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MICR223 > MODULE 1 - Sources of Infection and Preventing Transmission > Flashcards

MODULE 1 - Sources of Infection and Preventing Transmission Flashcards

1
Q

where can infection come from?

A

endogenous - our microbiota

exogenous - someone else’s microbiota, environment (air, water, soil, fomites), animals (foods)

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2
Q

what are fomites?

A

surface or material which can transmit an infectious organism

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3
Q

what is zoonosis?

A

an infectious disease that can be transmitted by animals

two kinds: direct and indirect

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4
Q

what is direct zoonosis?

A

direct contact with animal resulting in transmission

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5
Q

what is indirect zoonosis?

A

some vector involved e.g. an insect involved in transmission from animal to human

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6
Q

what are some examples of zoonotic microorganisms?

A

viruses

bacteria (e.g. campylobacter)

fungi (e.g. dermatophytes)

parasites (e.g. giardia)

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7
Q

what is campylobacter?

A

gram-negative spiral rods which are highly motile, bipolar flagella, microaerophilic (prefers less oxygen), capnophilic (likes some CO2), mesophilic (higher temps about 42 degrees) but can survive in refrigeration temps

the main one we need to know about is Campylobacter jejuni which is a common cause of gastroenteritis and often found in chicken cause internal gut temp. of chicken 42 degrees so commensal with chickens

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8
Q

what are the routes of infection for campylobacter?

A

ingestion of contaminated food

direct contact (e.g. with animals)

waterborne

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9
Q

what is the epidemiology of campylobacter?

A

infections peak summer

bimodal age distribution peaking at 0-4 and 15-29 (maybe due to immunological immaturity of young people and loss of immunity as you grow to early adulthood or just more risk exposure)

common asymptomatic infection (especially in children who can be a reservoir)

in NZ notified cases are much lower then actual cases (1 for every 30)

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10
Q

what is campylobacteriosis?

A

usually caused by campylobacter jejuni

low minimum infectious dose (500)

prodromal flu like symptoms

acute onset of GI symptom (cramping, nausea, bloody diarrhoea)

self-limiting disease

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11
Q

what are the two kinds of diarrhoea caused by campylobacter?

A

two kinds of diarrhoea caused (could mean different pathogenic mechanisms)

secretory - profuse, watery stool (occurs when jejunum and ileum of small bowl affected)

dysentry-like - blood, mucus inflammatory cells in stool (occurs when colon affected, more rare but more serious)

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12
Q

what are the virulence factors of campylobacter?

A

motility (penetration of mucus)

chemotaxis (towards sugars found in mucus so it can detect where wall of gut is)

adhesion (allowed by LPS, pili, fimbriae)

invasion (very important for disease)

toxins (cholera-like enterotoxin and cytolethal distending toxin)

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13
Q

how do the two toxins produced by campylobacter jejuni work?

A

cholera-like enterotoxin interferes with regulatory proteins causing production of lots of adenylate cyclase which results in a lot of cAMP produced which effects ion channels in cell membrane by permanently opening them resulting in loss of ions and so loss of water hence watery diarrhoea

cytolethal distending toxin is a DNase which causes apoptosis and cell death which is perhaps responsible for the bloody diarrhoea by killing of cells lining the colon

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14
Q

what does treatment of campylobacteriosis involve?

A

self limiting and doesn’t really cause any major problems so not a lot

can cause dehydration and antibiotics not really necessary and controversial as resistance developing

not really treated unless vulnerable patient or bad case

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15
Q

what are the main ways to prevent infection by campylobacter jejuni?

A

hand washing

washing fruit/veges

seperate chopping boards for animal products

proper food storage

treatment of drinking water

chlorination of recreational water

no contact with sick people or animals

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16
Q

what are dermatophytes?

