Module 7 - Host Parasite Relationships, Basics of Infectious Disease Flashcards

1
Q

Symbiosis:

A

-living together
-defined as a close relationship between 2 organisms but does not suggest benefit or harm

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2
Q

Parasitism:

A

-relationship that only benefits one organism - the parasite
-parasite is any pathogen that does harm to the host by deriving its nutrients
-parasites live at the expense of the host but that expense can be minimal
-ex. Giardia Lamblia: beaver fever - causes GI symptoms
Viruses H1N1 = flu, and COVID Virus

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3
Q

Mutualism

A

-a relationship that provides reciprocal benefits for both organisms
-ex. Bacteria in the vagina make the pH so low that many pathogen cannot survive, bacteria consume local glucose provided by tissue glycogen - in the absence of lactobacilli that produce acids, species like yeast Candida can become numerous

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4
Q

Commensalism: ‘eating at the same table’

A

-relationship where one organisms uses another often larger organism for nutrients, habitat, locomotion
-there is no effect on the host
-ex. staph. Epidermidis lives on our skin and has no particular effect on us
-organism could be commensalism on skin but parasitic if entering vagina and vice versa

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5
Q

Nonpathogenic

A

a microorganism that does not cause disease; may be part of the normal flora

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6
Q

Opportunistic pathogen

A

an agent capable of causing disease only when the host’s resistance is impaired (for example when the host is immunocompromised)

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7
Q

Pathogen

A

a microorganism capable of causing disease

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8
Q

Pathogenicity

A

the ability of an infectious agent to cause disease

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9
Q

Toxigenicity

A

ability of microorganism to produce toxins that contribute to development of disease

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10
Q

Adherence (adhesion, attachment):

A

the process by which a pathogen sticks to the surface of host cells

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11
Q

Infection

A

multiplication of an infectious pathogenic agent within the body (even if the person is asymptomatic)

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12
Q

Invasion

A

the process whereby bacteria, parasites, fungi and viruses enter the host cells or tissues and spread in the body

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13
Q

Carrier

A

a person or animal with an asymptomatic infection that can be transmitted to another susceptible person or animal

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14
Q

Virulence

A

the quantitative ability of an agent to cause disease. Virulent agents cause disease when introduces into the host in small numbers

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15
Q

Types of Pathogens

A

-primary pathogens: cause disease in otherwise healthy people
-ex. chlamydia trachomatis can infect most people who are exposed to it and is not normal flora of the body

-opportunistic pathogens: rarely cause disease in people with intact nonspecific and specific defences (emerges when resistance is low)
-ex. E. coli is not normally seen as a pathogen in the gut (it is normal flora) but it causes most UTIs
-ex. Candida albicans is usually found in small amounts on the body and causes no harmful effect, but it’s overgrowth can also cause several types of candidiasis such as thrush and yeast infections

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16
Q

Primary Pathogen vs Opportunistic Pathogens:

A

-chlamydia = primary
-candidiasis = opportunistic
-streptococci = opportunistic?
-H1N1 = primary
-HSV-2 cold sore forms from being tired = opportunistic

17
Q

Typical Stages of an Infectious Disease: 4 stages

A
  1. Incubation period: time between the moment the person is exposed to the microbe/toxin and the appearance of symptoms
  2. Prodrome period: time during which nonspecific symptoms occur. Prodrome comes from ‘precursor’. 3. An example may be a migraine aura, general lack of appetite or malaise
  3. Specific-illness period: time during which the characteristic features of the disease occur
    Recovery period: time during which the symptoms resolve and health is restored
18
Q

What Happens After..

