lecture 2 Flashcards
why is p.aeuginosa the epitome of an opportunistic pathogen?
Pseudomonas aeruginosa is considered the epitome of an opportunistic pathogen due to its remarkable ability to cause infections primarily in individuals with weakened immune systems or compromised health. This bacterium exhibits several characteristics that enable it to thrive in a wide range of environments and exploit vulnerabilities in hosts, making it one of the most challenging pathogens to control and treat. Here are the key factors that contribute to its status as a quintessential opportunistic pathogen:
- Versatile Metabolism and Adaptability
P. aeruginosa has a highly versatile metabolism, allowing it to survive and grow in diverse environments, including soil, water, hospitals, and even on medical equipment.
It can utilize a wide variety of organic compounds as energy sources, enabling it to thrive in nutrient-poor conditions that would be hostile to other bacteria.
This adaptability makes P. aeruginosa highly resilient and capable of colonizing both environmental surfaces and human tissues. - Biofilm Formation
One of the defining features of P. aeruginosa is its ability to form biofilms, which are structured communities of bacteria enclosed in a self-produced extracellular matrix.
Biofilms protect P. aeruginosa from the host’s immune response and significantly increase its resistance to antibiotics.
This trait is particularly problematic in hospital settings, where P. aeruginosa biofilms can form on medical devices like catheters, ventilators, and implants, leading to persistent infections. - Antibiotic Resistance
P. aeruginosa is intrinsically resistant to many antibiotics due to its low outer membrane permeability and the presence of efflux pumps that expel drugs from the cell.
It can also acquire resistance through horizontal gene transfer, mutations, and by producing enzymes that degrade or inactivate antibiotics, such as β-lactamases.
The emergence of multi-drug-resistant (MDR) and extensively drug-resistant (XDR) strains of P. aeruginosa has made treatment options very limited, posing a significant challenge in clinical settings. - Production of Virulence Factors
P. aeruginosa produces a wide range of virulence factors that enhance its ability to infect and damage host tissues. Some of these include:
Exotoxins (e.g., Exotoxin A) that interfere with host cell function and immune responses.
Proteases that degrade host tissues and immune molecules.
Pyocyanin and other pigments that generate reactive oxygen species, causing oxidative stress and tissue damage.
These virulence factors contribute to the severity of infections, making P. aeruginosa capable of causing acute and chronic infections. - Ability to Sense and Respond to Host Signals
P. aeruginosa has sophisticated quorum sensing systems, which allow it to detect cell density and regulate gene expression, including genes responsible for virulence and biofilm formation.
This ability to sense and respond to its environment enables the bacterium to adapt its behavior according to the host’s immune response or the availability of nutrients, enhancing its survival and pathogenic potential. - Predilection for Immunocompromised Hosts
P. aeruginosa rarely causes infections in healthy individuals but is a major cause of morbidity and mortality in immunocompromised patients, such as those with:
Cystic fibrosis (CF)
Severe burns or wounds
Cancer or undergoing chemotherapy
Organ transplant recipients
Patients with HIV/AIDS
Individuals on prolonged antibiotic or immunosuppressive therapy
The bacterium exploits weakened defenses, impaired tissue barriers, and medical interventions to establish infections in these susceptible hosts. - Infections in Multiple Sites
P. aeruginosa can cause a wide variety of infections, including:
Respiratory tract infections (especially in patients with cystic fibrosis or ventilated patients)
Urinary tract infections (often associated with catheters)
Skin and soft tissue infections (in burn wounds or surgical sites)
Bacteremia and sepsis, which can lead to life-threatening complications
This wide range of infection sites demonstrates its ability to colonize and damage multiple tissues within the host.
Conclusion
Pseudomonas aeruginosa is considered the epitome of an opportunistic pathogen due to its exceptional adaptability, resistance to antibiotics, ability to form biofilms, production of virulence factors, and capacity to exploit weakened immune systems. Its resilience and versatility make it a formidable challenge in healthcare settings, particularly for patients with compromised immune defenses.
what group is pseudomonas aeruginosa and the burkholderia genus apart of and why are the plant pathogens so environmentlally important?
Pseudomonas aeruginosa and the genus Burkholderia are part of the Proteobacteria phylum, specifically belonging to the Gammaproteobacteria and Betaproteobacteria classes, respectively. These groups consist of a diverse range of bacteria, including both human pathogens and plant-associated bacteria, which can be either beneficial or pathogenic.
Pseudomonas aeruginosa and the Burkholderia genus belong to the Proteobacteria phylum, with diverse roles ranging from human pathogens to plant-associated bacteria. Plant pathogens from these groups are environmentally important because they influence nutrient cycling, plant population dynamics, biodiversity, agricultural productivity, and the evolution of plant defenses. Their dual roles as both pathogens and beneficial organisms highlight their significance in both natural and managed ecosystems.
what are proteobacteria broadly split into?
enteric and non-enteric genera
what is the difference between enteric and non-enteric genera?