A

fungi which causes superficial infections of keratinised tissues (hair, skin, nails)

disease caused is dermatophytosis (i.e. tinea or ringworm)

named after the site it infects

can be zoophilic

3 genera of dermatophytes which are very distinguishable under a microscope by looking at spores

they are generally zoophilic (prefer to infect animals) and so less adapted to humans which means more intense inflammatory responses when they do infect humans

treatment involves antifungals (topical for feet and body, oral for hair and nails) and can take a long time to work

diagnosed through clinical appearance or macro/microscopic appearance

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17
Q

what is Giardia?

A

intestinal protozoan parasite which can be in two forms (cyst when in environment and trophozoite in gut which is motile and disease causing)

low minimal infection dose of 10-25 cysts

zoonotic

mostly infecting children in NZ

disease it causes is Giardiasis

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18
Q

what is giardiasis?

A

caused by Giardia

50% of people asymptomatic and these people act as reservoirs

acute symptoms include mild-severe cramping, diarrhoea, gassy

chronic symptoms can include malabsorption leading to malnutrition and dehydration and this can occur in immunocompromised people

quite long duration of disease (2-4 weeks)

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19
Q

what is the pathogenesis of Giardia?

A

not well understood

attachment by ventral adhesive disk to small intestine but doesn’t invade. This allows it to blunt the villi leading to loss off absorption and enzyme function

it also produces proteases which damage proteins disrupting tight junctions which perhaps causes water loss through leakage

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20
Q

what does treatment and prevention of giardia infection involve?

A

treatment involves rehydration and drugs only effective against trophozoites not cyst phase. Resistance also emerging

prevention involves avoiding risks since there is no vaccine

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21
Q

what are the categories of environmental pathogens?

A

native soil/water microbes (opportunistic)

microbes of human origin (obligate pathogens)

zoonotic microbes of animal origin (obligate pathogens)

saprophytic moulds (opportunistic)

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22
Q

what are obligate pathogens?

A

able to cause disease in anyone (not just vulnerable)

important causes of CAI (community acquired infection) and HAI (hospital acquired infection) mostly through infection of wounds, skin, RT and GIT

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23
Q

what environmental pathogens would you find in air, soil or water?

A

aspergillus (air)

pseudomonas (soil, water)

cryptosporidium (water)

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24
Q

what is pseudomonas aeruginosa?

A

gram-neg rod with unipolar flagella (motile), non-fermentative, can grow in a wide range of environments (even jet fuel)

found in soil, water, plants and animals and causes GIT, RT, oral cavity and skin infections

big problem in hospitals

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25
Q

what is the pathogenesis of pseudomonas aeruginosa?

A

opportunistic pathogen which needs susceptible host with immune dysfunction e.g. cancer, ICU or disrupted physical barriers e.g. burns, IV lines, catheters, ET tubes

requires a broad spectrum of antimicrobials cause of high rates of resistance

26
Q

what are the virulence factors of pseudomonas aeruginosa?

A

biofilms - composed of slime layer (alginate and polysaccharide) and can also form a polysaccharide capsule. EPS (extracellular polymeric substance) is what holds the biofilm together and polysaccharide and important component of this

motility - unipolar flagella allows chemotaxis to respiratory mucus

adhesions - fimbriae, pili, LPS, capsule

invasins - enzymes which break down tissues allowing better spread of microbe throughout host

toxins - LPS (endotoxin which binds to TLR and up regulates cytokine production and activates inflammation) and exotoxin A (inhibits translational elongation thus stopping protein synthesis and killing cell)

27
Q

what is advantageous to pseudomonas aeruginosa about forming a biofilm?

A

increases resistance to immune system (phagocytes, complement and antibodies) and acts as diffusion barrier giving antimicrobial resistance

28
Q

what are the key invasins in pseudomonas aeriginosa?

A

elastase (destroy connective tissues)

protease (breakdown of antibodies and complement and inactivates cytokines)

leukocidin (kills neutrophils)

haemolysins (break down RBCs and cell membranes)

pyocyanin (impairs ciliary function, apoptosis of neutrophils, inhibits IL-8 release, stimulates damaging inflammation)

29
Q

what disease is caused by pseudomonas aeruginosa?

