Pathogenesis of microbial Infection Flashcards

(46 cards)

1
Q

Symbiosis definition

A

-The close and often long-term interaction between two different
biological species

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2
Q

What are the 3 types of symbiotic associations

A

Commensalism:
-one organism benefits and the other derives neither benefit nor
harm.
Mutualism:
-association which is beneficial to both organisms involved
Parasitism:
-one organism, the parasite, benefits at the expense of the other

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3
Q

Obligate intracellular vs facultative parasites

A

-Obligate intracellular parasites can only reproduce within host cells (e.g. intracellular bacteria like Chlamydia and all viruses)
-Facultative parasites do not rely on
the host to continue their life-cycle and can live/reproduce inside and outside cells (e.g. Salmonella)

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4
Q

Normal flora definition and functions

A

-Population of microorganisms that reside in the skin, mucous membranes and intestinal tract of human body
1. Helps development of mucosal immunity
2. Protects host from colonisation with pathogenic microbes
3. Aids in digestion of food

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5
Q

Human microbiome definition

A

-Collection of genes of all the
microbes in normal flora

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6
Q

Why is knowledge of the normal flora of the human body important?

A

-Allows prediction of the pathogens causing infection as bacteria tend to grow in specific body sites
e.g. Pneumococci frequently colonize the
upper respiratory tract, and are believed to act as a reservoir for infection of the lower respiratory tract

-Investigation for underlying abnormalities in specific areas of the body when bacteria are
isolated from normally sterile sites
e.g. alpha-hemolytic streptococci in the
throat is considered normal flora, whereas in the blood is likely the cause of bacterial endocarditis

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7
Q

Resident vs transient flora in hand hygiene

A
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8
Q

Why does flora change during hospitalisation?

A

-Exogenous environmental
infections (e.g. hospital
flora found on linen,
equipment, water supply)
-Invasive techniques
employed increase risk of
infection (e.g. urinary
catheters, I.V. lines)
-Use of antibiotics

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9
Q

What are opportunistic infections?

A

-Caused by non-pathogenic microorganisms that act as pathogens in certain circumstances:
-Normal flora moves to other parts of the body causing
infection (e.g. E coli can ascend urethra and cause UTIs)
-If host defence mechanisms are weakened (e.g. immunocompromised patients)
-Lack of competition from normal flora due to its loss from body (e.g. vaginal yeast infections due to use of
antibiotics)

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10
Q

Infection definition

A

The presence of microorganisms in the body

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11
Q

Colonisation definition

A

Describes when a new microorganism grows on superficial body sites
(skin, mucous membranes and GI tract) without invading the body

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12
Q

Carrier definition

A

A person who harbours a microorganism and can be a source of infection for others

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13
Q

Pathogen definition

A

A microorganism capable of causing disease

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14
Q

Microbial pathogenesis

A

The process by which infection leads to disease

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15
Q

What is the course of infectious diseases?

A
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16
Q

What does immunopathogenesis cause?

A

Immunopathogenesis is a primary cause of cell death in many infections is due to killing of infected cells by the host immune system:
-Cytotoxic T cell mediated attack (e.g. Hepatitis B virus and liver damage)
-Antibody-mediated damage to the host (e.g. Streptococcus pyogenes and rheumatic fever)
-Antibody-mediated complement fixation (e.g. Hepatitis C virus exploits the complement system to establish persistence)

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17
Q

Symptom vs Sign vs Syndrome

A

-Symptoms: Subjective features of
disease experienced only by the
patient. Infections can be
asymptomatic (sub-clinical) or
symptomatic
-Sign: Objective manifestations of
disease that can be observed and
measured by others
-Syndrome: Group of symptoms and
signs characteristic of a disease

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18
Q

Local effects vs systemic effects in response to infection

A

Local effects:
-Inflammation (swelling)
-Tissue necrosis
-Nasal congestion

Systemic effects:
-Fever
-Altered immune response
-Muscle pain (myalgia)

