Lecture 12- Infectious Disease And The GI Tract Flashcards

1
Q

Bacterial infection factors

A

*opportunistic vs obligate pathogen;
-opportunistic = may be transmitted without causing disease
-obligate = must cause disease for transmission

*intracellular vs extracellular
*number of infectious units required for enteric pathogens;
Low= shigella dysenteriae (-10 cells)
High= escherichia coli (-100 cells)

*virulence factors= v.cholera only pathogenic if it has integrated bacteriophage DNA to allow toxin production

*damage= direct vs toxin-mediated vs indirect
*exposure= likely to come into contact?
*immuno-compromised host= elderly, very young, HIV

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2
Q

Stages of infectious disease

A

Exposure- first contact with the pathogen

Incubation period- time between exposure to pathogenic organism + the first appearance of symptoms

Length of incubation period depends on; virulence, portal of entry, infective dose, immune system health, site of infection + pathogen specific factors

Periods- slide 7

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3
Q

Stages of infectious disease

A

Prodormal period-
- early stage of a disease - when symptoms first appear
-generalised symptoms; malaise, fever, muscle aches
-associated with immune system activation

Gram negative bacterial cell recognition + fever= slide 7

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4
Q

Stages of infectious disease

A

Illness/acute period;
-infection has developed
Severe stage of infection; pathogen numbers are at their peak
-immune responses limited/developing
-transmission risk at its highest

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5
Q

Stages of infectious disease

A

Decline;
-immune response/medical intervention results in a killing/removal of the pathogen
Symptoms begin to subside
Immune response peak
Patient doesn’t enter this stage= disease is fatal

Convalescence;
-recovery of patient - tissue and systems are repaired
Length of time based upon; extent of damage, nature of pathogen, site of infection + overall health of patient

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6
Q

The chain of infection

A

Slides 12-13

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7
Q

Human reservoirs;
Diseases that are transmitted from person to person without intermediaries

A
  1. Symptomatic infections; symptoms of infections. Most likely already diagnosed/being treated. Patient contacts/activities are restricted
  2. Carriers;
    Incubatory carriers; transmit the infection before their own symptoms appear
    In apparent carriers; never develop the infection but can transmit
    Convalescent carriers; still infectious whilst recovering from the infection
    Chronic carriers; recovered but are still infectious

Examples of infections; human immunodeficiency virus, smallpox, measles, syphilis, group A streptococcus

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8
Q

Animal reservoirs; AKA Zoonoses

A

Both domestic, wild animals + insects are included

Direct contact= bite/scratch- rabies
Animal products= sheep wool
Consumption; shellfish

Non-living reservoirs;
Soil, water, food, faeces
^C.tetani, V.cholerae; legionella pneumophila, C. Botulinum + tetani

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9
Q

Barriers to infection + portals of entry

A

Human body= comprises skin + mucosal epithelia; digestive, respiratory + urinary tracts

Barriers= prevent pathogens from crossing epithelia + colonizing underlying tissues

Surface epithelium= provides mechanical, chemical + microbiological barriers to infection

Portals of entry; same pathogen uses diff routes- slide 19

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10
Q

Bacterial pathogenesis

A

Bacterial virulence factors play a key role in= colonisation, infection + invasiveness

Slide; 20

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11
Q

Relating bacteria to infection;

A

Koch’s Postulates; a set of criteria established to identify causative agent of infection
^gene associated with infection should be inactivated

Steps 1-4; slide 21

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12
Q

Origin of modern epidermiology

A

Epidemiology; study of the distribution + determinants of health-related status and events in specific population

Slides 23-25

Miasma theory; medical theory that disease was caused by noxious forms of air (bad air) from decaying matter

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13
Q

Bacterial biofilms

A

-aggregates of cells attached to a surface and/or each other, and that are surrounded by an extracellular polymeric matrix

EPS Defining feature with key roles in; structure, antimicrobial protection, retainer water/nutrients, virulence factor, adhesion, genetic transfer + communication

Composition of EPS varies based on species in the biofilm, external conditions; polysaccharides, extracellular DNA + proteins

Some biofilms generate an EPS composed of crystalline minerals; calcium or mg phosphates

5 stages; 26-27

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14
Q

The gastrointestinal tract

A

Consists of; oral cavity, pharynx, oesophagus, stomach, small intestine, large intestine + anal canal

