BIOL 2460 Microbiology Exam Four - Dylan Parks

disease

a condition where normal structure and/or function are damaged or impaired

infection

invasion of pathogen or parasite that lead to disease

signs

things that can be directly measured by clinician (ex: blood cell counts)

symptoms

things felt by patient that cannot be clinically measured (ex: nausea)

syndrome

groups of signs and symptoms that help indicate a particular disease

asymptomatic/subclinical

only signs can be observed through correct testing (ex: patient with herpes and no symptoms)

International Classification of Diseases (ICD)

World Health Organization codes that are used globally to classify and monitor diseases

infectious

disease caused by direct effect of a pathogen

communicable

capable of spreading person-to-person

contagious

easily spread

iatrogenic

acquired as result of medical procedure

nosocomial

acquired from hospital setting

zoonotic

acquired from animal

non-communicable

obtained from non-living thing such as soil or contaminated object

non-infectious

not caused by pathogen

malaria

- communicable

- infectious

- zoonotic

sickle cell anemia

- non-communicable

- non-infectious (genetic)

5 stages of infectious disease

1. incubation

2. prodromal

3. illness

4. decline

5. convalescence

incubation

initial entry of pathogen; replication begins

prodromal

replication continues; host shows signs and symptoms

illness

signs and symptoms are most severe in host

decline

pathogen number starts to decrease; host's immune system is weak and vulnerable to secondary infection

convalescence

host starts to recover

acute disease

relatively short (hours, days, week)

chronic disease

longer time (months, years, lifetime)

latent disease

comes in episodes; pathogen replicates when disease is active

Koch's postulates

set of standards that must be met to demonstrate that X pathogen causes X disease

Koch's postulates

1) The suspected pathogen must be found in every case of disease and not be found in healthy individuals.

2) The suspected pathogen can be isolated and grown in pure culture.

3) A healthy test subject infected with the suspected pathogen must develop the same signs and symptoms of disease as seen in postulate 1.

4) The pathogen must be re-isolated from the new host and must be identical to the pathogen from postulate 2.

Koch's assumptions (WRONG)

1) Pathogens are found only in diseased individuals.

2) All subjects are equally susceptible to infection.

3) All pathogens can be grown in culture.

Molecular Koch's postulates

identifies gene instead of pathogen; improved postulates that overcame some of Koch's limitations

Limitations of Molecular Koch's postulates

1. genetic manipulation of some organisms isn't possible with current techniques

2. some diseases do not have suitable animal models

pathogenicity

ability of a pathogen to cause disease

virulence

degree of pathogenicity

ex: highly virulent - Bacillus anthracis induces severe signs and symptoms

ex: low virulent - Rhinovirus induces low signs and symptoms

virulence curve

how virulence can be modeled in controlled experiments

median infectious dose (ID50)

number of pathogens required to infect 50% of those inoculated

median lethal dose (LD50)

number of pathogens required to kill 50% of those infected

- LD50 is 10^4 pathogen cells or virions

primary pathogen

can cause disease in a host regardless of the host's resident microbiota or immune system

ex: enterohemorrhagic E. coli (mainly due to Shiga toxin)

opportunistic pathogen

can only cause disease in situations that compromise the host's defenses (protective barriers, immune system, or normal microbiota)

ex: Candida albicans with disrupted microbiota

ex: UTI caused by E. coli

influencers of susceptibility

drugs, resident microbiota, genetics, & age

5 stages of pathogenicity/infection

1. Exposure to host

2. Adhesion

3. Invasion

4. Infection

5. Transmission

exposure (contact)

can occur in many ways: pathogens must be exposed to portals of entry to begin adhesion

- some portals are worse than others (ex: mucosa)

TORCH infections

pathogens that can cross placental barrier as portal of entry

Torch

toxoplasmosis --> Toxoplasma gondii (protozoan)

tOrch

syphilis --> Treponema pallidum (bacterium)

chickenpox --> Varicella-zoster virus (human herpesvirus 3)

hepatitis B --> Hepatitis B virus (hepadnavirus)

HIV --> Retrovirus

fifth disease (erythema infectiosum) --> Parvovirus B19

toRch

rubella (german measles) --> Togavirus

torCh

cytomegalovirus --> Human herpesvirus 5

torcH

herpes --> herpes simplex virus (HSV) 1 & 2

adhesion

pathogens' varying capability of colonization

adhesins

molecules/structures that bind to certain host receptors

biofilm

production of community glycocalyx

invasion

occurs when colonization is established; pathogens generally produce toxins to allow further colonization into body/tissue and protection from immune system

- virulence plays a role in degree of invasion

ex: Helicobacter pylori urease production

intracellular pathogens

invade via endocytosis and evasion of host immune defenses

invasion mechanisms

1. Effector proteins are secreted to trigger entry - membrane ruffling

(ex: Salmonella and Shigella spp.)