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19
Q

Obligatory steps for infectious agents

20
Q

Stages of infectious disease progression

A

1) Incubation: Time between exposure and onset of a specific clinical sign.
2) Prodrome: Period during which non specific “constitutional” symptoms occur (e.g. fever, malaise, loss of appetite) Not all infectious diseases have a prodromal stage.
3) Illness: Period when clinical features of the infection are present
4) Recovery (convalescence): Period when the illness abates and patient
returns to healthy state

21
Q

Communicable vs Non-communicable disease

A

Communicable: The infection can spread from host to host directly (e.g. HIV) or indirectly (e.g. noroviruses)
-The term contagious is applied to a highly communicable disease spread by contact

Non-communicable: The infection is non
transmissible between humans (e.g. botulism)

22
Q

What are the types of infections based on occurrence?

A

-Sporadic: the disease occurs only occasionally (e.g. tetanus)
-Endemic: the disease is continously present in a population, community or country (e.g. TB and chickenpox)
-Epidemic: the disease has greater number of cases than normal in an area within a short period of time i.e. outbreaks occur (e.g. SARS in 2003)
-Pandemic: epidemic disease that has
worldwide distribution (e.g. flu pandemic in 1918 and 2009)

23
Q

What are the types of infections based on site of infection?

A

Superficial:
-self limiting, microorganisms replicate in epithelium at the site of entry and local damage is caused (e.g. impetigo or folliculitis caused by Staph. aureus and
common cold caused by rhinovirus)
-immune response to superficial infections can give rise to constitutional
symptoms (e.g. cytokine storm and influenza)

Systemic:
-replication of microorganism at multiple sites due to infection of deeper tissues
-spread throughout the body primarily via lymph and blood (e.g. chickenpox, measles, Salmonella typhi)

24
Q

What are the types of infections based on outcome?

A

Acute infection:
-Rapid onset of disease with relatively brief period of symptoms. The pathogen is cleared within days (e.g. influenza, poliovirus, measles)

Persistent infection:
-The pathogen is not cleared from the host following primary infection, but remains in tissues of infected
individuals