A

shit loads (and they are all pretty bad too)

30
Q

how do you diagnose pseudomonas aeruginosa?

A

pigment production (pyocyanin causes blue pus)

fruity odour

oxidase positive

mucoid

beta haemolysis

also makes some fluorescent shit

31
Q

how do you treat pseudomonas aeruginosa infections and why is it so difficult to do so?

A

combinations of drugs or broad-spectrum

difficult to treat cause multi drug resistant (a result of exposure to soil organisms) and also has multiple drug resistance mechanisms (e.g. efflux pumps which pump antimicrobials out of cell and beta lactamases which break down beta lactic drugs). Also difficult due to resistance acquisition through mutation and MGEs and also biofilm formation

32
Q

what is aspergillus?

A

environmental mould (saprophyte) which causes invasive infections of susceptible hosts (usually respiratory)

33
Q

what is aspergillosis?

A

disease caused by aspergillus

results in allergy, aspergilloma (fungal ball in lung), and in bad cases erosion into blood vessels which results in spread around the body

34
Q

how do you treat aspergillosis?

A

treatment of aspergilloma through IV antifungals or surgery

treatment of invasive aspergillosis involves IV antifungals (poor response) or surgery but has high mortality due to rapid progression

35
Q

what is cryptosporidium?

A

non-motile protozoan parasite, many of which cause human disease (some found only in humans some in animals)

has a very low minimum infectious dose (10-100 oocysts) which is only 1-2 in susceptible people e.g. HIV patients

36
Q

what disease does cryptosporidium cause?

A

cryptosporidiosis which involves infection of distal ileum/proximal colon results in mild self-limiting diarrhoea (watery, mucoid, bloodless) and abdominal pain, nausea, vomiting, fever which lasts about 2 weeks

infection is often asymptomatic leading to carriers

in immunocompromised can cause chronic diarrhoea which can persist for years leading to rapid dehydration, malabsorption/malnutrition and electrolyte imbalance. Infection can spread out of intestine

significant cause of mortality in HIV patients

37
Q

what is the epidemiology of cryptosporidium?

A

found in domestic water, swimming pools, natural water sources, cross contaminated foods

oocysts are resistance to chlorination and disinfectants so treatment of water involves filtration or UV

most NZ cases in children and actual cases higher than reported cases

38
Q

what is the pathogenesis of cryptosporidium?

A

causes infection through hijacking host immune response to parasite. This involves TNF alpha and prostaglandins which increase intestinal permeability resulting in water loss and diarrhoea. They also cause malabsorption through villus blunting

parasite is intracellular but extracytoplasmic making it difficult for immune system or drugs to target as it fuses with cell membrane but doesn’t cross it and just chills in the brush border

39
Q

how do you diagnose, prevent and treat cryptosporidium?

A

diagnosis through microscopy, PCR or antigen detection

prevention through good hygiene, avoiding contact with animals, faeces, untreated water and try purify and filter or boil water

treatment not needed for immunocompetent cause self limiting disease however immunocompromised may require supportive therapy e.g. rehydration, electrolytes and also some drugs can be used with variable efficacy

there is no vaccine

40
Q

what is the chain of infection?

A

concept used in infection control to protect both the patient and the healthcare worker from HAI

identifies steps required for infection to occur in susceptible host and the key interventions to prevent transmission

the links of the chain are infectious agent, reservoirs, portal of exit, means of transmission, portal of entry and susceptible host

41
Q

what is the infectious agent?

A

an organism capable of causing infection

e.g. is it virus, bacteria (gpos or gneg), fungi or parasite, what’s its virulence, host-susceptibility

42
Q

what is a reservoir?

A

place an infectious agent survives

environment, human (acute, chronic, asymptomatic, microbiota)

prevention (screening, isolation etc.)