2. Surface proteins allow for binding to host cell (trojan horse approach)

Phagolysosome survivors

- Listeria monocytogenes

- Mycobacterium tuberculosis

local infection

small area of body

focal infection

pathogen or toxin spreads to secondary location

systemic infection

occurs throughout body (ex: septicemia)

primary infection

can lead to secondary infections of different pathogen

ex: HIV lowers immune system and opens door for yeast and others; rhinoviruses can lead to bacterial pneumonia

transmission

persistence passes on pathogen onto a new host through a portal of exit

virulence factors

pathogen product that assists in ability to cause infection and disease

- dictate how severe and extensive a disease is; some have more than one

ex: adhesion factors, exoenzymes, toxins, immune evasion

adhesins

proteins that aid in attachment to host cell receptors

- found in ALL microbial types (viral, fungal, bacterial, etc.)

- commonly found on fimbriae or pili

- can initiate biofilm formation in some species

-emia

presence of pathogen in blood

bacteremia

bacteria in blood

viremia

viruses in blood

toxemia

toxins in blood

septicemia

bacteria present and multiplying in blood

- patients with septicemia (septic) can lead to shock (life threatening disease in BP)

exoenzymes

extracellular enzymes used to invade host tissues

- glycohydrolases, nucleases, phospholipases, proteases

ex: collagenase produced by C. perfringens causing necrosis and gas gangrene

toxins

biological poisons that assist in ability to invade and cause tissue damage (toxigenicity)

endotoxins

lipopolysaccharides that triggers host inflammatory responses; can cause severe fever and shock

exotoxins

proteins mostly produced by Gram (+)

- targets receptors in specific cells

detectors of endotoxins

1. Limulus amebocyte lysate (LAL) test

2. Enzyme-linked immunosorbent assay (ELISA)

LAL test

blood cells of the horseshoe crab mixed with patient's serum; observed chromogenically or by coagulation

ELISA

uses antibodies to detect endotoxins

intracellular targeting

a division of exotoxins with A & B regions for activity and binding

ex: diptheria and botulinum toxin

membrane disrupting

division of exotoxins aka phospholipases that degrade bilayer membrane

ex: Bacillus anthracis and Rickettsia spp.

hemolysins and leukocidins

membrane disruptors that can target RBC, WBC, and other cells

superantigen

division of exotoxins that trigger excessive production of cytokines by immune cells

ex: Staphylococcus aureus and Toxic Shock Syndrome

host evasion

mechanisms to evade phagocytosis

ex: capsules that enlarge bacterial cell so phagocytes cannot engulf pathogens

ex: proteases digest host antibody molecules

antigenic variation

alteration of cell surface proteins to hide from immune cell recognition (example of host evasion mechanism)

antigenic drift

result of point mutations causing slight changes in spike proteins (H & N)

antigenic shift

major change in spike proteins due to gen reassortment

virulence in fungi

Many properties similar to bacteria; adhesins, proteases, and toxins

ex: Capsule (+) Cryptococcus spp. can cause pneumoniae and meningitis

mycotoxins

fungal toxins produced by Claviceps purpurea and Aspergillus spp. that contaminate grains and other staple crops

virulence in protozoans

have unique features for attachment

ex: Giargia lamblia uses adhesive disk of microtubules to attach to intestines

ex: Plasmodium falciparum quickly changes adhesive protein for RBCs to avoid immune recognition; causes chronicity in malaria patients

virulence in helminths

tissue penetration commonly achieved with proteases (worms that burrow into skin)

ex: roundworms produce cuticle to last longer against host defense assaults

ex: Schistosoma mansoni degrades host antibodies to halt immune defense

"Glycan gimmickry"

mimic host cells to evade immune system

epidemiology

field that studies distribution and timing of diseases (infectious and non-infectious)

Determines:

1) Etiology

2) Transmission

3) Susceptible populations

morbidity

number of individuals with disease

rate calculation: #/population

mortality

number of deaths from disease

rate calculation: #/population

prevalence

number of individuals at certain time

incidence

number of new cases

4 patterns of incidence

1. Sporadic

2. Endemic

3. Epidemic

4. Pandemic

sporadic

occurs occasionally without regional concentration

ex: tetanus, rabies, plague

endemic

constantly present in certain region

ex: malaria, ebola, chickenpox

epidemic

larger than normal amount of cases

ex: influenza, west nile

pandemic

epidemic that is cross continental

ex: virulent influenza, ebola, etc.

etiology

determining the causative (etiological) agent of infectious disease; epidemiology helps provide clues and the standard procedure is Koch's postulates

CDC (Center for Disease Control)

protects public from disease/injury by providing physicians and health-care workers with updates on public health issues & latest data on notifiable diseases

ex: publication of the MMWR (Morbidity and Mortality Weekly Report)

NNDSS (National Notifiable Disease Surveillance System)

system where all cases must be reported by physicians; these studies track notifiable diseases to determine risks

ex: west nile, HIV, measles, etc.

John Snow

British physician and father of epidemiology; his study led to the discovery of the contaminated water pump that was responsible for the 1854 cholera London epidemic