5 VL Wichtig an der Universität zu Lübeck

Karteikarten und Zusammenfassungen für 5 VL Wichtig an der Universität zu Lübeck

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Lerne jetzt mit Karteikarten und Zusammenfassungen für den Kurs 5 VL Wichtig an der Universität zu Lübeck.

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Mechanism associated with prost-translational regulation of bacteria? (3)

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The dual lifestyle of intracellular/extracellular bacterial pathogens: 3 phases and mordern view on exclusivity of bacteria lifestyle:

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Spotted fever Rickettsia: Rickettsia spreading/cell to cell movement (a-e)

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Immune sensing of intracellular bacteria. 3 main points. 2nd point with 2 (+1 each) subpoints

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Immune sensing of intracellular bacteria part 2. Examples of receptors and ligands: 5 points: ec, endosomal (3), cytosolic (3), cytosolic DNA, cytokine answers (2 classifications with 2 examples each).

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Protective immunity against Rickettsiaceae. Which cells are involved (3)?, typical course of Rickettsia sensing and immune answer (3, mit 3 a-c).

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Immune pathogenesis of Rickettsioses: Caused by what? Course of immune pathogenesis (1-5)

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Wolbachia (alpha-proteobacteria), close relatives of Rickettsia. endosymbionts of what, transmission, manipulation of hosts and reproduction

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Filaria, a family within the nematoda clade, are obligate carriers of the endosymbiotic Wolbachia. Why are Wolbachia important in human infections with filaria/ immune-pathologic mechanisms induced by wolbachia (5)?

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Query-Fever (Q-Fever). other name, caused by? Acute form different courses of the disease with different symptoms, chronic form and its symptoms. Short epidemiology. (4: 2nd with 3 points)

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Erreger Flussblindheit? Wolbachia? Symptome? Was ist der Sinn einer Antibiotika-Therapie hier?


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Pathogen niches 4 examples and 2 explanation

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Beispielhafte Karteikarten für 5 VL Wichtig an der Universität zu Lübeck auf StudySmarter:

5 VL Wichtig

Mechanism associated with prost-translational regulation of bacteria? (3)

Pathogen-Host-Interactions: 

  • Protein Transport Systems 
  • sec-dependent and –independent transport 
  • exported proteins fulfill a multitude of different functions

5 VL Wichtig

The dual lifestyle of intracellular/extracellular bacterial pathogens: 3 phases and mordern view on exclusivity of bacteria lifestyle:

  1. Intracellular phase: Transmission of bacterial pathogens to new host from infected hosts, vectors or environment (water, soil etc.). Intercellular transit from cell to cell.
  2. Switch from intracellular to extracellular phase: May be essential for the pathogenesis. Egress of intracellular pathogens to extracellular territories of the host leading to systemic dissemination and extracellular replication.
  3. Extracellular phase: Transmission of extracellular bacterial pathogens from infected hosts to vector and environment.


2012 Silva, Manuel: Classically, pathogenic bacteria are classified as extracellular, facultative intracellular and obligate intracellular. In my opinion, this classification is inadequate. For a microbial pathogen, what matters is whether intra- or extracellularity is in the context of the in vivo life and in association with pathogenicity.


5 VL Wichtig

Spotted fever Rickettsia: Rickettsia spreading/cell to cell movement (a-e)

a) Engulfment of bacterium by the cell
b) Bacterium inside a vacuole
c) Bacterium surrounded by a layer of actin filaments
d) Bacterium associated with a comet tail of actin
e) Bacteria into cell surface protrusions invading neighboring cells

5 VL Wichtig

Immune sensing of intracellular bacteria. 3 main points. 2nd point with 2 (+1 each) subpoints

Host organisms have developed many ways for immune sensing of intracellular pathogens:

  • Most intracellular bacteria have an extracellular stage where they can be detected by classical receptors for extracellular pathogens.
  • Intracellular receptors:
    1. Endosomal TLRs:
      • TLRs 9-13, only TLR9 is functional in humans. TLRs 9-13 all use MyD88 as adaptor protein.
    2. Cytosolic receptors: NOD-like receptors that sense peptidoglycan structures and the inflammasome receptors that can sense a variety of different ligands.
      • cGAS is a recognizer of cytosolic DNA. Once activated it promotes the expression of type-I interferons. This is important for virus sensing but also certain intracellular bacteria can activate cells through cGAS. 
  • Like most intracellular pathogens, anti-Rickettsia responses need the cellular immune mechanisms. Therefore IFN-gamma is a key cytokine.