43
Q

what is the portal of exit?

A

how infectious agent leaves reservoir

RT, GIT, skin, blood, contaminated medical equipment

if things infect one of these they prob leave via it too

44
Q

what is the mode of transmission?

A

transfer of infectious agent from reservoir to susceptible host

contact (direct or indirect), droplet (large and short distance), airborne (small particles and long distance), common vehicle (food, water, meds etc.), vector-borne (irrelevant to NZ healthcare setting but maybe tropical countries)

45
Q

what is the portal of entry?

A

how infectious agent enters a susceptible host (GIT, RT, skin, blood, contaminated medical device etc.)

46
Q

what is a susceptible host?

A

person lacking immunity or resistance to potential pathogen

host factors influencing susceptibility: age, comorbidities, lifestyle, genetics, immunisation, medical interventions, socioeconomic status, medications, trauma

47
Q

what are some standard precautions to prevent transmission of disease?

A

hand washing, gloves, PPE (masks, eye protection, face shields, gowns), safe disposal of sharps, aseptic technique, cough etiquette, cleaning/disinfection, waste disposal

48
Q

what is hospital acquired infection (HAI)?

A

infections not present and without evidence of incubation at the time of admission to a healthcare setting

49
Q

what are some common HAIs?

A

UTI, LRTI, SSI, BSI

50
Q

what is the pathogenesis of HAI?

A

susceptible host, virulent organism (AMR most HAI), portal of entry (catheters, IV etc.)

51
Q

what are the sources of microbes (reservoir) for HAI?

A

endogenous (patient microbiota)

exogenous (HCW, patients, hospital enviro)

52
Q

what are urinary tract infections (UTI)?

A

most common HAI and most often associated with catheters (bacterial retrograde movement up catheter and biofilms)

100% of patients on catheter for 30 days or more develop bacteriuria which is often asymptomatic

organisms involved mostly e coli and motile

53
Q

what are surgical site infections (SSI)?

A

source of organism can be either endogenous or exogenous

most infections due to colonisation during surgery

gram pos most common cause

also often obligate anaerobes from gut

infections often polymicrobial making treatment difficult

susceptible people are prone and likelihood of SSI can be somewhat predicted based off of the surgery being performed

54
Q

what are lower respiratory tract infections (LRTI)?

A

most deadly HAI and usually pneumonia which is infection of alveoli

most often ventilator associated pneumonia (VAP) which is usually caused by GIT microbes

most often caused by gram negs e.g. strep. pneumoniae

infections usually polymicrobial making treatment difficult

55
Q

what are blood stream infections (BSI)?

A

usually associated with central venous catheters

can be gram pos or gram neg or even fungi (candida)

retrogade migration up catheter or direct inoculation with catheter

can often involve biofilm infections which complicates treatment

56
Q

what are community acquired infections (CAI)?

A

an infection contracted outside a healthcare setting or diagnosed within 48 hour of admission

especially problematic with elderly and organisms are increasingly antimicrobial-resistant

57
Q

what are some CAI which were previously HAI and increasingly antimicrobial resistant?

A

MRSA
ESBLs
VRE

58
Q

what is MRSA?

A

HAI and CAI

CA-MRSA is less resistant and treatable as not multi drug resistant

HA-MRSA is more resistant, multi drug resistant and also resistant to beta lactams and others. Potential for vancomycin resistance in future

59
Q

what are ESBLs?

A

extended spectrum beta lactamases (an enzyme in some bacteria) allowing resistance to penicillin and cephalosporins (drug of choice for e coli and klebsiella)

HAI and CAI increasing rates

often not recognised till too late leading to treatment failure

treatable with carbapenems e.g. imnipenem however resistance emerging

60
Q

what is VRE?

A

vancomycin resistant enterococcus

opportunistic infection

multi drug resistant incl vancomycin

mostly an issue as HAI

MICR223 (7 decks)

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