Colonization, Infection And Transmission

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mutualistic

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benefit to both members often accompanied by co-dependency

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commensal

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one member benefits while causing minimal harm to the other

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parasitic

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one member of the relationship benefits at the expense of the other

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colonization

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establishment of a population for either a short time or a long time.
infection disease is the clinical effect of damage caused by infection/colonization not all colonizers cause disease

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pathogens

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microbes that cause disease

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pathogenesis

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the process whereby a microbe causes disease

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virulence / pathogenicity

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ability of a microbe to cause disease

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virulence factors

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produced by microbes and facilitate pathogenesis/ increase virulence
can determine whether a feature is a virulence factor using Koch's postulates

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Opportunistic pathogens

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can occur when:
gain entry to a normally sterile site with few defenses
when normal microbiota is disrupted
when the host's defenses are compromised

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strict pathogens

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parasitic microbes that almost always cause disease even in healthy individuals

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Adhesion

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crucial first stage of the infectious cycle as bacteria must combat expulsion mechanisms to colonize

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Non-specific adhesion

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a microbe sticks to the host cell via general physical characteristics (hydrophobic interactions) or the presence of exopolysaccharide

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Specific adhesion

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depends on the expression of two types of cell surface molecules:
Adhesins- ligand on the bacterial surface
Receptor- present on host cell surface
they fit together with high specificity which helps to determine the host and tissue that a microbe can colonize
very strong interaction
adhesins may be imbedded in the cell wall or outer membrane or distant from the cell, make good vaccine candidates

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Dissemination/ invasion

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ability of the microbe to move beyond the initial site of colonization

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Degradative enzymes

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help organisms spread through tissue by breaking down extracellular matrix materials
aids in invasion

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Toxins

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molecules that affect host cells directly including;
cytolysins and phospholipases which destabilize host cell membranes and lyse host cells
cell signaling toxins
injected toxins
toxins that bind a host receptor and are endocytosed

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Extracellular pathogens

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remain outside of the host cells

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Facultative intracellular pathogens

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may invade host cells but can replicate outside of them

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Obligate intracellular pathogens

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must replicate inside of host cells

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Transmission

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required for the long term survival of the microbe

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Vertical transmission

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occurs from parent to offspring
germline- as in retroviruses that are passed on in the DNA
prenatal- occurs primarily through the placenta
Perinatal- occuring during birth
postnatal- where the pathogen is passed on through milk or direct contact

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Horizontal transmission

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eg. human, animal or environment to human
sources:
respiratory tract- sneezing, coughing allow pathogens to be shed from nasal cavity and lungs and inhaled by others
GI tract- transmission occurs primarily through fecal-oral route
Urogenital tract- most infections transmitted sexually, few are passed on through urine
Oropharynx- several organisms including some respiratory pathogens and a number of viruses transmitted through saliva
skin- several diseases can be passed through skin either directly or through dust/shared items
Blood- must gain entry through skin or mucosa
invertebrates- blood-sucking arthropods
vertebrates- zoonoses transmitted through contact w/ or ingestion of meat, fecally contaminated water, bites or inhalation
environment- some live quiet happily in environment

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Resolution and recovery

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possible outcome of infectious disease
for many pathogens in otherwise healthy individuals tis will occur naturally and may be aided by chemotherapy

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Persistence

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possible outcome of infectious disease
some pathogens remain in the host for long periods of time or even permanently
ex. mycobacterium tuberculosis, herpes simplex virus, varicella-zoster virus

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Autoimmune disease

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possible outcome of infectious disease
some bacteria produce molecules that mimic host epitopes which can lead to sequelae of infection such as rheumatic fever, myocarditis, rheumatoid arthritis, and diabetes

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Progression

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possible outcome of infectious disease
for some pathogens if untreated will progress sometimes becoming lethal
may also occur in immunocompromised patients
some diseases include necrotizing fascitits which can progress so quickly that full medical support may not prevent a lethal outcome

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Infectious dose

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in lab generally defined as ID 50 the dose at which 50% of hosts become diseased under a specific set of conditions

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In real life infectious dose can vary depending on

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host species or genotype
route of introduction
health/immune status
etc.

