unit 8 Flashcards
Disease
abnormal state in which body is not capable of carrying on its normal function
Infection
invasion/ colonization of the body by pathogenic microbes
Pathogens
disease carrying microbes
Pathology
study of diseases
Etiology
cause of diseases
Normal flora or normal biota commensals
- location = skin/mouth/vagina/eyes
Why is concentration important in our normal flora?
abnormal concentration/change of location of normal flora could become pathogenic
Sporadic (occurence of disease)
disease occurs occasionally in a population’
ex: fever
Endemic (occurence of disease)
disease constantly in a population
Epidemic (occurence of disease)
many people in a given area acquire a disease in a short period of time
Pandemic (occurence of disease)
worldwide epidemic
- covid 19
Acute (severity/duration of a disease)
disease develops rapidly but lasts a short time
chronic
disease develops slowly
body reactions are less severe
recurrent or continuous for long time
subacute
disease intermediate between acute /chronic
sclerosing panencephalitis is an example of what kind of disease
subacute
Latent
become inactive for a some time then becomes active
HSV is an example of what kind of disease
latent
what is a localize infection
microbes limited to a certain area
boils/abscesses
what is generalized/systemic infection
microbes spread via blood/lymph system
ex= measles
What is focal infection
-arises from infections of teeth/tonsils/sinuses
- infection starts local than become systemic/generalized
what is primary infection
infection that causes inital illness
what is secondary infection
infection caused by an opportunistic microbe due to weakening of body
Nosocomial
hospital acquired infections (HAI’s)
HAI’s types of infections
- lower rt
-surgical sites - UTI’s
HAI’s types of microbes
e.coli/ enterococcus
staph/strep
pseudomonas
C.difficles
Bacteremia
bacteria in blood
Septicemia (sepasis)
pathogen multiplying in blood / blood poisoning
Toxemia
Toxins in blood ( tetanus)
Viremia
Viruses in blood (measles)
Pyemia
Pus forming microbes in blood (staph/strep)
Sign
= measured
Symptom
= felt
General patterns of infection
- period of incubation
- prodromal syndrome
- period of invasion
- acme or fastigium
-period of decline - period of convalescence
Period of incubation
interval between initial infection / appearance of signs and symptoms
Prodromal syndrome
mild sign/symptoms
Period of invasion
most severe
Period of decline
subside
Period acme or fastigium
equilibrium
Period of convalescence
recovering
EID’s emerging infectious diseases
new/ changing diseases
Host parasite relationships
-mutualism
- commensalism
- parasitism
Commensalism
most normal flora
Parasitism
live off host cell
Portals of entry
- RT
- GI tract
- skin/membrane
- paracentral
- Genitourinary tract
- placental
RT tract
inhaled
GI tract
mouth
Skin/membranes
mainly breaks in skin
Paracentral
deposited directly -> tissue / beneath the skin and mucous membranes (tetanus /injections)
Genitourinary tract
STD’s / STI’s
Placental
effects fetus (toxicplasmosis / HIV)
Purpose of pili
conjugation/ attachment
Purpose of flagella
movement
Purpose of capsules
resist host defenses
Cell wall M protein
attach to host/ resist WBC’s
Cell wall waxy layer
resist phagocyte digestion
Exoenzyme production
- hemolysins
- leukocidins
- Coagulase
-Kinase, Streptokinase , staphylokinase,
-Hyaluronidase - Immunogobulin A proteases
Exoenzyme purpose
-used for self protection against host defenses
- secrets enzymes
Hemolysins
breaks down RBC’s
Leukocidins
destroys WBC’s
Coagulase
coagulates the blood protein (firbinogen) -> fibrin
blood clots formed by staph
Fibrinogen
produce by liver
Kinase
enzymes that dissolve blood vlots
Streptokinase
(fibrinolysin)
Staphylokinase
activates plasmidogens
Hyaluronidase
- “spreading factor” holds cell togethers
- hydrolyzes hyualuronic acid to increase tissue permeability ( tissue blackening)
- produced by clostridium sp.
Immuniglobbulin A proteases
- antibodies
-enzymes that digest IgA
Which microbes penetrate through mucosal membrane of cell
H. influenzae and S. pneumoniae
Characteristics of exotoxins
-production of toxins
- found in gram + / bacteria (cytoplasm)
- produce when cells are growing / released in cell death
-heat labile protein
-susceptible to heat
-destroys cells
Mode of action for exotoxins
inhibits cell activity
How much dosage of exotoxins is lethal
small dosage
exotoxin that target nerve cells
neurotoxins
exotoxin that targets intestinal tissue
enterotoxins
exotoxin that targets heart muscle
cardiotoxins
exotoxin that targets kidneys
renaltoxins
what is produced by exotoxins
toxoids and antitoxins
toxoid
-harmless/ antigenic
- destroyed with heat
Toxoid if injected
produces antibodies (how vaccines are created)
When are are given if someone is exposed to exotoxin?
Antibodies
purpose of Antitoxin
neutralizes circulating harmful exotoxin
Diptheria, Scarlet fever, Botulism, Cholera, and Tetanus or lockjaw are examples of what kind of toxin
exotoxins
Diptheria (exotoxin)
-cytotoxin produced by cornybacterium diptheriae
- damages heart tissue/ nerve cells
-vaccine = prevent disease
-Antitoxin treats disease
Scarlet fever (exotoxin)
-produced by streptococcus pyogenes
-erthryogenic toxins
- antibiotics = vaccine
-red skin rash
Botulism (exotoxin)
-exotoxin of clostridium botulinum
- botox = botulinum toxin
- fatal food poisoning
- neurotoxin prevents release of ach
-paralysis/loss of muscle tone
Antitoxin is the treatment for what exotoxin?
Botulism
Cholera (exotoxin)
-enterotoxin of vibrio cholera
- bacteria does not invade tissue
-rice water stools
- toxins simulates secretions of fluids/electrolytes from small intestines
Tetanus lockjaw (exotoxin)
- neurotoxin produced by clostridium tetani
- causes uncontrollable skeletal/muscle contractions
- vaccines to prevent / antitoxins to treat
Endotoxin
-within part of cell
- produced by gram - bacteria only
- produced when cells die
-heat stable
-no toxoids or antitoxin
How much dosage of endotoxin is lethal
larger does than exotoxin
Mode of action for endotoxin
effect non-specific tissue
effects of endotoxin
-release fever inducing substances from neutrophils
- activates blood clotting proteins that obstruct capillaries result in tissue death (decreases blood supply)
-shock/death
-intravascular clotting disease (DIC)
Type of endotoxins
-typhoid fever
-meningococcal meningitis
How are typhoid fever /meningococcal meningitis treated?
- treat symptoms until endotoxins breakdown
-antibiotics release more endotoxins (improves when lipid lipase breaks down lipid endotoxin)
