BIOL 2460 - chapter 15 - PARKS - MICROBIOLOGY

Parks UTA

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 (e.g. blood cell counts, Heart rate, respiratory rates)

Symptoms

things felt by patient that cannot be clinically measured (e.g. nausea, headache, loss of appetite) (EXPRESSED BY PT)

Syndrome

groups of signs & symptoms that help indicate a particular disease

asymptomatic

only signs can be observed thru correct testing

Infectious

disease caused by direct effect of a pathogen

Communicable

capable of spreading person-to-person (contagious – easily spread) (STD’s/ HIV, Malaria)

Iatrogenic

acquired as result of medical procedure

Nosocomial

acquired from hospital setting

Zoonotic

acquired from animal (rabies, malaria, avian flu)

Non-communicable

obtained from non-living thing such as soil or contaminated object (tetanus, Sickle Cell Anemia)

Non-infectious

not caused by pathogen (Sickle Cell Anemia)

Infectious disease follow 5 stages:

Incubation, Prodromal, Illness, Decline, Convalescence

Incubation

initial entry of pathogen; replication begins; no signs or symptoms

Prodromal

Replication continues; host shows signs & symptoms

Illness

signs & symptoms are most severe in host (respiratory) (HIGHEST # OF PATHOGENS)

Decline

pathogen no. start to decrease; host’s immune system is weak and vulnerable to secondary infection (immunocompromised)

Convalescence

host starts to recover

Acute

relatively short (hours, days, week) (flu)

Chronic

longer time (months, years, lifetime) (TB, HIV, Hepatitis)

Latent

comes in episodes; pathogen replicates when disease is active (chickenpox and herpes)

Koch’s Postulates

determine whether a particular microorganism is a pathogen

1. The suspected pathogen must be found 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 wrong assumptions

Pathogens are found only in disease individuals
All subjects are equally susceptible to infection
All pathogens can be grown in culture

Molecular Koch’s Postulates

used to determine what genes contribute to a pathogen's ability to cause disease

Molecular Koch’s Limitations

1. genetic manipulation of some organisms isn’t possible with current techniques
2. some diseases do not have suitable animal models (HIV)

Pathogenicity

ability of pathogen to cause disease

Virulence

degree of pathogenicity
Highly virulent – Bacillus anthracis induces severe signs & symptoms
Low virulent – Rhinovirus induces low signs & symptoms

Median infectious dose (ID50)

no. of pathogens required to infect 50% of those inoculated

Median lethal dose (LD50)

no. of pathogens required to kill50% of those infected

Primary pathogen

can cause disease in a host regardless of host’s resident microbiota or immune system
- enterohemorrhagic E. coli (mainly due to Shiga toxin)

Opportunistic pathogen

can only cause disease in situations that compromise the host’s defenses (e.g. protective barriers, immune system, or normal microbiota) (ENVIRONMENTAL CHANGE)
- Candida albicans with disrupted microbiota, UTI caused by E. coli
- STAPH infection, E. coli

Stages of Pathogenicity

Exposure to host, Adhesion, Invasion, Infection, Transmission

Exposure/contact

pathogens must be exposed to portals of entry to begin adhesion 
i.e. (eye conjunctiva, nose, mouth, placenta (TORCH), anus, urethra, vagina, insect bite, broken skin)

Adhesion

capability of colonization
Adhesins - molecules/structures that bind to certain host receptors
Biofilm - production of community glycocalyx

Invasion

colonization is established
- Effector proteins are secreted to trigger entry –membrane ruffling(e.g. Salmonella & Shigella spp.)

- Surface proteins allow for binding to host cell, receptors that bind to epithelium cells and the cells allow them to enter (trojan horse approach)
~ some survive phagolysosomes within WBCs (e.g. Listeria monocytogenes, Mycobacterium tuberculosis)

Infection

1. Local infection – small area of body
2. Focal infection – pathogen or toxin spreads to secondary location
3. Systemic – occurs throughout body (ex. Septicemia, chicken pox)

Primary infections can lead to ________ infection of different pathogen

secondary
i.e. HIV lowers immune system and opens door for yeast and others; rhinoviruses can lead to bacterial pneumonia

Transmission

Portals of exit: eye (tears), mammary glands, placenta, vagina, skin (flakes), urethra (urine), nose, mouth (saliva & sputum), ear (wax), needle (blood), anus, insect bite, and broken skin

Virulence factors

pathogen product that assists in ability to cause infection and disease
Adhesion factors, Exoenzymes, Toxins, Immune evasion

Adhesins

proteins that aid in attachment to host cell receptors; initiate biofilm formation in some species
i.e. viral, fungal, bacterial, fimbriae or pili

-bacteremia

bacteria in blood

-viremia

viruses in blood

toxemia

toxins in blood

septicemia

bacteria present and multiplying in blood (active)

Patients with __________ can lead to shock (life-threatening decrease in BP)

septicemia

Exoenzymes

extracellular enzymes used to invade host tissues
i.e. glycohydrolases, nucleases, phospholipases, proteases

Toxins

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

Endotoxins

lipopolysaccharides (in G-) that triggers host inflammatory responses; can cause sever fever and shock

Exotoxins

proteins mostly produced by Gram (+); Targets receptors on specific cells; can be further divided

Detecting endotoxins

1. Limulus amebocyte lysate (LAL) Test: blood cells of the horseshoe crab mixed with patient’s serum; observed chromogenically or by coagulation

2. ELISA – enzyme-linked immunosorbent assay: uses antibodies to detect endotoxins

Intracellular targeting - EXO

with A & B regions for activity and binding; Ex. diphtheria & botulinum toxin

Membrane-disrupting - EXO

aka phospholipases that degrade bilayer membrane; Ex. Bacillus anthracis & Rickettsia spp.
- Hemolysins and Leukocidins: can target RBC, WBC, and other cells

Superantigen - EXO

trigger excessive production of cytokines by immune cells; 
Ex. Staphylococcus aureus and Toxic Shock Syndrome (causing high amounts of S. aureus since it is cultivated by blood

Host evasion

mechanisms to evade phagocytosis
- Capsules that enlarge bacterial cell so phagocytes cannot
engulf pathogens
- Proteases digest host antibody molecules
- Mycolic acid in acid fast bacteria (M. tuberculosis) helps evade
phagolysosomes
- Coagulase pos. microbes can coagulate blood cells to keep immune cells out of reach
- Alteration of cell surface proteins to hide from immune cell
recognition (antigenic variation)

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

Mycotoxins

adhesins, exoenzymes, & toxins
produced by Claviceps purpurea and Aspergillus spp. that contaminate grains & other staple crops
- Many properties are also similar to bacteria (adhesins, exoenzymes, & toxins)

Protozoans

Adhesins, toxins, antigenic variation
Unique features for attachment – Giardia lamblia uses adhesive disk ofmicrotubules to attach to intestines

Helminths

- “Glycan gimmickry” – mimic host cells to evade immune system
- Tissue penetration commonly achieved w/ proteases (e.g. worms that burrow into skin)
- Schistosoma mansoni degrades host antibodies to halt immune defense