Micro - ch.16 - Host Microbe Interactions

pathology

study of disease

• cause, mechanism, effects

etiology

study of finding causation or origin of disease

infection

invasion and multiplication of a pathogen

disease 

disruption in normal body function caused by infection, genetic defect, environmental stressors

transient flora

temporary microbes that live on body (skin)

microbial antagonism

normal microbiota inhibit harmful microbes (through competition)

symbiosis

close relationship between two organsisms

commensalism symbiosis

one organism benefits and the other is neither helped nor harmed

Mutualism symbiosis

both organism benefit

parasitism symbiosis

one benefits - one is harmed

Primary infection

initial infection caused by pathogen - weakens it

Secondary infection

during or after primary infection due to already having a weakened immune system

inapparent/subclinical infection

produces no noticeable symptoms

• pathogen is still present and potentially transmissible

immunocompromised

weakened/impaired immune system reducing bodies ability to fight off infection

What are some causes of immunocompromised immune system?

congenital (from birth)

acquired (HIV, diabetes, cancer)

induced (chemotherapy, transplant, immunosuppressor drugs)

What is Koch’s postulates?

questions to ask to determine the cause of a disease 

What are Koch’s postulates steps?

1. same pathogen must be present in every host

2. pathogen must be isolated from host and then grown

3. cultured pathogen must cause same disease when introduced into healthy host

4. pathogen must be re-isolated from new host and be identical to original host

Exotoxins

proteins secreted by bacteria during growth/multiplication

Endotoxins

components of outer membrane of G- bacteria that produce fever, weakness, aches

adherence 

ability of a microbe to attach to host safely

adhesions/ligands

surface molecules that bind objects and help them attach

virulence (recap)

strength of microbe to cause a disease

injectisome

type of aid invasion

needle like protein structure

G-

injects toxins/effector proteins directly into host 

C5a peptidase

type of aid invasion

an enzyme produced by certain pathogenic bacteria which helps bacteria invade host immune system by targeting and inactivating C5a

dismantling complement system/cascade

What is C5a?

inflammatory molecule produced by complement-system (hole punching) to recruit phagocytes to cite of infection

“calling over”

What is an example of C5a?

streptococcus pyogenes

M protein

type of aid invasion

surface virulence factor that helps bacterium invade the host immune system : C3b

allows binding host proteins → contributes to autoimmune complications

highly variable = complicates vaccines

Capsules

type of aid invasion

thick gelatinous layer that surround the cell wall

• prevents phagocytoses and help adhere to host 

fibronectin

host protein not being used by S. pyogenes

cell wall proteins and waxes

aid attachment and protects from phagocytosis

• resist drying out and disinfectants 

Leukocidins

type of enzyme

toxins that destroy WBCs

hemolysis

type of enzyme

toxins that destroy RBCs by lysing their membranes

coagulase

enzyme

cause blood plasma to clot

→ clot creates protective barrier around bacteria and they can invade immune system

kinases

enzyme

break down clots →allows bacteria to escape and spread through tissue 

DNase, streptodornase

breaks down DNA in pus so that bacteria can spread more easily 

hyaluronidase/collagenaase

breaks down hyaluronic acid and collagen (CT) and bacteria can spread deeper

necrotizing factors

destroy host tissue (necrosis) which makes it easier invasion with less tissue barrier (cell death) 

hypothermic factors

decrease host body temperature

• septic shock or severe infection

proteases

breaks down proteins

• structural protein (collagen)

• destroys antibodies 

Hygiene hypothesis

early exposure to microbes is essential for developing a balanced immune system

• overly clean environment: immune system may not learn

• increase risk of allergies, asthma, autoimmune disease

**does not apply to adults 

cytotoxins

toxins that damage/kill host cell by disrupting vital cellular functions

diptheria toxin

corynebacterium

• inhibits protein synthesis resulting to death 

neurotoxins

specifically targets nervous systems ability to send signals 

botulinum toxins

clostridium botulinum

• food borne - most potent 

• muscle weakness progresses to paralysis in extremes 

tetanus toxin

soil, dust, animal feces

neurotoxin that causes spastic (rigid) paralysis

muscle stiffness and spasms → lockjaw, arching back, difficulty swallowing/breathing = death

enterotoxins

specific in GI tract

disrupt normal fluid balance

diarrhea, vomiting, ABD cramps

food poisoning

choleragen

vibrio cholerae

intestinal lining

watery diarrhea → dehydration

erythrogenic

strains of streptococcus  scarlet fever

massive immune response = damage blood vessels → red rash

staphylococcal

staph strains

target protein outer layer of skin causing the skin to peel

• enterotoxins, DNases, hyaluronidses

cytokine storm

dangerous immune overreaction when body releases too many pro-inflammatory cytokines in short period

(messengers send signals)

cytokine → recruit immune cells → release more cytokines

What is the cause of a cytokine storm?

infection, autoimmune disease, cancer therapies, transplants

What are the consequences of a cytokine storm?

fever, fatigue, rash, organ failure, shock, high mortality 

Cross reactive antibodies

bind to more than one antigen due to structural similarity between those antigens

• past infections recognize new variants 

Rheumatic fever

triggered by poorly treated strept throat

• immune system produces antibodies against streptococcal M protein

• antibodies cross react with host tissue

• heart, joints, skin, brain

communicable disease

illness caused by a pathogen that can transmit from one person to another

contagious disease

type of communicable

• spreads easily and rapidly 

noncommunicable disease

does not spread from person to person

• genetics, lifestyle, environment

• Ex. cancer or even asthma

Incubation period

time between initial infection and appearance of first S/S

• lag phase

prodromal period

early stage of illness following incubation

mild symptoms (fatigue)

• beginning of log phase

period of illness

stage when symptoms are most severe

• peak - stationary phase 

period of decline

phase when symptoms begin to subside - starts to recover - vulnerable to secondary infection

convalescence period

final stage of recovery - return to normal functioning and strength