Session 3: Pathogens and Disease Flashcards

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1
Q

What is pathogenicity?

A

The ability to produce a disease in a host organism. It is a qualitative measurement, it is less specific in explaining the degree of harmfulness of a pathogen.

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2
Q

What is virulence?

A

The degree of pathogenicity of the microbe. It describes the quantitative negative effect, it can be used to express the degree of harmfulness of a pathogen.

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3
Q

Define infection.

A

the entry, establishment, and replication of pathogens inside a host organism

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4
Q

Define incubation time.

A

the period of time between exposure to an infectious agent and the appearance of symptoms of the infection or disease it causes

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5
Q

Define morbidity

A

the relative occurrence of a disease or a condition that causes illness

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6
Q

Define mortality

A

the number of deaths in a given time or place

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7
Q

Define vector

A

an organism (usually an arthropod such as a mosquito or tick) that carries an infectious agent from one host to another

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8
Q

Define a disease being endemic.

A

regularly occuring disease in a community

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9
Q

Define epidemic

A

the sudden increase in the level of disease in a specific population over a given period of time

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10
Q

Define pandemic

A

an increase above endemic levels that spreads over a large geographic region such as a continent or multiple continents

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11
Q

Define acute

A

fast onset, often with shorter duration

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12
Q

Define chronic

A

slower onset and longer duration, or recurring

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13
Q

Define latent infection

A

currently not producing or showing any symptoms but has the potential of being reactivated and then manifesting symptoms

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14
Q

Describe Bacteria.

A

Bacteria are prokaryotic, single celled microorganisms. Bacteria inhabit soil, water, and also live in and on plants and animals, etc. Of the many species of bacteria, relatively few cause disease in humans. Bacteria infect a host to exploit the food potential of the host’s body tissues. The natural reservoir, or source of the infection, varies from species to species. Bacteria can be beneficial, they break down material, they are decomposers.

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15
Q

What are the shapes/types of bacteria?

A

There are other but the main two: Cocci (round), bacilli (oval/cylinder shape).

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16
Q

Describe bacterial cell walls.

A

Bacterial cell walls are made of a peptidoglycan polymer (amino acid + carbohydrate) which is unique to bacteria. Bacteria are often broadly categorized into two groups based on differences in their cell wall composition: Gram -positive have a much thicker layer of peptidoglycan. Gram -negative have a thinner layer of peptidoglycan with an additional outer membrane with a lipopolysaccharide component

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17
Q

How does gram staining differ for gram positive and gram negative

A

Gram staining works as a result of the different effects of ethanol in the gram stain technique on the cell wall: Gram -positive bacteria’s thick peptidoglycan layer is dehydrated by ethanol, trapping the crystal violet stain. Gram -negative bacteria have an outer lipid membrane which is dissolved by ethanol, releasing the crystal violet stain so the red counterstain is visible without the violet colour

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18
Q

Describe the two qualities of bacterial pathogenicity.

A
  1. Invasiveness - their ability to invade tissues. It includes: Colonisation (adherence and initial multiplication). Production of extracellular substances which facilitate invasion. Ability to avoid the host defence mechanisms. 2. Toxigenesis - the ability to produce toxins. Bacteria may produce two types of toxins called exotoxins (proteins) and endotoxins (lipopolysaccharides).
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19
Q

Describe invasiveness - colonisation.

A

Colonisation is when bacteria grow on body sites exposed to the environment, without necessarily causing any infection. This involves establishment at the appropriate portal of entry - (urogenital tract, digestive tract, respiratory tract etc). Usually have tissue adherence mechanisms and some ability to overcome or withstand the constant pressure of the host defences/ immune response.

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20
Q

Describe invasiveness - adherence.

A

Adhesins are cell-surface components or appendages of bacteria that facilitate adhesion or adherence to other cells or to surfaces, usually in the host they are infecting or living in. Adhesins are a type of virulence factor. Adherence is an essential step in bacterial pathogenesis or infection, it allows them to infect the host, it makes them difficult to remove, makes it harder to eradicate them/fight them with antibiotics, etc.

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21
Q

Describe invasiveness - invasins.

A

Invasion may be aided by the production of substances which break down defenses of the body, referred to as invasins. Most invasins are proteins (enzymes) that act locally to damage host cells and/or have the immediate effect of facilitating the growth and spread of the pathogen. Invasins can help to dissolve the membrane to allow the bacteria to access the inside of the cell of the host.