5 VL Wichtig

Immune sensing of intracellular bacteria part 2. Examples of receptors and ligands: 5 points: ec, endosomal (3), cytosolic (3), cytosolic DNA, cytokine answers (2 classifications with 2 examples each).

  • Sensing during extracellular stages
    • e.g. O. tsutsugamushi can be sensed by TLR2
  • Endosomal TLRs (Only TLR9 in humans)
    • TLR9: CpG DNA e.g. of M. tuberculosis
    • TLR11: Flagellin e.g. of uropathogenic E. coli
    • TLR13: 23s rRNA e.g. of Streptococcus pyogenes)
  • Cytosolic receptors
    • Cell wall receptors (NOD1, NOD2, NALP3)
    • Flagellin receptors (NAIP5, IPAF)
    • Toxin receptors (NALP1b)
  • Cytosolic DNA receptors (cGAS, …)

=> Type I IFNs (IFN-alpha, IFN-beta), proinflammatory cytokines (IL-6, TNF-alpha)

5 VL Wichtig

Protective immunity against Rickettsiaceae. Which cells are involved (3)?, typical course of Rickettsia sensing and immune answer (3, mit 3 a-c).

 Cells involved:

  • NK cells: Early phase (2-4 days post-infection), early source of IFN-γ 
  • CD4+ Th1 cells: IFN-γ, TNF-α, activation of antibacterial effectors (ROS, iNOS, IDO) in endothelial cells and macrophages 
  • CD8+ T cells: IFN-γ, TNF-α, cytotoxicity 


Course Rickettsia immune answer:

  1. Rickettsia typically target macrophages and endothelial cells
  2. Dendritic cells sense the pathogens and move to the lymphatic tissue where they elicit a cellular immune response
  3. The response comprises both, CD4+ and CD8+ T cells which move to the sites of infection. 
  1. CD4+ Th1 cells are an important source of IFN-gamma which activate macrophages and target cells to express antimicrobial effector mechanisms like iNOS or IDO
  2. CD8+ T cells act with their cytotoxic functions 
  3. Activation of endothelial cells lead to an inflammation of the vasculature and increased vascular permeability which can drive further pathology

5 VL Wichtig

Immune pathogenesis of Rickettsioses: Caused by what? Course of immune pathogenesis (1-5)

The typical manifestations of Rickettsioses are caused by the immune system.

 

Course immune pathogenesis of Rickettsioses:

 

  1. Pathogen proliferation at infection site
  2. Hematogenous and lymphogenous spread, proliferation in endothelia and vascular associated tissue
  3. Cell death activation of endothelia  
  4. Inflammation, increasing levels of IFN-gamma, TNF-alpha, ROS, NO. Vasodilatation, vascular permeability goes up, necrosis
  5. Skin: Rash, Petechia
    Organs: Pneumonia, Hepatitis
    Systemic manifestations: Hypoxia, disseminated intravascular coagulation, thrombosis, shock, multi organ failure

5 VL Wichtig

Wolbachia (alpha-proteobacteria), close relatives of Rickettsia. endosymbionts of what, transmission, manipulation of hosts and reproduction

 

  • Endosymbionts in insects, arachnids, and filari. NO human pathogens
  • Solely vertical transmission: Only females trans-ovarially transfer bacteria to their offspring, males cannot transfer their infection to offspring. They survive in gonads of their hosts.
  • To effectively infect a whole population, they manipulate the reproductive capabilities of their hosts:
    1. Males are turned into femalesm
    2. Male killing
    3. Reproduction without males
    4. Cytoplasmic incompatibility: infected males are incompatible with uninfected females

5 VL Wichtig

Filaria, a family within the nematoda clade, are obligate carriers of the endosymbiotic Wolbachia. Why are Wolbachia important in human infections with filaria/ immune-pathologic mechanisms induced by wolbachia (5)?

Wolbachia influencing human health => Immune-pathologic mechanisms: 

  • Induce accumulation + activation of neutrophils surrounding filaria and activated macrophages 
  • Neutrophils: connected to micro-filaria killing + disassembly, neutrophils contribute to cyst formation inside onchocercoma
  • Contribute to neg. side-effects of filariasis chemotherapy (mouse model) 
  • Determining role in keratitis development 
  • Wolbachia-infested filariae are threat and also attractive target for medicine


Full text:

This is why Wolbachia have to be considered in human health:

  • Wolbachia induce immune-pathologic mechanisms: 
    • Wolbachia induce accumulation and activation of neutrophils surrounding filaria and activated macrophages 
    • Neutrophils are connected to the killing and disassembly of micro-filaria, neutrophils contribute to the formation of cysts inside the onchocercoma, where the worms copulate 
    • Wolbachia are thought to contribute to negative side-effects of chemotherapy of filariasis, inside the mouse model of onchocerciasis, Wolbachia play the determining role in keratitis (eye cornea inflammation) development 
    • Wolbachia-infested filariae are a threat, but the Wolbachia might also be an attractive target for medical intervention 
  • Wolbachia are associated with Onchocerciasis (Onchocerca volvulus), lymphatic filariasis (Wucheria bancrofti, Brugia malayi, B. timori) and with non-pathogenic Mansonella oozzardi

 

5 VL Wichtig

Query-Fever (Q-Fever). other name, caused by? Acute form different courses of the disease with different symptoms, chronic form and its symptoms. Short epidemiology. (4: 2nd with 3 points)

  1. Q-fever = „slaughterhouse fever“: Bacterial infection by Coxiella burnetii
  2. Acute Q fever 95-99%: 
    1. 60% asymptomatic or mild 
    2. 38%: flu-like symptoms 
    3. Complications (2%): Pneumonia, ARDS, Hepatitis, hepatomegaly…
  3. Chronic form 1-5%: 
    1. Usually, endocarditis: Fatal if left untreated, otherwise 10% case fatality. 
  4. Epidemiology: Worldwide distribution, no effective vaccine 

 

Full text: 

Q-fever is also known as „slaughter house fever“ and a bacterial infection caused by the bacteria Coxiella burnetii. Acute Q fever 95-99%: In about 60% the infection is asymptomatic or mild. Otherwise 38%: flue-like symptoms: fever (7-14 days), fatigue, headaches, myalgia, loss of appetite, cough, confusion. Complications (2%): Pneumonia, ARDS (acute respiratory distress syndrome), Hepatitis, hepatomegaly, jaundice(icterus) 

Chronic form 1-5%: endocarditis, normally fatal if left untreated, otherwise 10% case fatality. The rare chronic form is dangerous because it usually presents as an endocarditis (Endocarditis is an infection of the endocardium, which is the inner lining of your heart chambers and heart valves.)

Epidemiology: Worldwide distribution, no effective vaccine. Infections are rare (2013: 115 cases; 2014: 262 cases in Germany (RKI)). Outbreak in Netherlands 2009: 2300 men were infected, 25 died 

5 VL Wichtig

Erreger Flussblindheit? Wolbachia? Symptome? Was ist der Sinn einer Antibiotika-Therapie hier?


  • Onchocerca volvulus: Nematode that causes onchocerciasis (river blindness) and is the second-leading cause of blindness worldwide after trachoma.
  • Onchocerciasis symptoms: Eye and skin disease. Symptoms are caused by the microfilariae, which move around the human body in the subcutaneous tissue and induce intense inflammatory responses when they die. Severe itching and various skin changes. Sometimes eye lesions which can lead to visual impairment and permanent blindness. In most cases, nodules under the skin form around the adult worms.
  • Wolbachia: Genus of gram-negative bacteria sharing an endosymbiotic relationship with most filarial nematodes and against which antibiotic therapy makes sense (are no human pathogens). In the absence of Wolbachia, larval development of O. volvulus is disrupted or ceased.
  • Wolbachia is also suspected to enhance symptoms and severity of onchocerciasis by triggering inflammatory responses in the host (immunopathologic mechanisms):
    • Induce accumulation and activation of neutrophils surrounding filaria and activate macrophages
    • Neutrophils are connected to the killing and disassembly of micro-filaria (stage between egg and larva), neutrophils contribute to the formation of cysts inside the onchocercoma, where the worms copulate
    • Wolbachia are thought to contribute to the negative side-effects of chemotherapy of filariasis. Mouse model of onchocerciasis: Wolbachia play determining role in keratitis (eye inflammation) development

5 VL Wichtig

Pathogen niches 4 examples and 2 explanation

  1. Biofilms
  2. Protected capsules (abscesses)
  3. Immune privileged infection sites
  4. Intracellular infections


  • Pathogens have to find their specific niches in the body to hide from immune attacks of the host and from being outcompeted by bacterial competitors. Intracellular lifestyle of bacteria is one of these strategies. 
  • Host cells have developed strategies to fight ic bacteria and the coevolution of ic bacteria and hosts have given rise to various forms of ic lifestyle in different compartments o the host cells. Some bacteria have successfully evolved by customizing compartments for their specific needs.

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