A

-after recovery period, some people become chronic carriers of the organism and in others latent infections develop
-some people have subclinical infections during which they remain asymptomatic but can still spread it → chlamydia, Epstein Barr Virus (mononucleosis), rhinovirus
-or some people completely clear it (ideal)
-The presence of antibodies often reveals that a period infection has occurred. This is used diagnostically (ex. Primary HIV test is for antibodies against HIV)

19
Q

Pathogenesis

A

-our body is supposed to protect us from pathogens so we have physical/chemical, innate and adaptive immune responses
-however we can still get sick from pathogens because most common infectious organism have developed answers to the problem of host defences - their ability to survive as parasites depends on how well they resist host defences

20
Q

Aspects of Pathogenesis:

A

Colonisation and transmission
Adherence
Invasiveness
Toxins
Ability to evade immune response/antimicrobials

21
Q

colonisation/transmission (1/aspects of pathogenesis)

A

-1st step
-establishment of a pathogen at an appropriate site of entry
-pathogens usually colonise host tissues that are in contact with external environment - urogenital tract, skin, respiratory tract/lungs, conjunctiva (eye), digestive tract

22
Q

Types of Transmission and Their Control:

A

-respiratory/salivary: covid, flu, common cold

-faecal/oral: giardia, can be e.coli, parasites

-venereal (STIs): HIV, Chlamydia

-vector: ex. West nile virus, zika, bug bites (spread between bug and human)

-vertebrate reservoir: rabies, animals-humans

-vector vertebrate reservoir: plague, fleas and rats, often spread historically but still outbreaks in present day

23
Q

Routes of Infection for Baby:

A

-prenatal (in utero/congenital): passes through placenta from mom to baby
-perinatal: occurs during birth - mixing of blood, passing through birth canal
-postnatal: from milk, umbilical stump

24
Q

How Many is too Many:

A

-id50 = infectious dose = 50% of sample population will be infected
-number of microbes that will infect 50% of the population
-a measure of virulence
-a smaller number entering the body might still be overcome by non-specific immunity
-vibrio cholera has an ID50 of 10^8 cells, but if gastric pH increases (less acidic) the ID50 decreases
-id50 = infectious dose = 50% of sample population will be infected
-number of microbes that will infect 50% of the population
-a measure of virulence
-a smaller number entering the body might still be overcome by non-specific immunity
-vibrio cholera has an ID50 of 10^8 cells, but if gastric pH increases (less acidic) the ID50 decreases

-toxins: LD50 = lethal dose = 50% of sample population will die
-shiga toxin 250 ng/kg (body weight)
-staphylococcal enterotoxin 250 ng/kg
-c. Botulinum toxin 0.03 ng/kg

25
Q

Adherence (2/aspects of pathogenesis)

A

-pathogen adherence to a host cell requires:
-receptor: usually specific carbohydrate or peptide resides on the host cell
-adhesin: a macromolecule (lipoprotein of glycoprotein) on the pathogen surface which interacts with the host cell receptor
-ex. E Coli binding in bladder

26
Q

Specificity of Adherence:

A

-some bacteria have preferences for certain tissues over others
-streptococcus mutans is abundant in dental plaque but does not occur on epithelium of tongue
-some bacteria only infect one species of animals
-neisseria gonorrhoeae infections are limited to humans
-these effects are due to the interaction of specific receptor and adhesins

27
Q

Examples of Adherence:

A

-Hiv:
-has a glycoprotein gp41/gp120 (adhesin) on its envelope that binds to a CD4 molecule (receptor) and CCE5 or CXCR4 (co-receptro) on a helper T-cell
-if you have a mutant or missing CCR5 co-receptor you are not susceptible to the HIV virus

-e.coli:
-produces proteins (adhesins) that bind tightly to certain sugars (receptors) on the host cell membrane
-the adhesion of e.coli can be partially blocked by proanthocyanidins which are found in cranberry juice

28
Q

Without Adherence:

A

-adherence for pathogens in essential for survival, so failure to adhere will result in explosion by one of the body’s mechanical mechanisms (mucus, cilia)
-ex. Chlamydia that are introduced into the vagina that DON’T adhere to living cells are expelled in vaginal secretions
-superficial cells (the squamous epithelium) on the lumen of the vagina are dead and are sloughed off
-chlamydia needs to attach to living endocervical columnar epithelium

29
Q

Invasiveness (3/aspects of pathogenesis)

