General Bacteria fun facts (virulence factors, unique characteristics) Flashcards
Which virulence factors allow for adhesion to fibronectin and vitronectin
*Protein A
*Techoic acid
3 mechanisms of bacterial gene transfer
1) Transduction
-Bacteriophage
2) Conjugation
-Sex pili to share plasmid
3) Transformation
-Uptake of DNA from lysed bacteria
What is a biofilm? How do bacteria survive in it?
Aggregate of bacteria with a polymer matrix
Has water channels within to disseminate O2 and nutrients?
What makes the cell wall of mycobacteria special
NO cell wall!
They have a plasma membrane
Do not pick up gram stain, variable
What is the benefit of a peptidoglycan layer for Gram + bacteria
Resist heat and dessication
List superantigens
Staph enerotoxins A, B, C, D (SE-B)
Toxic shock syndrome toxin-1 (TSST-1)
Protein A (avoids complement binding by FcR; upregulates KC adhesion mc)
Staphyloferrins function
Lyse RBC
Use the iron for growth
CHIPS protein function
Evade C5a
SCIN function
Staph complement inhibitor protein
Virulence factors of Streptococcus
*M protein (inhibits phagocytosis)
*Streptolysin O
S equi: ELISA for M protein for Strangles/Purpua hemorrhagic diagnosis
Virulence factors of Pseudomonas
*Biofilm
-Increases MIC
-In 40% of OE isolates
-Quorum sensing, slime, plasmid exchange
*Pyocyanin
-Pigment, proinflammatory
*Elastase
-Cleaves collagen
Virulence factors of Nocardia
*Thick peptidoglycan layer (heat, dessication resistance)
*Superoxide dismutase
*Catalase
Virulence mechanism of Mycobacteria
*Intracellular: Block fusion of lysosome in macrophage
Prevents MHC2 expression
*No cell wall, so resistant to B-lactams
*Can act as a SUPER ANTIGEN- strong T cell response
*Can vary surface antigens to avoid immune identification
Function of coagulase
Converts fibrinogen to fibrin (clot scaffold)
-Tissue invasion
-Microabscesses
-Protection from granulocytes
Indicator of pathogenicity
BlaZ gene
In Staphylococcus
Encodes for beta lactamase
Which Streptococcus are more pathogenic: alpha or beta hemolytic
Beta: lysis RBCs
Alpha are commensals on MM and skin
Bacteria that can cause:
-Necrotizing Fasciitis and Myositis
-Toxic Shock Syndrome
Streptococcus canis!
-M Protein: antiphagocytic, destroys C3 convertase
-Proteases: help spread through fascial planes and into muscle
Which Mycobacteria causes conjunctivitis in cats
*Mycoplasma felis
T or F: detection of Mycoplasma in lungs of dogs is diagnostic for infection
False. Mycoplasma is a commensal in respiratory tract of dogs
What do Mycoplasma colonies look like on culture plate
Fried eggs!
Central zone of growth
Treatments for mycoplasma
BACTERIOSTATIC – long duration of tx
Macrolides, clindamycin, FQs, tetracyclines, chpc, aminoglycosides
Streptococcus that causes mastitis in cows
S. agalactiae
What do superantigens bind to induce a massive inflammatory response
MHC cl II and TCR
Which antibiotic can TRIGGER Toxic Shock Syndrome
Fluoroquinolones.
Can trigger more expression of superantigen TSST-1 by S. canis!
Best treatment for Toxic Shock Syndrome
Clindamycin
-Inhibits M protein synthesis
-Suppresses LPS-induced TNF production
Age, Inciting incident for Toxic Shock Syndrome
<1 year old
Bite wound, URI
Best antibiotic for Enterococcus
Worst antibiotic for Enterococcus
Best = ampicillin, penicillin
Worst = TMS (even if S in vitro. can bypass folic acid synthesis blockade)
Luckily, rarely pathogenic
Doppleganger for Enterococcus
Streptococcus
Both cocci, grow in chains. Enterococcus less pathogenic than Strep. Some sp of strep have been reclassified as Enterococcus
Where does Rhodococcus equi invade?
Lymphatics, macrophages
Facultative intracellular bacteria
Virulence factor that allows Rhodococcus equi to persist inside macrophages
VapA
Clinical signs in CATS with Rhodococcus equi infections
Abscesses! Check FIV/FeLV
(Horses = pyogranulomatous pneumonia.
Cows/Pigs = pyogranulomatous lymphadenitis)
Treatment Rhodococcus equi
Erythromycin/ Clarithromycin + rifampin
–> lipophilic drugs to penetrate cell wall
Surgical excision + drainage
What’s special about Listeria monocytogenase
Facultative intracellular gram + rod in MACROPHAGES
Escapes humoral immune response
What type of immune response is important for clearing Listeria monocytogenes
Cell mediated
It’s hiding in macrophages, where Ig can’t find it
What virulence factor allows Listeria monocytogenes to be phagocytosed by macrophages
Internalin
=induces phagocytosis by KCs, then pushes pseudopod projections out to be ingested by macrophage
What enables Listeria monocytogenes to escape host cell killing
Listeriolysin O
Where in the body can Listeria monocytogenes be found
GI, CNS, placenta
Form intestinal inflammation, fever, v+, abscesses
–> die from septicemia
How do animals get Listeria monocytogenes
Ingestion of contamination food
Causative agent of Anthrax
Bacillus anthracis
Large, gram +, aerobic, spore-forming
What induces Bacillus anthracis to produce spores
Exposure to atmospheric O2
(Spores are NOT produced in intact carcasses!)
Bacillus anthracis on cytology
String of box cars
Virulence factor for Bacillus anthracis
Thick capsule to avoid phagocytosis (plasmid pX02)
Stains to ID Bacillus anthracis
Methylene blue, Giemsa stain
Pick up polypeptide capsule around organism
Clinical sign of Bacillus anthracis
Swelling of the head and neck
GI, inhalation, cutaneous forms
*Acute hemorrhagic gastroenteritis
*Black eschar if cutaneous exposure (cut)
*Pulmonary nodules
How do animals develop Bacillus anthracis
Eat grass contaminated with spores; Eat infected meat –> GI signs