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Normal microbiota acquired during birth

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baby picks up microbes from the mother that were ideally part of the normal microbiota of the genitourinary tract, large intestine, skin but may be pathogens

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Normal microbiota acquired just after birth

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colonization begins as soon as baby is born
major sources include contact w/ mother and caregivers passing on normal skin and URT microflora as well as environment
hospital stays are assoc. w/ colonization by more potential pathogens

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Normal microbiota acquired during feeding

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much of gut microbiota comes from what goes into it

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Normal microbiota and antibiotic use

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treatment w/ antibiotic inhibits normal development of microflora
appears to allow colonization by more potentially pathogenic bacterial strains

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Family members

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pick up the microbiota of the people we are in contact w/ the most
if normal microbiota is disrupted, recolonization may occur primarily w/ species present in/on those around us

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Situations in which normal microbiota can become opportunistic pathogens

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when a barrier is breached allowing microbes to reach areas w/ few defenses
when normal defenses are disrupted
depression of immune system allowing for uncontrolled growth of commensal microbes
antibiotic treatments

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factors in which normal microbiota physically prevent the establishment of other potentially pathogenic organisms

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occupying binding sites and receptors, thereby preventing adhesion
keeping available nutrient levels low
producing waste or antimicrobial compounds that discourage microbial growth
maintaining an acid pH

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important functions that normal microbiota play a role in

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metabolic reactions converting indigestible food to nutrients we can absorb
growth factor production

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Microbes in upper respiratory tract

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mostly anaerobic
Peptostreptococcus
Veillonella
Actinomyces
Fusobacterium
Candida (oral thrush, esophagitis, endocarditis, sepsis)
Streptococcus * (can cause tooth decay, abscesses, sepsis, meningitis, endocarditis)
Haemophilus *
Neisseria *

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Microbes in lower respiratory tract

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normally sterile but can transiently be colonized by upper airway microbes

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Microbes in Ear

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coagulase negative staphylococci are most commonly found
opportunistic pathogens that colonize the ear include streptococcus pneumoniae, pseudomonas aeruginosa and enterobacteriaceae such as E. coli

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microbes in eye

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coagulase negative staphylococci

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Microbes in esophagus

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transiently colonized by oropharyngeal bacteria and yeast

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Microbes in stomach

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only acid tolerant microbe can survive for long periods and numbers tend to stay low
Lactobacillus
Streptococcus
Helicobacter (causes peptic ulcers in some individuals)

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Microbes in SI

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mostly anaerobes including
Peptostreptococus
Porphyromona
Prevotella

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Microbes in LI

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literally full of microbes
most anaerobes but also facultative bacteria
Bifidobacterium
Eubacterium
Bacteroides (B. fragilis often causes post-traumatic intraabdominal abscess)
Clostridium
Enterococcus (important nosocomial pathogen)
Lactobacillius
enterobacteriaceae

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Microbes in urethra

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stable colonizers are usually avirulent and include
Lactobacillus
Streptococcus
coagulase-negative staphylococci
Transient colonization w/ opportunists can also occur
enterococcus
enterobactericeae
candida

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Microbes in Vagina

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composition of this population can change quiet dramatically usually linked to hormonal changes or antibiotic treatment
common stable colonizers include
lactobacillus
staphylococcus
streptococcus
enterococcus
gardnerella (common opportunist)
mobiluncus (common opportunist)
mycoplasma (common opportunist)
ureaplasma
several anaerobes
enterobactericeae
candida (causative agent of yeast infection/ thrush)

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microbes in skin

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skin can support the growth fo a few microbes due to its drynes, pH and saltiness, colonizers are tough usually gram-positive or fungi
common skin colonizers include:
Staphylococcus (common opportunist in hospital and community settings)
micrococcus
propionibacterium (common opportunist)
corynebacterium (opportunist)
peptostreptococcus (occasional opportunist)
streptococcus (usually transient)
clostridium perfringens (opportunist)
candida (candidemia, candidiasis, endocarditits, diaper rash)
Malassezia