infections 1 Flashcards
what is the definition of infections
The invasion and multiplication of a pathogenic organism in a host organism
what are the 6 stages of infectious disease?
Acquisition
Colonisation
Penetration
Spread
Damage
Resolution
what is endogenous infections?
organisms present in/on the body (e.g. bacteria, fungi – some examples are shown on the right)
what is exogenous infection?
exogenous microbes that are not part of our typical body flora
what are example bacterias present in oral cavity, nasopharynx , skin , GI tract, Vagina?
Oral cavity
Streptococcus spp
Actinomyces
Nasopharynx
Streptococcal spp
Neisseria spp
Corynebacteria spp
Skin Staphylococcal spp Streptococcal spp Corynebacteria spp Some fungal species
GI tract Enterobacteriaceae Enterococci spp Clostridium spp Bacteroides spp Candida spp
Vagina
Lactobacillus spp
1st line- Intact skin & mucous membranes
what is the bodys defence?
Sweat (pH), mucous traps bugs, antibacterial secretions e.g. stomach acid, lysozyme in tears
2nd line
Phagocytosis & inflammation
What is the bodys defence to this?
Phagocytic cells in blood (monocytes, neutrophils), tissues and lungs (macrophages) engulf & destroy microorganisms
Along with phagocytic cell increase at local site, body tries to limit spread of the organism e.g. by forming clot
what are some exogenous infection transmission?
Direct contact
e.g. STIs
Inhalation / droplet infection
e.g. common cold
Ingestion / faecal-oral route
e.g. gastroenteritis
Trauma / inoculation
e.g. tetanus, malaria, infected atopic dermatitis
Trans-placenta
e.g. congenital toxoplasmosis
Explain the stage colonization
Organism must survive and multiply in the environment
pH, temperature, competing endogenous organisms
Some have evolved mechanisms to help colonisation
Mucolytic enzymes to penetrate mucous layers
Adhesins to help stick to colonisation site
Once established in a site (internal or external), organism has colonised but may not necessarily go on to invade & damage host tissue
what are the features of Bacteria seldom lone cells
Bacteria seldom lone cells - usually form complex colonies termed “biofilms”
Have co-operation of organisms, often have slimy protective outer layer
More difficult to treat than isolated bacteria in a culture / spread plate
what is penetration
To invade, organism must breach the surface barrier (skin, mucous membrane..)
can skin avoid penetration and how?
Skin: most bacteria can’t penetrate intact skin
how can upper respiratory tract avoid penetration
Upper respiratory tract: muco-cilliary clearance and cough reflex protect against particulate exposure
Influenza “sticks”
Droplets <5μm can reach alveoli and establish infection
how does gastrointestinal tract prevent penetration?
Gastrointestinal tract: stomach acid defence but:
Organisms can damage mucosal surface by releasing toxins e.g. causing dysentery
Or get taken into cells - e.g. Salmonella typhi taken in by M cells in Peyer’s patches
invading organisms can spread where?
Along tissue planes
By extension of colony into surrounding area
Via vasculature / lymph (effective rapid spread
what are some damages which can take place?
Mechanical damage from bulk effects
Toxins
Altered function of host cell
Host response
what is mechanical damage from bulk effect?
e.g. Bacteria/biofilm can obstruct a hollow organ, e.g. cystic fibrosis
what are exotoxins
Exotoxins produced inside bacteria (G+/-ve) and diffuse out, usually proteins
Very toxic e.g. Clostridium tetani neurotoxin → tetanus
Strongly antigenic
what is endotoxins
Endotoxins are LPS-protein complexes
Mainly in cell wall G-ve bacteria (shed)
Typically less specific toxic reactions
Weakly antigenic, often cause fever
e.g. meningococcal disease and sepsis
from Neisseria
what does altered function of host cell mean?
Can affect functioning of cell, tissue or organ - Common with viruses
Can be as the body tries to combat infection - e.g. increased bowel motility in diarrhoea
what does host response mean?
Host response
Host damage through response to infection
Can have chronic inflammation and immune response
Can get swelling, pus, scarring, necrosis
what are the stages of resolution?
Recovery: organism cleared from body, no lasting effects
Latent infection: Initial symptoms resolve but infection not cleared and can re-occur. Often occurs with viruses – Herpes, CMV, EBV (more in Part 3)
Clinical latency: can have a period of no symptoms but the infection course is continuing. Examples include – HIV, syphilis (more in Part 3) or also during the initial incubation period
Chronic infection: some infection may never clear (HIV, chronic hepatitis), or can take long time to clear. Some may be cleared by have long-term effects.
May recover (clear infection) but have long-lived effects due to damage from infection. Example – from inflammation or leading to autoimmune disorders
Pathogen:
an organism capable of causing disease
Virulence:
degree of pathogenicity of an organism (ability to cause disease)
Attenuation:
a reduction in the virulence of a pathogen (if gone = avirulent)
Exaltation:
an increase in virulence
Chemotherapeutic agents –
chemicals intended to be toxic for the pathogenic organisms but safe for the host
Parasite
– general term used to describe protozoa and helminths
what are the three classes of biochemical reaction:
Three general classes of biochemical reaction are potential targets for chemotherapy of bacteria:
Class I: reactions that utilise glucose and other carbon sources are used to produce ATP and simple carbon compounds
Class II: pathways utilising energy and class I compounds to make small molecules (e.g. amino acids and nucleotides)
Class III: pathways that convert small molecules into macromolecules such as proteins, nucleic acids and peptidoglycan
Class I reactions are poor targets.
Class II reactions are better targets:
folate synthesis is inhibited by sulfonamides and trimethoprim (bacteria), pyrimethamine (malarial parasite), methotrexate (cancer cells)
Class III reactions are important targets:
bacterial peptidoglycan synthesis selectively inhibited by β-lactam antibiotics
bacterial protein synthesis selectively inhibited by antibiotics that: prevent binding of tRNA (e.g. tetracyclines), promote misreading of mRNA (e.g. aminoglycosides), inhibit transpeptidation (e.g. chloramphenicol) or inhibit translocation of tRNA from A site to P site (e.g. erythromycin)
nucleic acid synthesis inhibition (e.g. chain termination such as by antiviral aciclovir) or by inhibiting DNA gyrase (e.g. the ciprofloxacin)