Non-Enteric Bacteria
Definition: Non-enteric bacteria are bacteria that do not typically inhabit the intestines and are often found in other environments, such as soil, water, air, or on various surfaces.
Enteric Bacteria
Definition: Enteric bacteria are a group of bacteria that primarily inhabit the intestines (gut) of humans and animals. The term “enteric” is derived from the Greek word “enteron,” meaning intestine.
what diets are more likely to carry pseudomonadaseae aeruginosa?
vegetarians
Pseudomonadaceae characteristics- what kind of physical properties do bacteria of this family poses
Gram-negative bacilli
Polar flagella
Aerobic (could this possibly be dogma?)
Non-fermentative
Many genera, including:
✓Pseudomonas
✓ Burkholderia
✓ Xanthomonas
✓ Ralstonia
✓ Zymomonas
✓ Sphingomonas
✓Stenotrophomonas
✓ Common human pathogens
✓Uncommon human pathogens
what do we mean by “opportunistic”
Opportunistic: cannot invade intact tissue, and so exploits failing host defences to initiate infection
Pseudomonadaceae aeruginosa infections in humans
Endocarditis: Mostly heart valves of IV drug users
Respiratory infections: 80% of CF patients colonised in lungs, cats and dogs with chronic illness
Bacteraemia and septicaemia: in immunocompromised patients (AIDS, diabetes mellitus, and severe burns)
Pseudomonadaceae aeruginosa infections in humans
Central Nervous System infections: meningitis and brain abscesses after invasion from contiguous structure (eg. inner ear or paranasal sinus)
Ear infections including external otitis: a predominant bacterial pathogen in external otitis, chronic in cats and dogs
Eye infections: causes devastating infections in the human eye
Bone and joint infections: most often seen in lV drug users, and in conjunction with urinary tract or pelvic infections
Urinary tract infections: usually hospital-acquired after catheterization,
P aeruginosa: infections in humans in skin, soft tissue and gastrointestinal
Skin and soft tissue: After breakdown of integument
(burns, dermatitis) and high moisture conditions can exacerbate risks
(swimmers; toe webs; perineum; under nappies).
Gastrointestinal: any part (oropharynx to rectum) in
immunocompromised. Does not cause typical diarrhoeal / vomiting disease.
Organs: Bladder and lungs are common
Burn Toe web Hot tub folliculitis Eye
the different virulance factors mean that P aeruginosa can adapt and affect hosts in multifactoral mechanisms- what are they?
opportunistic pathogens dont have one specific powerful pathogen that is capable of overcoming the bodies defences but rather a general affect that overcomes peoples immune system when theyre down so it can affect people wiith a range of virulance factors to take advantage of possiblle weaknesses
Fimbriae & other adhesins-
Attachment to host cells. Formation of biofilms
Neuraminidase- Modifies host receptors to aid fimbriae attachment
Polysaccharide capsule-Attachment to host tissues. Protects against immune system, and antibiotics
Endotoxin- May cause septic shock in host
Exotoxin A / Exoenzyme S- Inhibits host cell protein synthesis
Elastase, protease, haemolysins- Breaks down host cell fibres, and IgA / IgG
Pyocyanin- Generates superoxide and peroxide
radicals – tissue damage. Stimulates
inflammatory response. A siderophore that steals iron from host cells
Exopolysaccharides Facilitate biofilm formation which makes it very difficult for antibiotics to fight it off
P. aeruginosa characteristics
Can multiply in nutritionally poor environments
* API 20NE assimilation tests
* Aviation fuel
* Distilled water
* Photographic chemicals
* Cosmetics
* Plasticisers
P aeruginosa: routes of spread
Ubiquitous in the environment (potentially dogma):
* Soil & vegetation
* decaying organic matter
* Water
* Domestic environment
* Hospital environment
Spread via:
* Person – to – person
* Fomite spread
* Exposure to environmental sources
key facts about Burkholderia pseudomallei – melioidosis
A saprophytic bacterium found in parts of Southeast Asia, India, Africa, and North Australia
Found in soil, water, rice paddies. Long term
environmental survival: > year so is usually causing infections in people that are exposed to the soil and have skin breakages
Melioidosis: a severe infection in animals and humans in some tropical countries (~165 000 cases annually)
Localised infection from a break in the skin – may
progress to the bloodstream.
