Pathogenesis Flashcards

1
Q

What is symbiosis and give typesd

A

Close+often long term interaction between 2 different biological species
Commensalism (one organism benefits and the other neither benefit nor harmed), Mutualism (association which is beneficial to both organisms involved), Parasitism (parasite benefits at the expense of other organism)

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2
Q

Difference between obligate intraceullar parasite and facultative parasites

A

Obligate: can only reproduce within host cells
Facultative: don’t rely on host to continue life cycle as can live and reproduce inside and outside cells

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3
Q

Normal flora definition and functions

A

population of microorganisms that reside in skin, mucous membranes and intestinal tract of healthy human body
Functions:
Helps development of mucosal immunity
Protect host from colonisation with pathogenic microbes
Aids in digestion of food

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4
Q

Human microbiome what

A

collection of genes of all microbes in normal flora

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5
Q

Difference resident and transient flora

A

Resident-disturbed but reestablish themselves, usually not removed by routine hand wash, usually not associated with transmission of infecdtion e.g. staph epidermis
transient-do not reestablish themselves, easily removed by hand wash, usually assocaited transmission of infection e.g. staph aureus

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6
Q

Why does hospitalisation cause change in flora

A

Exogenous environmental infections
invasive techniques employted increase risk of infection
use of antibiotics

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7
Q

What are the different types of opportunistic infections and give examples of them

A

caused by non pathogenic microorganism that act as pathogen in certain circumstances
Normal flora moves to other parts of body causing infection e.g. E.Coli can cause UTI
If host defence mechanisms are weakened (immunocompromised( e.g. fungal/bacterial infections such as candida spp, aspergilllus spp, peseudomonas aeruginosa
Lack of competition from nnormal flora due to its loss from body e,g, vaginal yeast infection due to antibiotic use

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8
Q

What are local and systemic effects for infections

A

Local-inflammation, tissue necrosis, nasal congestion

Systemic-fever, altered immune response, muscle pain

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9
Q

What are the obligatory steps for infectious organisms

A

Entry+spread: attach and enter with local or general spread in the body by evading host’s primary defenses
Evasion: Evasion of host’s immune system by evading immune defenses long enough for full cycle in host to be completed
Multiplication-Increase in number by rapid growth/replication
Transmission-exit from body into next portal of entry on a scale that ensures spread to fresh host

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10
Q

What are the strages of infectious disease progresion

A

Incubation: time between exposure and onset of a specific clinical sign. Determined by virulence of pathogen, infective dose, health of the patient’s immune system, generation time of the pathogen or the site of infection. Incubation period differs depending on the pathogen involved
Prodrome: period during which non specific constitutional symptoms occur. Not all diseases have this stage
Illness: period during which the clinical features of the infection are present
Recovery (convalescence)): Period during which the illness abates and patient returns to the healthy state

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11
Q

Define: spordiac, endemic, epidemic, pandemic

A

Spordiac: disease only occurs occasionally
Endemic: Disease continuously present in population
Epidemic: disease has greater number of cases than normal in an area within a short period of time
Pandemic: epidemic disease that has worldwide distribution

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12
Q

What are superficial and systemic infections

A

Superficial: self limiting microorganisms replicate in epithelium at the site of entry and local damage is caused. Immune response to superficial infections can give rise to constitutional symptoms
Systemic: replication of microorganissm at multiple sites due to infection of deeper tissues. Spread throughout the body primarily via lymph nodes and blood.

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13
Q

Acute and persistent infections

A

rapid onset of diseases with relatively brief period of symptoms. The pathogen is cleared within days
Persistent: Pathogen is not cleared from host following primary infection but remains in tissues of infected individuals. Latent=microorganism persists after initial clearance and may have asymptomatic or symptomatic reactivation, Chronic=continued production of infectious organism and immune evasion. Infected hosts are carriers

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14
Q

Nosocomial infection what

A

Infection acquired in hospital or medical facility. Can affect patients are health care workers and are common because: i) easily to moved around by staff/patients/visitors, II) not always prevented by proper handwashing

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15
Q

Give types of nosocomial pathogens which can be prevented by handwashing and can be prevented by hand washing.

