Microbiology Exam 3 Material

Healthcare-associated infection

An infection linked to care that was not already present or incubating

when care began.

Endogenous

source of infection might be patients own microbiota

Exogenous

source of infection might be external person

Host vulnerability

Immunosuppression, burns, major surgery, and extremes of age reduce

protective defense

Added exposure

Invasive devices bypass barriers. Antibiotics can alter microbiota and

select resistant organisms

Care-system reliability

Crowding, staffing, equipment handling, and missed prevention steps

affect transmission opportunities

Bloodstream and urinary infections

Vascular and urinary catheters provide access across normal barriers.

Surgical site infection

An incision creates a vulnerable site affected by procedure, host, and

wound-care factors.

Pneumonia and C. difficile infection

Airway risks and antibiotic-associated disruption of microbiota require

different prevention strategies

Medical asepsis

Reduce contamination and

transfer; Hand hygiene; environmental

cleaning

Surgical

asepsis

Maintain a sterile field and

key items; Sterile catheter insertion; operative field

Aseptic

practice

Protect key parts and entry

sites; Avoid touching a disinfected

access site

Expected exposure, what to do?

Choose gloves, gown, and face or eye protection for the contact or

splash the task may create; Use hand hygiene, safe injections, sharps protection, and appropriate

equipment and linen handling.

Handhygeine when?

Clean hands before patient contact, after body fluid risk/glove removal; apply alcohol based hand rub and soap and water when visibly soiled

PPE

personal protective equipment; match ppe to task/precautions

Contact

C. difficile; selected

MDROs; Gown and gloves on entry; equipment controls

Droplet

Seasonal influenza;

pertussis; Medical mask on entry; patient

source control

Airborne

Pulmonary TB; measles;AIIR; appropriate N95 or higher

respirator

Norovirus

Enteric Precaution like C. diff; Control exposure to stool and vomit. During outbreaks, continue Contact

Precautions for at least 48 hours after symptoms resolve

Colonization versus infection

A resistant organism may be present without causing the patient's

current illness

Interpret the specimen

Consider collection quality, specimen site, symptoms, and the possibility

of contamination.

Critical Reprocessing

Sterile tissue or bloodstream; Sterilization

Semicritical Reprocessing

Mucosa or nonintact skin; At least high-level

disinfection

Noncritical Reprocessing

Intact skin; Appropriate low-level

disinfection

Sharps & Waste

Disposes in correct container

Airborne Isolation Rooms

Negative pressure, air stays in room

Protective Environment Room

Positive pressure, air sucked into hallway, immunocomprimised patients

The clinical question comes before the test

Localize the suspected infection

History, symptoms, examination, and exposures guide the specimen site

and test.

Estimate the likelihood

Host risk, illness timing, and prior treatment change what a positive or

negative result means.

Interpret the evidence together

Distinguish infection, colonization, contamination, and a residual signal

after recovery

Specimen quality begins before collection

Select the site and test

Sample the suspected process. Confirm the required specimen,

container, and transport medium.

Collect enough, at the right time

Obtain the required volume before antimicrobials when feasible, without

delaying urgent treatment

Protect identity and integrity

Use approved identifiers, accurate source labeling, and a technique that

limits contamination

Blood culture

bottles

Prompt delivery; usually room temperature

Delay or inappropriate storage is a concern

Urine for culture

Prompt processing; approved cooling or preservative if delayed

Overgrowth can inflate the count is concern

CSF for bacterial culture

STAT delivery; do not routinely refrigerate

Loss of fragile bacterial pathogens is concern

Blood culture yield depends on volume and technique

Recover the organism

Use the ordered number of sets and the system's recommended fill

volumes. Adult and pediatric volumes differ.

Limit contamination

Prepare skin and bottle septa correctly, allow required drying, and

protect the prepared site.

Preserve interpretive context

Document collection sites, times, method, and antimicrobial exposure.

Evaluate the pattern across sets

A urine culture requires a clinical indication

Choose the collection method

Use clean-catch midstream urine when appropriate. For an indwelling

catheter, collect aseptically from the sampling port.

Prevent false information

Avoid the drainage bag for culture. Preserve the specimen appropriately

if processing will be delayed.

Interpret with symptoms

Bacteriuria and pyuria alone do not establish symptomatic UTI.

Collection method and clinical findings matter.

Colony counts

growth into CFU per mL

0.001 mL

100/0.001 = 100,000 CFU/mL - HIGHER NUMBER INDICACTES INFECTION

0.01 mL

100/0.01 = 10,000 CFU/mL

General rule

Colonies/volume plated

Meningitis

affects the meninges

Encephalitis

affects brain tissue

Lower respiratory infection

true sputum/indicated lower airway sample; saliva may indicate oral contamination

Suspected pulmonary TB

Sputum for AFB, NAAT, and culture; AFB posititve alone does not indicate TB

Pharyngitis

throat swab and targetted testing; wrong site or test might miss target

Deep wound infection

Appropriate tissue or aspirate when feasible

Surface colonizers obscure the process

Infectious diarrhea

Stool in the test's approved container or medium

Wrong preservative or unneeded panel

Skin, hair, or nail mycosis

Targeted scrapings or clippings as directed

Too little or wrong-site material

Specimens are eventually used for:

evidence of infectious cause

Microscopy / stain test

Cells, organisms, or characteristic structures

-bad: limited sensitivity/ specificity

Culture

Viable organisms that grow under the conditions used

-prior treatment/special needs limit recovery

NAAT / PCR

A targeted nucleic-acid sequence

-detection doesn’t prove viability

Antigen / antibody

Microbial antigen or the host immune response

-timing and crossreactivity matters

Alpha colony indicates:

Partial hemolysis

Beta colony indicates:

Complete hemolysis

Gamma colony indicates:

No hemolysis

Disk diffusion

Standardized growth around antibiotic disks

-zone diameter interpreted by breakpoints

Broth microdilution

Growth in serial drug concentrations

-minimum inhibitory concentration

Gradient diffusion

Drug-gradient strip on inoculated agar

-MIC at inhibition-ellipse intersection

MIC definition

The lowest tested concentration that inhibits visible growth under the 是pecified laboratory conditions.

