Micr 121 Midterm Flashcards
Enterobius vermicularis
pinworm
most common worm infection in north america
Enterobius vermicularis life cycle
direct
human-enviro-human
Ascaris Lumbricoides
foot long worm
Ascaris Lumbricoides life cycle
Direct
ingest eggs, larvae hatch in small intestine
Taenia saginatum
Beef tapeworm
Taenia Solium
Pork tapeworm
Diphyllobothrium Latum
Fish tapeworm
Tapeworm life cycle
indirect life cycle
human-eggs into environment - cow - muscle- human
Schistosomes
Fluke (bird schistosomes)
Schistosomes life cycle
indirect life cycle
intermediate host - egg taken up by snail
Parasite detection (2 ways)
intestinal
tissue and blood
intestinal parasite detection
stool sample in preservative (formalin) to maintain the parasite structures
tissue and blood parasite detection
antibody detection
Biopsy
depends on where it infects
(GI- intestinal so look under microscope)
Beef and pork tapeworms are not found in north america because
cow must be exposed to human waste in sewage.
not happening in north america
Entamoeba histolytica
and transmission
intestinal protozoa
major pathogen where poor sanitation
Transmission: water/food
human only
direct transmission
Dientamoeba Fragilis
and transmission
intestinal protozoa
Worldwide, primarily in children
Human only
Transmission:Direct contact
does not have a cyst form therefore, will not survive in environment.
(often see kids with pinmarks may be through pinworm)
Giardia Lamblia
and transmission
intestinal protozoa
Beaver Fever
Transmission: Fresh water - camping
Cryptosporidium Parvum
and transmission
intestinal protozoa
Transmission: cattle, water system (rural pops with wells)
Cyclospora
and transmission
contaminates food
Rasberries lettuce
human pathogen
which intestinal protozoa is resistant to chlorine?
Cryptosporidium
therefore, water tx plants need to
1. chlorinate water
2. Filter water
Intestinal protozoa structures
Trophozoite: feeding form
Cyst Stage: Infective resting stage: resistant to adverse conditions in environment
only form that will survive in the environment.
Trichomonas Vaginalis
Human only
Wet prep of vag swab for motile trophozoites
Toxoplasma Gondii
Commonly infects other vertebrae hosts - found in cats
Human infection often asymptomatic
Evades immune system and is stored in tissue cysts indefinitely.
Reactivated by:
1. immunocompromised - neurotoxoplasmosis
2. pregnant women - blindness and intellectual complications
Malaria: plasmodium species life cycle
indirect life cycle
asexual in vertebrae RBC
Sexual in mosquito
mosquito- blood-liver-blood-differentiate to gametocytes - mosquito - sexual stage.
to determine mortality rate of malaria
count number of RBCs
incr RBC number = incr mortality rate
Critical prevention of malaria
chemoprophylaxis
Chloroquin
common
not expensive
mefloquin
1X/week
causes nightmares
malarone
1X/day
not long time before
majority of malaria death is in
kids
if adults have survived have developed immunity
but if take out of environment will lose immunity
chemoprophylaxis issues:
Dosing (Daily/wkly)
side effects
resistant *chloroquin)
Cost
diagnosis of malaria
giemsa stain of thick and thin blood smear
Sebaceous glands
secrete complex lipids = substrate for G+ bacteria
end products of G+
are inhibitory for G -
Majority of organisms on are skin are
G +
part of skin that is mostly G-
Midsection
because colon is full of G-
Lysozyme
in our eye
breaks down peptidoglycan similarly to pennicilins (inhibit cross linking of peptidoglycans)
Conjunctival infections are from
mechanical deposition not aerosol spread.
Few G+ in GI tract because
Bile - inhibitory to G+
bacteria upper GI tract
Facultative
grows in presence or absence of oxygen
bacteria in lower GI tract
Anaerobes
only grow in absence of oxygen
less risk of infection after GI surgery in
upper GI tract d/t peristalsis
this type of bacteria thrive in GI
anaerobes b/c competition for oxygen
G+ bacteria that can grow in GI
enterococcus species
resistant to bile.
Lactobacillus species
nonpathogenic organism
in female genital tract in women of child bearing age.
coat epithelial cells - bacteria can’t grow
acidic environment - bacteria can’t grow
how lactobacilli are controlled
estrogen - epithelial cells - glycogen - incr lactobacilli(eat glycogen) - lactic acid
Gram __ primarily in resp tract
+
resp tract non specific resp defenses
- mucociliary elevator (ciliated hairs) - move material towards larynx and swallowed f
- cough reflex
- lysozyme
- lactoferrin: Binds free iron and limits bacteria using it to grow
- Secretory IgA
- alveolar macrophages
IgM
early in infection
IgG
long lasting memory
Cytotoxic T cells
recognizes antigen on surface of cells
(pathogen multiples in cytoplasm - antigens carried to the surface - proliferation of these cells - T cells kill cells expressing the antigen
Natural killer T cells
kill tumor cells
vrius infected cells
inflammation
fills a gap between exposure and immune system response = critical defense at this time.
inflammation works against and doesn’t work against
works: bacteria and fungal
does not: viral because cannot engulf viral cells.
polymorphonuclear leukocyte
WBC “pus cell”
ingest all of the bacteria
Phagocytic killing steps
- bacteria ingested in phagocyte (pocket)
= phagosome - phagosome fuses with the lysozome (digestive enzs)
= phagolysozome
=>killed by enzs
opsonophagocytosis
antibody coated antigen
needed to enable phagocytosis of organisms with a capsule
Slime layer
many organisms on medical device have a capsule and produce a slime layer -> biofilm
biofilm
cannot be penetrated by:
antibody
antibiotics
Inflammation cells
Organism that produces slime layer
staphylococcus epidermidis
avoiding phagocytosis by killing the white cell
production of leucocidins (toxins) specific for WBCs
avoiding phagocytosis (3)
capsule
slime layer
leucocidins (kill the WBC)
Avoiding phagocytic killing (3)
- survive in the cytoplasm of the cell (phagocyte)
- inhibit fusion of phagosome and lysozome
- resist enzymatic killing
surviving long term in phagocytic cell long term
macrophage
transport to other sites and spread infection
latency
virulence factors
once avoidance of phagocytosis assists the organism ini initiating disease, produce these factors to cause further disease
adherence
virulence factor
organisms must adhere to host tissues to establish a focus of infection
-> initiates the ability to cause disease.
receptor for adherence
adhesin
exotoxins
virulence factor
protein with enzymatic effects - only need small amount to get big effect
specific action on tissues
ability to convert to toxoids: a toxin that is recognized by our immune system that cannot fxn, make excellent vaccines against actual toxins.
endotoxin
LPS in outer membrane of G- cell envelope.
generic
LPS survives due to
heat stability
injectable package says pyrogen free, does not have endotoxin been tested past the autoclave test
host response to endotoxin
binds to macrophage - induces immune modulators (cytokines) ->fever and hypotension (septic shock)
mechanisms of action of exotoxins on GI
- cytolytic: lyse cells -> bloody diarrhea
- Inhibit intracellular metabolic functions.
a. protein synthesis -> cell death
b. alter cAMP (=ion and water transport) across cells = decr H2O absorption from gut and secretion into gut -> watery diarrhea
which organisms cause both exotoxin effects
E. COli
C.Difficile