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22
Q

Describe invasiveness - defence avoidance.

A

Many pathogenic bacteria can avoid the host defences by: Avoiding contact with phagocytes (immune cells - phagocytes engulf and kill bacteria). Invade or remain confined in regions inaccessible to phagocytes (e.g. skin). Induce minimal or no inflammation required to focus the phagocytic defences. Inhibit phagocyte processes. Surviving inside phagocytes. Some species have specific mechanisms to get into their host cell as well as special mechanisms to survive once they are inside, including immune cells. Produce substances that kill or damage phagocytes. Some can produce extracellular enzymes or toxins that kill phagocytes. Phagocytes may be killed by a pathogen before or after ingestion

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23
Q

Describe toxigenesis.

A

At a chemical level there are two types of bacterial toxins: Lipopolysaccharides or endotoxins and Proteins or exotoxins.

24
Q

What are the properties of endotoxins.

A

Source: Part of the outer membrane of gram-negative bacteria, composed of lipopolysaccharides and are usually only released when the bacteria are reproducing or dying. Toxicity: Less toxic than exotoxins but more heat stable, Relatively high dose needed, The immune system can not neutralise them with antitoxins

25
Q

What are the properties of exotoxins?

A

Source: Proteins produced by gram-positive bacteria and some gram-negative bacteria released as part of normal growth and metabolism. Toxicity: Some of the most toxic compounds known, Soluble so they can diffuse easily in host tissue, Very small doses can cause symptoms.

26
Q

Describe all the factors of helicobacter pylori (bacteria study).

A

Shape: Bacilli shape with flagella at one end that move it in a corkscrew motion
Gram positive or negative: Gram negative (spiral shaped)
Endo or exotoxin: Endotoxin
Chain of infection: Reservoir: other humans, Portals of exit: mouth or excreted through anus, Transmission: (oral-to-oral (stomach contents are transmitted from mouth to mouth) or fecal-to-oral (from stool to mouth)), Portal of entry: mouth generally, Susceptible host: children, people living in crowded areas and/or in developing countries, people who have been exposed to someone who has the disease.
Disease caused: H. Pylori infection or peptic ulcer disease
Symptoms: ache or pain in stomach, nausea & vomiting, loss of appetite, bloating, unintentional weight loss, burping and indigestion, dark stools.
Treatments: Antibiotics (Amoxicillin, clarithromycin (Biaxin), metronidazole (Flagyl), tetracycline (Sumycin), or tinidazole (Tindamax)) and acid-reducing proton pump inhibito

27
Q

What is a virus?

A

Sub microscopic entity consisting of a single nucleic acid surrounded by a protein coat and capable of replication only within the living cells of cellular organisms. Viruses are not cellular structures because they don’t have cell organelles that make proteins for them - they infect the host cell and take over the host cell’s organelles and machinery to make proteins for themselves.

28
Q

What is the viral life cycle?

A

All viruses depend on cells for reproduction and metabolic processes. By themselves, viruses do not encode for all of the enzymes necessary for viral replication. However, within a host cell, a virus can hijack cellular machinery to produce more viral particles (they act non-living outside of a cell and become living and able to replicate once they take over a cell). Viruses have the following infection stages: Attachment (attaching to a target cell), Penetration (the cell engulfs the virus by endocytosis), Uncoating (viral contents are released), Biosynthesis (viral RNA enters the nucleus, where the viral RNA polymerase replicates it), Maturation (new phage particles (virus that infects and kills cells) are assembled), Release (new viral particles are made and released into the extracellular fluid. The cell is not killed in the process and it continues to make the new virus).

29
Q

What is tissue tropism?

A

Many viruses are host specific, meaning they only infect a certain type of host; and most viruses only infect certain types of cells within tissues. E.g. poliovirus exhibits tropism for the tissues of the brain and spinal cord.

30
Q

If the viral genome is RNA, describe the viral life cycle.

A
  1. Virus fuses to the host cell surface
  2. Virus RNA reverse transcriptase (enzyme), integrase, and other viral proteins enter the host cell.
  3. Viral DNA is formed by reverse transcription
  4. Viral DNA is transported across the nucleus and integrates into (combines with) the host DNA
  5. This new combined DNA then makes RNA which is identical to the RNA that was in the virus that first fused to the host cell surface
  6. New viral RNA is used as genomic RNA and to make viral proteins
  7. New viral RNA and proteins move to the cell surface and a new immature virus forms
  8. The virus matures (and is released) when protease releases the proteins that form the mature virus
31
Q

What are the ways that viruses are transmitted?

