12 Bacteria: Spirochetes Flashcards
General characteristics
Inner and outer membrane, thin peptidoglycan layer, flagellum located on inner membrane to periplasm
Leptospira
hosts
disease
General
Hosts
rodent natural asymptomatic host, humans accidental host, no human to human transmission
Disease
Leptospirosis: cold symptoms, systemic Weil’s disease possible
General (way of invading, microscopy, life cycle)
mostly extracellular, but can survive inside macrophages, very motile, penetrate through small skin lesions, bind to cell components via Adhesins and surive, replicate and exit from macrophages, barely detecable with common microscopy
Virulence mechanism / gene evolution
different species, only some pathogens, evolution of virulence via horizontal gene transfer, gene duplication and genome reduction
Genomic islands
Genomic islands
mobile genetic elements, often pathogenicity islands, that have a different GC content often flanked by repeat sequences or contain tRNA genes and contain integrases or transposases genes
Function
Antibiotic resistance, new metabolic pathways and virulence
Treponema
Disease and stages
transmission
Therapy
Disease
Syphillis
Primary phase: lesions, resolves after 3 weeks
Secondary phase: 6-8 weeks systemic rash
early latent phase
Tertiary phase: if untreated 15-40% severe lesions after 10-30 years, evades immune response
Transmission
sexually transmitted, can persist for >10 years if untreated
‘
Therapy
Penicillin
Special facts (doubling time, life cycle, flagellum)
30h gen time, extracellular, 3 periplasmic flagellar filaments
Antigenic and phase variation
example bacterium
results in heterogenic phenotype of clonal bact population to adapt to changing enviroment
antigenic variation is expression of different antigens, e.g. induced by hairpins, repeats, recombination
phase variation is altered antigen expression (on/off switches)
Example
Treponema pallidum 12 tpr genes and poly G stretch in promoter region, more than 9Gs means gene is silenced leading to phase variation
Recombination (copy/paste mechanism) in tprK genes
Borrelia
species
vector
mechanism / characteristics
Antigenic / phase variation example
species
burgdorferi
vector
tick species
mechanisms / characteristics
no LPS, exchange of lipids with host plasma membrane to evade immune system
genome lacks genes required for nutrient synthesis, conclusion is membrane transporter to get nutrients from host
Antigenic / phase variation example
phase variation: Blood meal enviroment leads to expression of mammalian lipoproteins, e.g. OspC
antigenic variation: reacts to host immune system by replacing OspC with variable VIsE
Interaction with tick to evade mammalian immune system
Even in tick gut it starts to produce mammalian antigens like OspC and OspC can bind to a tick protein SALP15 working as a shield to protect against immune response from mammals
Chlamydia
shape and life cycle
genome
Morphology
Secretion system
shape
gram- rod shaped obligate intracellular bacteria
genome
super small 1Mbp, 10% virulence factors, energy vampire (ATP from host)
Morphology and mechanism
Infectious elementary bodies that cant replicate and replicating reticulate bodies
Mechanism: EB endocytosed via type 3 secretion system and injects effectors in host cell, conversion to RB, persitance or transition to EB to exit cell and infect others
Secretion system
Type 3: Inclusion membrane derived from host vacuole proects from host cytosol, secretion system ranges from inclusion membrane to inner bact. membrane (3 membranes), there are also other secretion systems only ranging from inner to outer bact. membrane,
60-80 effectors, prevents lysosome function, prevents host cell apoptosis, exit from host, recruits motor dynein to migrate along microtubules
Rickettsia
Shape and life cycle
Genome
Species
Disease
transmission
Treatment
Mechanisms
Shape and life cycle
gram- intracellular bacteria, life cycle involves anthropod vector and vertebrate host
Genome
very small, again relying on different host synthesis of aa and nucleotides
Species
R. rickettsia, R. prowazekii (bio weapons)
Disease
Typhus, fecer
transmission
Tick, louse, mites
Treatment
antibiotic
Mechanism to infect
Variation of Transcriptom related to temperature: human body temperature needed to switch to infectious transcriptom
Induced phagocytosis > escape from phagosome > recruitment of actin filaments to actively move through cell and infect neighbouring cell > increased vascular permeability
Coxiella
disease
life cycle
diease
acute Q-Fever (apoptosis of infected cells) and chonic (1-2%) (no apoptosis), >50% asymptomatic
Life cycle
1 bacteria can cause disease (contaminated air), obligate intracellular can develop spore like cells (bioweapon)
Large cell variant (host) <> Small cell variant (enviroment spore like)
Phagocytosis (actin dependent) -> vacuole (5 min after contact), then accidification, SCV -> VCL after 8-48h and expansion of vacuole
Mycoplasma pneumoniae
disease
genome
special
how to evade immune system
disease
atypical pneumonia, usually mild or asymptomatic,, epidemics every 4-7 years
Genome
very small, almost no genes for biosynthesis of aa, ….
Special
no cell wall at all (antibiotica resistance) and molecular mimicry via changes in lipoprotein repertoire
Evasion
via Protein M that is a universal binder for monoclonal antibodies, binding results in reduction of immune response
Antivirulence therapeutics
advantages
different targets and
one example
new tyoe targeting virulenbce factors to disarm pathogen and not kill
advantages
>weaker selection resistance
>may overcome acquired resistances against antimicrobials
>preserves host microbiota
>strain specific
Targets
>physically block pilli to attach
>inhibit pili assembly/biogensis
>prevent toxin production (block genes or step in pathway)
>prevent toxin binding, activation
Secretion System:
>block secretion system assembly
> block host interaction
> blocxk effector secretion
Example
LED209 inhibits virulence in EHEC, Salmonella via toxin blocking
