Pathogens and Hosts Flashcards
What signs/symptoms characterise clinical infection
- inflammation
- pain
- pyrexia
- tachycardia
- rigors
- increased white cell cound
- increased C reactive protein (CRP)
note: infection can be latent or sub-clinical
Pathogen
organism that can cause disease
Commensal
organism which is part of normal flora (e.g. E.coli in gut, S.aureus in nose, axilla)
What is fighting during pathogen/host interactions
host defence (immune system) vs organism pathogenicity
Pathogenicity (infectivty and virulence)
Capacity of microorganism to cause an infection
Requirements:
* infectivity; ability to becoem established
* virulence; ability to cause harmful effects once established
Infectivity
Ability to become established on or within a host
Needs:
* Attachment; E.Coli
* Acid resistance; helicobacter pylori
Virulence
Capacity to cause harmful effects (disease) once established
Conferred by virulence factors: genetically determined microbial components:
* Invasivness
* Toxin Production
* Evasion of immune system by microorganism
Specific to strains, not species
Invasiveness
give example and what it does
Streptococcus pyogenes (Group A streptococci)
* Necrotising fasciitis
* Cellulitis
* CT breakdown (through enzymes/toxins)
* Fibrinolysis
Toxins
- Exotoxins are released extracellularly by the microorganism
- Enterotoxins are exotoxins which act on the GI tract
- Endotoxins is structurally part of the G-ve cell wall
Explain the Exotoxin: tetanus
- Clostridium.tetani
- Infection of dirty wounds
* Toxin production: binds to nerve synapses, inhibits release of inhibitory neurotransmitters - Death caused by respiratory paralysis
- Treatment by debridement, antibiotics and antitoxin
Explain the enterotoxin: cholera
- Toxin affecting the intestines (e.g. cholera)
- Vibrio cholerae (colonises small intestine)
- Enterotoxin production: Inc cAMP levels: (inhibits uptake of Na+ and Cl- ions, stimulates secretion of Cl- and HCO3- ions. Passive, large outflow of H2O from gut.
- Causes death by dehydration
- Treated by rehydration
Superantigens
- certain exotocins of s.pyogenes and s.aureus
- able to stimulate division of T cells in absence of specific antigen
- Overwhelming cytokine production causes “toxic shock”
Endotoxin
- Componet fo G-ve bacterial cell wall: LPS: Lipid A, Oligosaccharide core, spicific polysacchariide chain
- e.coli and other G-ve bacilli
- Induces severe uncontrolled host response: cytokine production, fever/rigors/hypotension/tachycardia/collapse
what form of MRSA is easier to treat
community required MRSA as opposed to hospital required MRSA
bacillus anthracis
human infections associated with exposure to infected animals or contaminated animal products
Can often be cutaneous and is rarely fatal with treatment
what are pathogenic bacteria
those capable of causing disease
what are pathogenic bacteria
those capable of causing disease
Requirements of pathogenicity
2
infectivity and virulence
What is virulence conferred by
invasiveness, toxin production and immune evasion
What can harmful effects from bacterial infection be caused by
2 things
- The bacterium
- the host response
often both
Virus pathogenic mechanisms
3
- Cell destruction following virus infection
- Virus-induced changes to cellular gene expression (e.g. tumor viruses)
- Immonopathogenic disease (e.g. Influenza A)
Sites of viral entry
- Conjunctiva
- Capillary
- Skin
- Respiratory tract
- Alimentary tract
- Urinogenital tract
What is the case with the majority of viral infections
Most is unarrparant (either dormant or infection doesn’t show) - like iceberg: only small portion shows
4 different types of viral infections
name and breifly describe each
- Acute infection: arise and then goes away
- Latent infection: arises, lies dormant, (stimulus) arises again
- Chronic infection: arises, small dec but remains
- Tumor virus infection: small inc, stable, suddenly shoots up in late diesease stage
Examples of acute viral infections
- Influenza A -respiratory infection
- Enterovirus - enteric (GI) and neurological infections
Summarise process of acute virus infection
- Viral infection
- Multiplies and inc exponentially
- Reaches peak (symptoms worst)
- Host immune system activated and begins to fight back
- host develped enough antibodies, and viral numbers dec
- Reduce to 0
2 features of acute virus infections
Localised to specific site of body (e.g. infulenza in resp. tract)
Development of viraemia with widespread infection of tissues
Explain Influenza A virus infection
- Virus infects cells of respiratory tract
- Destruction of respiratory epithelium: (secondary bacterial infections)
- Altered cytokine expression leading to fever
Explain Influenza A virus infection
- Virus infects cells of respiratory tract
- Destruction of respiratory epithelium: (secondary bacterial infections)
- Altered cytokine expression leading to fever
Explain Influenza A virus infection
- Virus infects cells of respiratory tract
- Destruction of respiratory epithelium: (secondary bacterial infections)
- Altered cytokine expression leading to fever
How are novel influenza viruses generated?
2 mechanisms
- Antigenic drift: minor changes (natural mutations) in genes of virus occur gradually over time to generate antigenic varients
- Antigenic shift: abrupt major changes in virus antigenic structure
Give some commone enterovirus infections
- Poliomyelitis (poliovirus)
- Aseptic meningitis (many enteroviruses)
- Myocarditis (coxsackie B viruses)
- Pancreatitis (coxsackie B virus)
- Respiratory infections (many enteroviruses)
Breifly describbe process of enterovirus infection
- oral —> GI system (gut)
- Viraemia: non-neuronal tissues, neuronal tissues (e.g. CNS) —> paralysis
- Virus also extreted in faeces
Where do enteroviruses live/infect initially
The Gut/intestines (GI tract)
Give example of a latent virus infection
Herpes simplex virus (cold sores = type 1, genital lesions = type 2)
Give brief overview of herpes virus infection and latancy
- Primary infection:
* Virus infection of epithelium (e.g. cold sore)
* Virus migrates to ganglia
* Virus latent in nucleus - Reactivation:
* Stimulus occurs (e.g. neurological, phycological, immunocompromised)
* Virus migrates to epithelium leading to virus replication
* Cold sore again
* Viral release
Give 2 examples of virus-induced tumors
- Papillomaviruses (HPV) - cervical carcinoma
- Retroviruses - lymphomas and leukemias
Summarise the retrovirus replication cycle
- Attachment
- Membrane fusion
- Uncoating of viral RNA in cytoplasm
- Reverse transcriptase acts and converts to viral DNA
- Virus DNA integration into nucleus
Summarise retrovirus-induced tumours
- Virus infects cell
- Virus nucleic acid, as DNA, integrates into ceullular genome
- Virus causes changes in cellular gene expression
- Uncontrolled cell multiplication and tumor formation
Colonisation
presence of a microorganism on/in a host, with growth and multiplication of the organism, but without interaction between host and organism
Latent
the time interval between when an individual or host is infected by a pathogen and when they become infectious, i.e. capable of transmitting
Asymptomatic infection
An infection without symptoms
Example of tumor causing virus
Human T-lymphotropic virus-1 (HTLV-1): causes abnormal gene expression
features of viral pathogenesis
Pathogenesis is the process by which an infection leads to disease. Pathogenic mechanisms of viral disease include:
1. implantation of virus at the portal of entry
2. local replication
3. spread to target organs (disease sites)
4. spread to sites of shedding of virus into the environment.