Accessory organs; teeth, tongue, glandular organs etc

Functions; digestion, adsorption + excretion + immune response

IR= maintains homeostasis
-protects from pathogens we may ingest
-tolerance
-IBS

GI= defence against infections
Typical high-income diet- 200,000 microbes each day

GI tract contains- 100 trillion microorganisms; diff species of bacteria in the colon

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15
Q

Oral infections- tooth decay

A

Infectious disease of teeth- bacteria may be transferred to others; biofilms form on tooth surface + eventually degrade the structure

Compound by plaque (biofilm) formation;
25+ streptococcus
S.mutans produces an enzyme;
-converts sucrose to a dextran-based polysaccharide
-produces a thick+ sticky substance = plaque
-“secondary colonisers”= can adhere to

S.mutans can ferment carbs to organic acids
-pH < 5.5= allows tooth demineralization
-overtime enamel is broken down= decay

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16
Q

Dental abscess; result of infection extending into the pulp of the tooth

A

Pulp can become necrotic
-associated with tooth decay; breaks down the enamel allowing bacterial access to the dentin + underlying pulp

Severe throbbing pain; tooth tender to touch

Without treatment= dental abscess persist, pain may subside as the nerves die; abscess may burst

Treatment= root canal treatment/ tooth removal; antibiotics

Not treated= infection can spread inside + outside of the mouth

17
Q

Periodontal disease

A

Chronic bacterial infection affecting the gums + bone supporting the teeth

Gingivitis (inflammation) -> periodontitis (gums recede- teeth become loose + may fall out)

Host response makes infection worse; gingival inflammation -> temp increases -> increased flow in gingival crevicular fluid (GCF)
- break down of GCF; contains iron + tissues; more nutrients for bacteria
-continuous cycle until tooth loss

18
Q

Oral thrush- Candida Albicans

A

Fungal infection; overgrowth of the mucous membranes in the mouth- C.albicans

Commensal member of the human microbiome;
50% have C.albicans in oral cavities
Newborns >64% get colonised during passage through birth control

Overgrowth of C.albicans usually associated with immune system suppression
Opportunistic pathogen- risk factors
-elderly/newborns, chemotherapy, HIV/AIDS, antibiotics + steroids

19
Q

The human stomach

A

Function; temp storage, mechanical digestion (muscular contractions) + chemical digestion (gastric acid secretion)

Gastric acid= digestive fluid secreted by gastric gland cell, comprises of; hydrochloric acid, gastric lipase, pepsin (breaks down proteins into peptides/amino acids)

Lowers stomach pH to 1-2; intolerable of microbial life

20
Q

Helicobacter pylori

A

Gram negative, spirochete + highly motile
Associated with; gastritis, ulcers + gastric cancers

Adapted to survive in stomach acid;
-secretes urease= breaks down urea into ammonia + bicarbonate
-produces a cloud of increased pH around the bacterial cells
-cells = survive stomach acid

Virulence factors= VacA- cytotoxin; exotoxins, LPSA- endotoxin
^ = localised tissue destruction + ulceration

-can also infect the duodenum
- found in 80% of patients with the infection -> leads to duodenal ulcers
Slide 39-41

21
Q

H.pylori- detection + treatment

A

Detection;
Urea breath test- using carbon isotopes
Blood/stool test for H.pylori antibodies

Treatment;
Antibiotics + proton pump inhibitors
Amoxicillin, clarithromycin + metronidazole
PPIs= reduce stomach acid production -> allows ulcers to heal

Antibiotic = 1 week treatment, tested again for H.pylori after 4 weeks

22
Q

Emerging infectious disease

A

Either newly recognised in a population/ exist but are rapidly increasing in incidence/geographic age

Contributing factors; population growth, increase immunocompromised patients, travel, climate change, AMR + breakdown in living conditions

Examples; COVID-19, HIV, Mpox

23
Q

ESKAPE Pathogens

A

6 extremely virulent + highly antibiotic-resistant bacteria pathogens

Gram + and Gram - = evade/escape commonly used antibiotics; increasing multi-drug resistance MDR

24
Q

Staphylococcus aureus- food poisoning

A

Eating good contaminated with toxins produced by S.aureus= food contam during handling process

Enterotoxin= super antigen -> diarrhoea + vomiting
30 mins-8hrs = after consumption

Symptoms= fever, abdominal cramping, diarrhoea, headache
^ resolve in 24hrs