Pulmonary infection – mild bronchitis to severe
pneumonia
problematic because it can survive in the environment for a long time and takes advantage of people with underlying conditons
burkholderia mallei primarily affects horses and another difference is that its geographic and habitat distribution is different
how are infections caused by burkholderia pseudomallei- casuing the infection melioidosis
Infections
as the disease has extremely long incubation periods and remain dormant in people; can give infections to people who have laten melioidosis decades after when their health starts getting worse
Patients with latent melioidosis may be symptom-free for decades. The longest period
between presumed exposure and clinical presentation is ~62 years. Dubbed the “Vietnam
time-bomb” following military activity and soil disturbance.
Animals
Widespread. In 1975 a panda introduced to a Paris zoo caused a major outbreak – serious
damage to a number of zoo populations and equestrian clubs.
how bukholderia pseudomallei attack the bodies cells
are capable of polymerising host actin, stopping the host cell from killing the bacteria and also breaks the walls of the phagocyte cell
gram positive vs gram negative
Gram-positive and Gram-negative bacteria are two major groups that differ significantly in their cell wall structure, chemical composition, and response to the Gram stain test. These differences play a crucial role in their physiology, pathogenicity, and how they interact with antibiotics. Here is a detailed comparison of Gram-positive and Gram-negative bacteria:
- Cell Wall Structure
Gram-Positive Bacteria:
Thick Peptidoglycan Layer: Gram-positive bacteria have a thick layer of peptidoglycan (20-80 nm) that makes up most of the cell wall. This layer provides rigidity and structural support.
Teichoic and Lipoteichoic Acids: They contain teichoic acids and lipoteichoic acids, which are embedded in the peptidoglycan layer and play roles in cell wall maintenance, ion regulation, and adherence to surfaces.
No Outer Membrane: Gram-positive bacteria lack an outer membrane, making their cell wall simpler in structure compared to Gram-negative bacteria.
Gram-Negative Bacteria:
Thin Peptidoglycan Layer: Gram-negative bacteria have a much thinner peptidoglycan layer (2-7 nm) located between the inner cell membrane and an outer membrane.
Outer Membrane: They possess an additional outer membrane that contains lipopolysaccharides (LPS), phospholipids, and proteins. The outer membrane provides an extra barrier, contributing to their resistance to certain antibiotics.
Periplasmic Space: The space between the inner membrane and the outer membrane is called the periplasmic space, where various enzymes and proteins involved in nutrient acquisition and defense are found.
2. Gram Stain Reaction
Gram-Positive Bacteria:
Color: Stain purple or dark blue.
Reason: The thick peptidoglycan layer retains the crystal violet stain even after being treated with a decolorizing agent (like alcohol or acetone).
Gram-Negative Bacteria:
Color: Stain pink or red.
Reason: The thin peptidoglycan layer and the outer membrane cannot retain the crystal violet stain after the decolorizing step, so they take up the counterstain (usually safranin).
3. Chemical Composition
Gram-Positive Bacteria:
High peptidoglycan content (up to 90% of the cell wall).
Presence of teichoic acids.
Absence of lipopolysaccharides (LPS).
Gram-Negative Bacteria:
Low peptidoglycan content (only about 5-20% of the cell wall).
Presence of LPS in the outer membrane, which is a potent endotoxin that can trigger strong immune responses.
Presence of lipoproteins and porins (proteins that form channels in the outer membrane).
4. Sensitivity to Antibiotics
Gram-Positive Bacteria:
Generally more sensitive to antibiotics like penicillin and other β-lactams that target peptidoglycan synthesis.
The lack of an outer membrane makes them more susceptible to antibiotics that target the cell wall.
Gram-Negative Bacteria:
More resistant to many antibiotics due to the presence of the outer membrane, which acts as a barrier to certain drugs.
Often require antibiotics that can penetrate the outer membrane or inhibit specific cellular targets (e.g., aminoglycosides or fluoroquinolones).
5. Pathogenicity and Immune Response
Gram-Positive Bacteria:
Can produce exotoxins, which are proteins secreted by the bacteria that cause damage to the host.
Examples of Gram-positive pathogens: Staphylococcus aureus (causes skin infections), Streptococcus pneumoniae (causes pneumonia), Clostridium botulinum (causes botulism).
Gram-Negative Bacteria:
Produce both exotoxins and endotoxins. The lipopolysaccharide (LPS) in the outer membrane acts as an endotoxin, which can trigger severe immune responses and inflammation.
Examples of Gram-negative pathogens: Escherichia coli (causes food poisoning), Salmonella (causes typhoid fever), Pseudomonas aeruginosa (causes opportunistic infections).
Conclusion
The differences between Gram-positive and Gram-negative bacteria, particularly in their cell wall structure, Gram stain reaction, and sensitivity to antibiotics, have significant implications for their treatment and the strategies used to control infections. Understanding these distinctions is crucial in microbiology, medical diagnostics, and the development of targeted therapies.
