, peripheral neuropathy, and impaired cell-mediated cytotoxicity.

Defect in lysosomal trafficking.

49
Q

DiGeroge Syndrome

A

22q11 deletion hemizygous (only one copy of a gene.

Impaired development of thymus, parathyroid, conotruncal heart, facial dysmorphisms.

Moderate T-cell deficiency and partial DSG

50
Q

What infections aren’t indicitative of immunodeficiency

A

Recurrent Strep and UTIs

51
Q

What labs can you use to diagnose these immunodeficiencies?

A

CIDs: HIV, T-lymphocyte/NK panel, TRECs

Ab deficiency, Ab response to vaccines

Neutrophil count.

CGD has replaced the NTB

LAD- flow cytometry for CD18

Genetic testing for many PIDDs via Invitae.com

52
Q

Treatment options of Primary Immunodeficiencies PIDD

A

Hematopoietic stem cell transplant for those with SCID, start with cotrimoxazole

Gene therapy.

Bovine-ADA replacement

Thymidine transplant for complete DGS (DiGeorge syndrome)

LAD: HSCT (Leukocyte Adhesion Deficiency)

Neutropenia: regular injections of G-CSF

CGD: prophylactic cotrimoxazole and itraconazole with IFN-y, or HSCT (Chronic Granulomatous Disease)

BIIC Part 2 (5 decks)

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