Three checks before acting on a laboratory result

Specimen check

Was the material collected from the right site, in adequate quantity, and transported correctly?

Method check

Did the laboratory detect growth, a nucleic-acid target, an antigen, or a host antibody?

Patient check

Does the result fit the syndrome, timing, and clinical trajectory? What information is still pending?

CSF

Cerebral spinal fluid

exposure

contact w microbe

-clinical interp: entry/persistance may never occur

colonization

organism present w/o attributable disease

-positive specimen may reflect carriage

infection/disease

infection may be asymptomatic, disease produces harm

-interpret organism w symptom

pathogencity

ability to cause disease

pathogenesis

jouney involved in development of disesase

exposure doesn’t always mean disease

suitable site is required: organism needs an appropriate environment, host receptor

Local defense stops establishment: intact barriers, antimicrobial secretion, resident microbiotal limit growth

host contains process: phagocytes + prior immunity

phases of infectious disease

• The incubation period

• The prodromal period: nonspecific sx

• The period of illness

• The convalescent period: recovery towards baseline

disease patterns + diff dimensions

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extent

localized/disseminated (ex. skin abscesses may remain local/spread)

time course

acute, subacute, chronic (duration doesn’t equal severity)

observed evidence

signs are objective, symptoms are subjective

latency

pathogen persists w/o active clincial disease, may reactivate

reactivation

varicella-zoster virus can persist in sensory ganglia + later cause shingles

secondary infections

new infection follows earlier one (ex. bacterial pneumonia followers viral respiratory illness)

Localized infections

Once an infectious process is initiated, the disease may remain localized or it may spread; examples of localized infections are pimples, boils, and abscesses

Systemic infections

When the infection spreads throughout the body, it is

said to have become a systemic or generalized

infection; an example is miliary tuberculosis, caused

by Mycobacterium tuberculosis.

chronic disease

slow onset and lasts a long time;

examples are tuberculosis, leprosy, and syphilis

mechanisms in disease development

1) entry and attachment

2) multiplication + persistance

3) tissue injury

pathogenecity

capacity to cause disease under suitable conditions

Virulence

degree of disease-causing ability in a defined host and setting, express degree of pathogenicity

virulence factors

traits that support attachment, persistence, immune evasion, or injury

examples of virulence factors

• Adhesins (ligans): vriulence factors, enable pathogens to bind to particular host cell receptors

• Pili (bacterial fimbriae): enable bacteria to attach to surfaces

intracellular survival and immune evasion

---

intracellular growth

use of protected cellular niche

-ex. chlamydia requires host cell for replication

altered phagosome handling

enables survival after engulfment

-m tb disrupts normal killing process

antigen change or IgA cleavage

reduced effectiveness of recognition or mucosal defense

-Antigenic variation: changing surface antigens 

-IgA protease (enzyme that destroys host’s antibodies)

camouflage/molecular mimicry

some organisms conceal foreign nature + coat themselves w host proteins (adult schistosomes)

Exoenzymes

major mechanisms by which pathogens cause disease

Bacterial enzymes can support spread + tissue injury

-tissue barriers disrupted (hyaluronidase + collagenase alter extracellular structures)

-host cells can be damaged: hemolysis and other membrane-damaging products can injure cells

-local survival can be promoted; coagulase promotes clotting, kinases dissolve fibrine barrier

Necrotizing Fasciitis

infects soft tissue, it dies; rots and falls off body

Toxins

poisonous substances released by various pathogens

Endotoxins

Part of the cell wall structure of Gram-negative bacteria

Can cause serious, adverse physiologic effects such as fever and shock/strong inflammatory signaling can contribute to shock

Exotoxins

Poisonous proteins secreted by a variety of pathogens, proteins made by certain bacteria

• gram-positive or gram-negative bacteria

• Specific cellular targets or broad immune activation

Examples: neurotoxins, enterotoxins, exfoliative toxin, erythrogenic toxin, and leukocidins

neurotoxins

disrupts neural signalling (ex. Botulinum and tetanus toxin)

enterotoxin

alter intestinal function (ex. Cholera toxin, e. Coli toxin)

cytotoxin/superantigens

cell injury or extensive immune activation (ex. C. diff, toxic shock toxin)

hosts can amplify injury

local inflammation can be protective: recruitment of defenses can contain microbes + support repair

-dysregulated response harms host: excessive/poorly controlled inflammation -> contribute to organ dysfunction

-sepsis: clinical emergency, infection-associated organ dysfunction requires prompt recognition + treatment

plausible mechanism and mechanism-based review

Plausible mechanism: helps generate a differential diagnosis

-mechanism-based review

• Attachment vs evasion

  • Pili and adhesion supports binding (capsules + intracellular survival can help organism persist)

• Injury vs extent

  • Toxins or host responses may cause severe effects even when organisms remain at local site

• Timeline vs infectiousness

  • Clinical phases do not supply a universal rule for when transmission occurs

First line Defence

Limits entry and establishment; skin, mucus, clearance, secretions, microbiota

Second Line Defense

Recognizes and responds within tissues

Phagocytes, inflammation, complement, fever