Spring Bugs Flashcards
Lab ID of Mycobacterium Leprae
Gram-positive, bacilli, nonmotile, non-sporeforming, acid-fast, mycolic acid: (mycoside)phenolic glycolipid (PGL-I), high lipid content of cell wall, lipoarabinomannan (LAM), obligate intracellular parasite, strict aerobe
Virulence factors of M. Leprae
PGL-I, laminin binding protein, lipoarabinomannan, high lipid content of cell walls
Mechanism of phenolic glycolipid I virulence
Binds to the basal lamina of Schwann cells
Mechanism of laminin binding protein virulence
Binds to the basal lamina of Schwann cells
Mechanism of M. Leprae high lipid content of walls
high lipid content of cell wall made of mycolic acids and LAM -> prevents many pharmacological compounds from crossing bacterial cell membrane into cytosol; CD8+ Tc unable to insert perforin for cell lysis
What is the predominant organism that causes dental caries?
Streptococcus mutans
Why is streptococcus mutans so prevalent in dental caries?
Metabolizes sucrose more efficiently than other oral bacteria
Salmonella Enterica lab ID
gram negative, bacilli, non-spore forming, non-acid fasting, motile, flagella (H antigen), LPS (O antigen), capsule (K antigen), pili, produces H2S when fermenting glucose on Hektoen agar (Black), non-lactose fermenting
Transmission of Salmonella Enterica
food preparation practices allowing infecting dose of bacteria by growth in food before ingestion, turtles
Identification of Shigella
Gram-negative, Bacilli, Pili, Non-motile, Unencapsulated, Non-lactose fermenting, no flagella, non-sporeforming, non-acid fasting
O-antigen (lipopolysaccharide outer membrane LPS) Serogroup A- Shigella dysenteriae
Serogroup B- Shigella flexneri
Serogroup C- Shigella boydii
Serogroup D- Shigella sonnei
Grows on Hektoen enteric agar- Fermenters of glucose- but does not produce gas in this process (green)
What is O antigen?
lipopolysaccharide
What is K antigen?
capsule
What is H antigen?
Flagella
How is shigella acid resistance a virulence factor
able to survive acidic climate of stomach to reach intestines, where it enters and infects host
virulence of Invasion plasmid antigens (Ipa)
protein antigens injected by type III secretion system ➡️ induce cytoskeleton reorganization and actin polymerization ➡️ induces engulfment and internalization of Shigella into host cell by endocytosis
Virulence of shiga toxin (Stx)
B unit directs binding to a specific glycolipid receptor (Gb3) present on eukaryotic cells ➡️ internalized in an endocytotic vacuole ➡️ Inside the cell, the A subunit crosses the vacuolar membrane in the trans-Golgi network ➡️ exits to the cytoplasm ➡️ enzymatically modifies the ribosome site (28S-RNA of 60S subunit) where amino acyl tRNA binds ➡️ blocking protein synthesis ➡️ leading to cell death
Virulence of shiga toxin (Stx)
B unit directs binding to a specific glycolipid receptor (Gb3) present on eukaryotic cells ➡️ internalized in an endocytotic vacuole ➡️ Inside the cell, the A subunit crosses the vacuolar membrane in the trans-Golgi network ➡️ exits to the cytoplasm ➡️ enzymatically modifies the ribosome site (28S-RNA of 60S subunit) where amino acyl tRNA binds ➡️ blocking protein synthesis ➡️ leading to cell death
Virulence factors for salmonella enterica
Flagella, pili, Injection (type III) secretion system
Virulence of injection (type III) secretion system for salmonella
S. Enterica adheres to cell via pili binding to mannose receptor ➡️ injection (type III) secretion system create a membrane “ruffles” (specialized plasma membrane site of filamentous actin cytoskeleton rearrangements) ➡️ salmonella endocytose and enter cell
Identification of clostridium difficile
gram positive, bacilli, spore forming, anaerobic, catalase negative, superoxide dismutase negative
Virulence factors for clostridium difficile
toxin A (TcdA) enterotoxin, toxin B (TcdB) a cytotoxin, C. difficile transferase (CDT), spores
virulence of c. diff toxin A and toxin B
Toxin A and B glucosylate and inactivate GTPases ➡️ disrupts the signal transduction of G proteins ➡️ rearrange actin filaments ➡️ disrupts intracellular tight junctions ➡️ increase membrane permeability and fluid secretion
virulence of c. diff transferase toxin (CDT)
exerts ADP-ribosylation ➡️ inhibit actin polymerization in enterocytes
What does the pseudomembrane of C. difficile consist of
inflammatory plaques ➡️ coalesce into pseudomembrane (made of fibrin, leukocytes, and necrotic colonic cells)
What kind of helminth is ascaris lumbricoides?
nematode
What kind of helminth is diphyllobothrium latum?
cestode
What are the five species of plasmodium which infect humans?
P. falciparum P. vivax P. ovale P. malariae P. knowlesi (rarely causes disease)
Lab ID/Characteristics specific to P. falciparum?
1) Infect RBCs of any age
2) Bind to glycophorin A on RBCs
3) Form knobs on RBC surface ➡️ produce high-molecular weight adhesive protein (PfEMP1) ➡️ used to bind to ligands on endothelium
4) large, banana-shaped gametocytes
5) Double chromatin dots
6) May have double infection (>1 parasite per RBC)
7) Maurer dots (RBCs)
Lab ID/Characteristics specific to P. ovale?
1) Has dormant stage (hypnozoite)
2) Only invade reticulocytes
3) Enlarged & pale RBCs
4) RBCs are oval and fimbriated (fringed borders)
5) Schuffner dots (RBCs)
Lab ID/Characteristics specific to P. vivax?
1) Has dormant stage (hypnozoite)
2) Binds to Duffy antigen on RBCs
3) Only invade reticulocytes
4) Enlarged & pale RBCs
5) Schuffner dots (RBCs)
Lab ID/Characteristics specific to P. malariae?
1) only invades senescent cells
2) trophozoites are band-shaped
3) merozoites arranged in rosettes
General lab ID/characteristics of plasmodium?
1) Non-motile
2) Gametocytes larger & lack nuclear division compared to asexual stages
3) red nuclear chromatin
4) blue cytoplasm
5) brown/black pigment (hemozoin) with ⬆️ ferroprotoporphyrin IX (breakdown product of hemoglobin)