A

-ability to invade or spread, penetrating the host’s defences
-surface infections: some microbes multiply in the epithelial layer (cells) at the site of entry
-they fail so spread to deeper structures or throughout the body
-local spread takes place on fluid covered mucosal surfaces (some bacteria have mechanisms to counter the mechanical effect of mucous - motility: flagella, cilia)
-systemic infections: other microbes spread systemically through the body via lymph and blood - often undergo stepwise invasion of various tissues

30
Q

SLIDE ON GRAPH FOR SURFACE/SYSTEMIC SPREAD

A
31
Q

Pathogenic Factors for Invasiveness:

A

-some bacterial pathogens secrete enzymes which aid in the invasion by digesting surround tissues
-staph. Aureus can excrete hyaluronidase which breaks up connective tissue so the organism can penetrate deep into the tissue
-staph, aureus produces lipases which allow it to penetrate into the oily sebaceous glands
-lipases break down fats
-other microbial enzyme: coagulase, collagenase

32
Q

Bacterial Toxins (4/aspects of pathogenesis)

A

-bacteria can cause disease by secretion of toxins
-toxin production: exotoxin (release for call) and endotoxin (part of cell)
-exotoxin:
-typically polypeptides release (exported) by bacteria into surrounding environment
-antigenic and include antibodies called antitoxins
-specific to a particular bacterial strain
-can be modified to form toxoid → antigenic but not toxic
-toxoids such as tetanus toxoid, are used to immunise against disease (tetanus vaccine)

33
Q

chart on page 6

A
34
Q

Exotoxins in Disease:

A
  1. Cholera toxin causes diarrhoea, by stimulating intestinal epithelial cells to secrete sodium, bicarbonate and water
  2. Diphtheria toxin causes cell death by stopping protein synthesis by ribosomes
  3. Tetanus toxin causes muscles spasms by blocking ingenuity pathways in motor neurons

-newborns display body rigidity of neonatal tetanus from tetanus toxin

35
Q

Endotoxins

A

-typically part of the bacterial outer wall or membrane (gram negative only)
-ex. Lipopolysaccharides (LPS) located in the outer membrane only of gram negative bacteria (ex. e.coli)
-LPS is composed of a core and Lipid A. Lipid A is the toxic component of LPS

36
Q

Endotoxin (LPS) in Disease:

A

-LPS binds to TLR4 (an innate PRR) on tissue macrophages
-this leads to the high production of proinflammatory cytokines
-can lead to high fever/shock

37
Q

Ability to Evade the Immune Response and Antimicrobials (5/aspects of pathogenesis)

A

Microbes have developed easy to evade most of our immune defence mechanisms and antimicrobial drugs
a) evasion of innate immune defence
Evade mechanical barriers: fluid and mucous can remove most virus, bacteria and protozoa from the surface of epithelial cells. Specific receptors or mechanical means to bind firmly to epithelial cells
Evade phagocytosis by neutrophils or macrophages: kill phagocytes by release of toxins (PVL Panton-Valentine leukocidin) - forming leukocidin by pathogenic staph aureus. Prevent phagocyte from engulfing microorganisms, prevention of the fusion between phagosome and lysosome
- b) evasion of adaptive immune definition
-concealment of antigens: latency or microbes in privileged tissue sites
-changinging antigens
-suppressing the immune response
-resistance to anti-microbial treatments
-penciilin ressitance is because of enzyme production beta-lactamase
-malaria resistance

38
Q

Aspects of Immune Function in Pregnant Person and Foetus/Newborn:

A
  1. Pregnancy hormones result in reduced cellular immunity but maintains antibody immunity
  2. Foetal tissue is protected from immune rejection by specific functions of placental tissue and immune regulation in that tissue
  3. Some viruses and systemic bacteria can cross the placenta. The foetus has only parental igG antibody and innate immune function to control infection (T cells and B cells are not fully developed)
  4. Newborns have parental IgG (but only for a few weeks) and IgA (breastmilk) as protection. They rapidly develop B-cell antibody immunity on their own, and more slowly. T cell mediated immunity
  5. Newborns can be treated with protective antibodies (immune globulins) and some antimicrobial or antiviral drugs
39
Q

how pregnancy can affect disease chart

A