25
What are the 2 types of persistent infections?
Latent: -The microorganism persists after initial clearance, and may have asymptomatic or symptomatic reactivation (e.g. latent TB, herpes simplex virus and varicella zoster Chronic: -With continued production of the infectious organism and immune evasion (e.g. chronic diabetic foot infection, Hep B, HIV) -Infected hosts become carriers
26
What are nosocomial infections?
-Any infection acquired in a hospital or medical facility -Can affect patients and health care workers and are common because: -they are easily moved around by staff, patients or visitors -they are not always prevented by proper hand washing
27
What factors contribute to the appearance of antibiotic resistance?
-Mutation and transfer of resistance genes through plasmids -Transmission of resistant bacteria via the hands of healthcare staff -Incorrect/excessive use of antibiotics -Transmission of resistant bacteria from surfaces within the healthcare facility
28
What is the epidemiological triad?
29
What factors affect host susceptibility to infection?
-Age (e.g. Infants and elderly are more susceptible to influenza infection) -Underlying characteristics that increase susceptibility (e.g. asthma, obesity, diabetes, malnutrition) -Genetic variation (e.g. sickle cell trait provides protection to malaria; HIV long-term non-progressors) -Immunodeficiency (e.g. opportunistic infections in AIDS patients) -Immune response (e.g. “cytokine storm” in influenza infection) -Trauma/surgery/foreign body (e.g. surgical implants) make it easier for bacteria to cause infection and more difficult to eradicate it
30
What are iatrogenic infections?
-Factors that can disrupt the body’s non-specific mechanical barriers to infection make it easier for microorganisms to cause infection: -Injury associated with therapy (e.g. damage sustained through procedures such as endoscopy, surgery or radiotherapy) allows microorganisms to enter normally sterile parts of the body -Plastic and metal “foreign bodies” such as prostheses (hip joints; heart valves) or IV lines provide surfaces that microbes can colonize more easily than the natural equivalents e.g. coagulase-negative staphylococci like Staph. epidermidis/aureus are members of the normal flora that can produce an adhesive slime material and grow as biofilms on plastic surfaces -Treatment is difficult and device must be replaced to avoid chronic infection or sepsis
31
How does attachment affect pathogenesis of bacteria?
-Bacteria have specific molecules on their surface (adhesins) that bind to specific host cell surface components (receptors) -Adhesins are often proteins, although they can be polysaccharides or glycolipids and include glycocalyx, capsule and pili -Upon receptor binding, adhesins mediate a series of signalling events that affect bacterial uptake and can promote inflammatory events by affecting innate immune receptors
32
How does attachment affect pathogenesis of viruses?
-Viral surface proteins bind to receptors on host cell membrane. Host cell receptors serve some function for the host cell, and the pathogen takes advantage of them (e.g. HIV binds to CD4) Also, the receptor can be different for different cell types. -The interaction of virus with receptor induces conformational changes that lead to membrane fusion and penetration. -Attachment factors (e.g. heparan sulfate proteoglycans) help to concentrate the viral particles at the cell surface. Unlike binding to receptors, the interactions with attachment factors are often not highly specific.
33
What is a host range?
-The different species of hosts a given pathogen can infect -The host specificity of viruses is predominantly defined by the interactions of viral proteins with their cognate cellular receptors -The molecular mechanisms of host specificity are less understood for bacterial pathogens
34
What is tissue tropism?
-The different tissues within a given host that are infected by the pathogen (e.g. rhinoviruses infect only the respiratory tract) -Attachment is one of several factors that determine tissue tropism as the need for a specific cell receptor narrows the species and the type of cells the pathogen can enter
35
What is a permissive cell?
-A permissive cell is one that allows a pathogen to replicate -It has the required receptor, allows the pathogen to replicate and lacks defences against the pathogen (e.g. interferon production) -Or the pathogen has evolved mechanisms to overcome such defences (e.g. Vpu and Vif genes in HIV)
36
What is invasiveness?
-The capacity of a microbe to enter and damage a tissue -Bacteria spread to deeper tissues by producing specific enzymes (invasins)
37
Examples of invasins
-Collagenase and hyaluronidase: Degrade collagen and hyaluronic acid disrupting the epithelial basal lamina and allowing bacteria to spread through subcutaneous tissues (e.g. S. pyogenes) -Coagulase: Triggers the formation of a fibrin clot around the bacteria to protect them from phagocytosis (e.g. S. aureus) -Leukocidins: Degrades white blood cells (e.g. S. aureus) -Hemolysins: Degrades red blood cells (e.g. Streptococci, staphylococci and clostridia )
38
What is pathogenicity?
The ability of a microbe to cause disease
39
What is virulence and what determines it?
-The degree of pathogenicity in an organism -Determined by its tropism, invasiveness and the production of factors that can increase toxicity/the permissive state of the cells it infects
40
What are measures of virulence?
-Lethal dose 50 (LD50) - Number of pathogens that will kill 50% of an experimental group of hosts -Infectious dose 50 (ID50) - Number of pathogens that will infect 50% of an experimental group of hosts
41
What are endotoxins?
-Lipopolysaccharides (LPS) present in the cell wall of Gram-negative bacteria
42
What are exotoxins?
-Secreted proteins produced by Gram-positive and Gram-negative bacteria (e.g. diphteria, tetanus, cholera and botulinum toxins) -Exotoxins have different mechanisms of action and different targets within the cell, hence cause a variety of diseases
43
Exotoxins vs Endotoxins
44
How do viral virulence genes work?
They: -Alter the ability of the virus to replicate -Modify the host defense mechanisms (e.g. viral proteins secreted by infected cell that mimic cytokines) -Enable the virus to spread in the host -Act as toxic proteins
45
What are super antigens?
-Toxins that stimulate the immune system -In contrast with classical peptide antigen recognition, superantigens do not require processing to small peptides -They can bind to MHC-II molecules non-specifically and stimulate a large number of T cells
46
Give 3 examples of bacteria that cause healthcare associated infections and are resistant to antibiotics
-Methicillin-resistant S. aureus (MRSA) -Vancomycin resistant Enterococcus faecalis (VRE) -Carbapenemase producing Enterobacteriaceae (CPE)