A

Respiratory transmission, Faecal -oral transmission, Blood- borne transmission, Sexual Transmission, Animal or insect vectors.

32
Q

How do virus induced tumours occur?

A

Viruses can induce tumours/ cancer: Virus infects cell, Virus nucleic acid, as DNA, integrates into cellular genome, Virus causes changes in cellular gene expression, Uncontrolled cell multiplication and tumour formation

33
Q

Describe fungi as infectious agents.

A

Fungi (molds & yeasts) are widely distributed in air, dust, fomites (objects or materials which are likely to carry infection, such as clothes, utensils, and furniture), and normal flora (microorganisms that live on another living organism). They are relatively nonpathogenic, they are the most common plant pathogen, few have been linked to disease in animals (referred to as mycoses), but human mycoses are caused by true fungal pathogens and opportunistic fungal pathogens (true are stronger and more invasive than opportunistic).

34
Q

What are true fungal pathogens?

A

True fungal pathogens are virulent regardless of the immune adequacy of the host (have well developed, high virulence), and the host can be perfectly healthy individual (have a normal immune system). The host must have high or low immune resistance. True pathogens usually enter through respiratory pathways, infections are primary pulmonary and systemic (often asymptomatic), the immunity after infection is well developed/specific, the infecting form is primarily conidial, natural habitat is soil, and they are restricted to endemic regions (geographically).

35
Q

What is thermal dimorphism?

A

Thermally dimorphic fungi are a unique group of fungi that respond to shifts in temperature by converting between hyphae (22–25°C) and yeast (37°C). The conversion to yeast within healthy and immunocompromised mammalian hosts is essential for virulence. In the yeast phase, the thermally dimorphic fungi upregulate genes involved with subverting host immune defences in order to cause a disease state.

36
Q

What are conidia?

A

Conidia are asexual, non-motile spores of a fungus. They are haploid cells produced via mitosis that can develop into new organisms if conditions are favourable. They are dispersed via the wind or other external transport and are a primary method of fungal reproduction

37
Q

What are opportunistic fungal pathogens?

A

Opportunistic fungal pathogens are organisms that have low/limited virulence. Disease production usually depends on diminished host resistance to infection. Recovery from an infection does not establish a specific immunity, and reinfection may occur if general resistance is lowered again (e.g. unlike viruses, if you contract it once you do not develop immunity and you can contract it again). The fungus does not convert from one form to another. The host must have low immune resistance, the pathogen usually enters through respiratory tract or mucocutaneous (skin) areas, the infection varies from superficial (skin) to pulmonary and systemic (goes throughout the entire body), usually symptomatic infections. The infecting form is usually conidial or mycelial, thermal dimorphism is absent, their natural habitat varies from soil to flora of humans and animals (human flora can refer to flora that exist in the gut), and infections can be distributed world wide.

38
Q

Describe pathogenesis of fungi.

A

Pathogenicity is influenced by the portal of entry: Respiratory portal - inhaled spores. Subcutaneous - inoculated skin – trauma/skin damage. Cutaneous - contamination of skin surface (e.g. subcutaneous means under the skin, etc.). Some can become systemic infections where they spread to other tissues.

Virulence factors – pathogenic fungi have a range of features that contribute to their ability to cause damage and disease: Thermal dimorphism, toxin-like substances, capsules and adhesion factors, hydrolytic enzymes (break down areas that allow them to infect cells and tissues), and inflammatory stimulants.

39
Q

What are dermatophytes?

A

Dermatophytes are fungal pathogens that require keratin (a protein in hair, skin and nails) for growth. They can cause superficial infections of keratin tissues. Dermatophytes are one of the most prevalent fungal infection types. Many cases go undiagnosed or misdiagnosed

40
Q

What are the three main parasite categories?

A

There are three main categories of parasites associated with infectious disease: Protozoa, helminths, and arthropods as vectors

41
Q

Describe Protozoa.

A

Unicellular. Life cycle stages: Trophozoite – feeding stage, mostly motile, Cyst – dormant stage, protective thick wall. Most are free living in water and soil. Classified by motility and life cycle. Subdivided by location in human host (E.g. GI tract, blood)

42
Q

Describe helminths.

