BIOL 2460 - chapter 15 - PARKS - MICROBIOLOGY

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

invasion of pathogen or parasite that lead to disease

things that can be directly measured by clinician (e.g. blood cell counts, Heart rate, respiratory rates)

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

groups of signs & symptoms that help indicate a particular disease

only signs can be observed thru correct testing

disease caused by direct effect of a pathogen

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

acquired as result of medical procedure

acquired from hospital setting

acquired from animal (rabies, malaria, avian flu)

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

not caused by pathogen (Sickle Cell Anemia)

Incubation, Prodromal, Illness, Decline, Convalescence

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

Replication continues; host shows signs & symptoms

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

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

host starts to recover

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

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

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

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

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

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

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

2. some diseases do not have suitable animal models (HIV)

ability of pathogen to cause disease

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

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

no. of pathogens required to kill50% of those infected

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

• enterohemorrhagic E. coli (mainly due to Shiga toxin)

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

Exposure to host, Adhesion, Invasion, Infection, Transmission

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)

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

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)

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)

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

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

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

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

bacteria in blood

viruses in blood

toxins in blood

bacteria present and multiplying in blood (active)

septicemia

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

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

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

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

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

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

aka phospholipases that degrade bilayer membrane; Ex. Bacillus anthracis & Rickettsia spp.

• Hemolysins and Leukocidins: can target RBC, WBC, and other cells

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

mechanisms to evade phagocytosis

• Capsules that enlarge bacterial cell so phagocytes cannotengulf 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)

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

major change in spike proteins due to gen reassortment

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)

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

• “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