A

Hand wash: staph. aureus, clostridium difficile, pseudomonas aeruginosa, enterococcus spp, respiratory syncytial virus, norovirus
Can’t be prevented by hand wash: influenza, chicken pox, measles

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16
Q

What are the determinants of pathogenesis (epidemiological triad)

A

Host (age, underlying characteristics, genetic variation, immunodeficiency, immune response, trauma/surgery/foreign body)
Pathogen (opportunism, attachment, invasiveness, viirulence, effect of infection on cell/cellular pathogenesis)
Environment

17
Q

iatrogenic infections what is it and what caused by

A

relating illness caused by medical treatment or examinations
Injury associated with therapy e.g. damage allows microbes to enter normal sterile parts of the body
Plastic and metal foreign bodies provide surface that microbes can colonise. Produce adhesive slime, material and grow as biofilm on surface

18
Q

How do adhesins work in pathogenesis

A

bacteria have adhesisns on surface that bind to specific host cell surface components aka receptors
Adhesins=often proteins though they can be polysaaccharides or glycolipids and include glycocalyx, capsule and pili. Interaction of virus with receptor induces conformational changes that lead to membrane fusion and penetration.
Adhesins mediate series of signalling events that affect bacterial uptake and can promote inflammatory events by affecting innate immune receptors

19
Q

Define host range

A

different species of hosts a given pathogen can infect. Host specificity of viruses predominantly defined by interactions of viral proteins with their cognate cellular receptors.

20
Q

Define tissue tropism

A

Different tissues within a given host that are infected by the pathogen. Attachment is one of several factorss that dertermine tissue tropism as thee need for a specific cell receptor narrows the species and the type of cells the pathogen can enter

21
Q

Define permissive cell

A

Allows pathogen to replicate. Has the required receptor, allow the pathogen to replicate and lacks defenses against the pathogen or the pathogen as evolved mechanisms to overcome such defenses

22
Q

Give examples of invasins and what they do

A

Collagenase and hyaluronidase: degrade collagen and hyaluronic acid disrupting the epithelial basal lamina and allowing bacteria to spread through subcutaneous tissues
Coagulase: triggers the formation of a firbrin clot around the bacteria to protect them from phagocytosis
Leukocidins: degrade WBC
Hemolysin: degrade RBC

23
Q

Pathogenicity and virulence define

A

Pathogenicity-ability of microbe to cause a disease
Virulence-degree of pathogenicity in a microorganism. Virulence determined by its tropism, invasiveness and production of factors that can increase toxicity or permissive state of cells it infects

24
Q

How is virulence meassured

A

LD50-number of pathogens that will kill 50% of experimental group of hosts
ID50-number of pathogens that will infect 50% of an experimental group of hosts

25
Q

Give examples of bacterial virulence factors

A

adhesins, invasins
endotoxins-LPS present in cell wall of gram negative bacteria
exotoxins-secreted proteins produced by gram positive and gram negative bacteria. Exotoxins have different mechanisms of action and different targets within cell hence cause variety of diseases

26
Q

Compare exo and endotoxins in terms of: source, whether secreted from cell, chemistry, location of genes, toxicity, clinical effects, antigenicity, heat stability

A

Exotoxin: gram positive+negative, yes, polypeptuide, plasmid or phage, high, various effects, high, destroyed rapidly at 60 deg
Endotoxin: gram negative, no, lipopolysaccharide, bacterial chhromosome, low, fever+shock, poor, stable at 100 deg for 1 hour

27
Q

What can viral virulence genes do

A

Alter ability of viruss to replicate
Modify the host defense mechanissms
Enable the viruss to spread in the host
Act ass toxic proteins

28
Q

what are superantigens (SAgs))

A

toxins that stimulate the immune system
In contrast with classical peptide antigen recognition, SAgs do not require processing to small peptides. They can bind to MHC II molecules non specifically and stimulate large no. T cells.