A

Large, multicellular endoparasites (live and feed in living hosts): Nematodes – round worms, Platyhelminths – flat worms (flukes and tapeworms). Many are intestinal worms, some reside in blood vessels. Eggs are often released externally and can last for long periods of time in the environment (soil, water etc)

43
Q

Describe arthropods as vectors.

A

Various arthropod species are transmission vectors for infectious agents such as viruses, bacteria and even other parasites such as protozoa: Ticks – Lyme disease (bacteria), Tick-borne Encephalitis (virus), Lice – Typhus (bacteria), Fleas – Bubonic Plague (bacteria), Flies – Typhoid (bacteria), Leishmaniasis (parasite), Mosquitos – Malaria (parasite), Dengue (virus)

44
Q

Describe prion disease.

A

Prion diseases are neurodegenerative conditions in mammals that are caused by an infectious protein agent without the involvement of nucleic information or additional transport vectors. The theorized prion agent is a modified form of the cell membrane protein PrPC, which is misfolded into the pathogenic form of the protein, which is referred to as PrPSc. These prion proteins are able to convert normal protein molecules into the prion form. The mechanics of the disease are still largely unknown. They can affect many lineages of mammals, from rodents to ruminants, as well as humans. There is no current cure, inoculation, or treatment for prion diseases, and livestock protection strategies largely include quarantine and destruction of infected organisms. They are resistant to denaturation by temperature or chemical agents, making them both difficult to destroy once in a host as well as capable of surviving in an exposed environment for an extended period of time.

45
Q

Describe the pathogenesis of prion diseases.

A

While prion diseases are not completely understood, it is clear the disease is caused by an accumulation in the brain of misfolded protein. During this process PrPc misfolds (post- translationally) into PrPSc which contains a high number of β -sheets. The process during which the normal protein changes to the abnormal takes place when some of the α-helices and coils of its structure refold into β - sheets. The changes have been shown to act as a template upon which PrPc is refolded into PrPSc. This is how the misfolded protein is able to become infectious to other prion proteins around it.

46
Q

What is transmissible spongiform encephalopathies?

A

Prion diseases are also referred to as Transmissible Spongiform Encephalopathies or TSEs. TSEs occurs in a number of different mammals, and strains of prion disease typically only affect peers in the species and closely-related lineages. There are three primary categories of prion diseases: Sporadic, where the cause is unknown, Familial, where the disease is caused by the genetics of the host, and Acquired, which is transmissible between organisms, either directly or through the environment.

47
Q

Define what it means for viruses to be obligate, intracellular, and a parasite:

A

Obligate: need a living host cell to replicate.
Intracellular: come alive within cells
And they are a parasite: take over host cells which then die after they have been used.

48
Q

Describe the nucleic acid of a virus.

A

It can be DNA or RNA (if its DNA it will make RNA (transcription) and then the RNA will make proteins (translation), if its RNA it will just make proteins)

49
Q

What is endocytosis and exocytosis?

A

Endocytosis: something going into the cell. Exocytosis: something going out of the cell

50
Q

What are antigenic drift and antigenic shift?

A

Antigenic drift: virus slowly, gradually mutating to something else (no other organisms are involved - not multiple species). Antigenic shift: two viruses combine in a short period of time and mutate into one virus → antigenic shift is interspecies (happens through multiple species, e.g. birds are infected with something, a human eats it, and so it mutates and becomes a virus that infects humans)

51
Q

Go through the steps for the life cycle of a lysogenic bacteriophage: lytic cycle and lysogenic cycle.

A

Lytic Cycle: 1. The phage attaches itself to a specific host cell, and inserts its nucleic acid and some enzymes into the bacterium. 2. Phage DNA circularises and enters the lytic cycle or lysogenic cycle. 3. Viral components are produced and assembled by the host cell into virions. 4. The host cell bursts and new phages emerge to infect new cells. Back to step 1.
Lysogenic cycle: Step 2 above into 5. A prophage forms when the phage DNA integrates into the bacterial DNA. 6. Lysogenic bacterium reproduces normally. 7. Prophages can be induced (by mutagens) to excise from the bacterial chromosome and enter the lytic cycle. Back to step 2.

52
Q

Describe Ebola: Virus Study.

A

Ebola is spread by direct contact with blood or other bodily fluids (sweat, vomit, urine, etc.) of an infected person or person who has recently died from Ebola. Ebola is a disease that some animals (bats, nonhuman primates, and antelope) contract and the first human case occurred in 1976 when a human came in contact with the bodily fluids and/or organs of an infected animal in Congo (Africa). Ebola enters through cuts in the skin, the eyes, nose, or mouth. Ebola has an incubation period of 2 to 21 days (generally 8 to 10 days when symptoms appear). The virus penetrates the host cell membrane which triggers endocytosis. Once inside the cell, the virus releases its nucleocapsid into the host cell cytoplasm. There have been 38 outbreaks since 1976, around 15000 people have died. There is often a 50 per cent mortality rate for people who contract Ebola, but this has varied between outbreaks. Infected people should receive treatment immediately, treatment includes oral or intravenous fluids and medicines provided in hospital, blood transfusions are also beneficial, and medicines to ease pain (symptoms of ebola include: nausea, vomiting, diarrhoea, and general pain). Treated with antibodies.

53
Q

Describe Candida albicans - fungus study topic

A

Morphology: can grow in multiple morphologies: yeast, pseudohyphae and hyphae. Candida albicans is the type of yeast that lives in your body. It can overgrow and become an infection if the balance of healthy bacteria and yeast is disrupted. It causes thrush, vaginal yeast infections, and invasive candidiasis.
Pathogenicity: most common human fungal pathogen causing diseases ranging from mucosal to systemic infections, uses both endocytosis and active penetration to invade host cells (can secrete hydrolases to assist this).
Symptoms: skin redness, itching, blisters, lumpy white patches, pain, soreness, discomfort, burning sensation, vaginal discharge. Causes: Feeling stressed, having unmanaged diabetes, having a weak immune system, eating a diet with excess refined carbohydrates, yeast and sugar, taking antibiotics, steroids, hormones or oral contraceptives. Symptoms can be seen: inside mouth and throat, inside vagina and rectum, near the diaper region of infants (thighs, genitals, etc.), on the fold of skin (armpits, groin, under breasts).
Treatment: antifungal medicine (oral or topical (creams))

54
Q

Define endogenous and exogenous.

A

Endogenous → protein that is part of your body
Exogenous → protein you consume, accumulate, etc.

55
Q

Describe Kuru (prions research task)

A

Cause/transmission: cannibalism or consuming people who died of kuru, transmits through tissue of an infected person to another person, can be transmitted through contact with open sores or wounds
Symptoms: muscle twitching/spasms, loss of muscle control, loss of coordination, extreme emotional fits - laughing fits or bursting into tears, difficulty walking, moving, speaking, etc. and eventually death
Treatment: no known treatment

56
Q

Define Malaria (parasites research task)

A

Cause: parasites that are transmitted through the bites of female mosquitoes, and rarely though blood transfusions and and contaminated needles
Signs/symptoms: fever, chills, headaches, nausea/vomiting, diarrhoea, abdominal pain, muscle/joint pain, fatigue, (seizures, difficulty breathing)
Treatment/prevention: avoiding mosquitoes and places that have the specific mosquitoes that transmit malaria, there are many drugs and medicines that treat it and reduce symptoms
Statistics (global, Australia): Globally: estimated 249 million cases and 608 000 deaths in 85 countries in 2022. Australia: overall Australia is said to have eliminated the disease but there is about 700-800 cases a year in travellers who contract it elsewhere and bring it here
Current and future developments for treatment: artemisinin-based combination therapy (ACT) is a combination of two or more drugs that work against the malaria parasite in different ways

57
Q

Describe HIV (virus research)

A

Cause: HIV is a virus spread through sexual contact, sharing of needles, and contact with infected blood. It is a disease that attacks the immune system, specifically white blood cells, causing immune system failure and the thriving of diseases, cancers, etc. HIV causes AIDS.
Symptoms: fever, headache, weight loss, cough, etc. Without treatment, people with HIV infection can also develop severe illnesses: tuberculosis (TB), cryptococcal meningitis, severe bacterial infections, and cancers such as lymphomas and Kaposi’s sarcoma
Treatment/Prevention: medicine treatment that controls the level of HIV in the body, allowing the immune system to maintain function. Prevention: using protection, getting checked for STDs, etc.