Gram + or - cause
Thickness of peptidoglycan cell wall
Why does gram + or gram - matter?
Thickness of peptidoglycan wall will determine the type of antibiotics we will use
Fungi divisions
Yeasts
Molds
Molds shape
Hyphae - fingerlike
Yeasts shape
Buds
Fungi cell walls can produce
vitamin D
Helminth
Worm parasite
4 infectious agent categories
Bacteria
Virus
Fungi
Parasites
Adaptive immune system consists of
T & B cells
Innate immune system consists of
Macrophages
Neutrophils
Eosiniphils
Basophils
Monocytes
Nonspecific immune system consists of
Skin, mucous membrane, stomach acid, lysozomes
Gut Microbiota/Microbiome
Diverse microorganisms in and on the human body. Need to be fed to produce properly.
Microbiota produces most of this vitamin in the body:
Vitamin K
Nosocomial infections
occur when replacement of the normal flora occurs in the hospital setting
Innate immune system
General system we are born with
Adaptive system
Specific, takes exposure
Immunization gives exposure for:
Adaptive immunity
Virus can cause damage to tissues in two was
directly/indicrectly
Chigella produces cytotoxin that causes
intestinal cells to die off. This produces hemorrhagic diarrhea
Cell being infected hurts the host
Immune system removes that cell
Direct cell damage from microorganism
cytoxin
Indirect damage from microorganism
inflammation
Acute
<4 weeks
Subaccute
4-12 weeks
Chronic
12 weeks or longer
Recurrent acute
4 or more episodes per year
IL-1
cytokine that is proinflammatory, produces fever
opportunistic infection
waits dormant for immune system to be distracted, takes the opportunity
Symptoms of a UTI
Burning, have to pee a lot.
Gram positive bacteria
Have thicker peptidoglycan walls so they hold on to dye more
Gram negative bacteria
Thinner wall
Infective endocarditis
Almost always infects the left side of the heart
IV Drug user endocarditis affects:
The right side
PRR stands for
Pattern Recognition receptors
What type of receptors fall under the PRR category?
Toll-like receptors, nucleotide binding oligomeriation domain like receptors
What activates PRRs
Exogenous organisms interacting with host cells
What does PAMP stand for?
Pathogen-associated molecular patterns
What happens when Pathogen associated molecular patterns are activated?
Activation of a pro-inflammatory cascade that plays a role in pathogen recognition and inactivation.
Pathogen associated molecular patterns
PAMPS
Which type of hypersensitivity response causes creation of immune complexes?
Type III
Diarrhea classified as
Secretory
Inflammatory
hemorrhagic
Secretory diarrhea
Presents as watery, Enterotoxins activate intestinal enzyme activity, loses water and electrolyes
Inflammatory diarrhea
Presents as mucus-y,
Comes from cell death, cell destruction.
Hemorrhagic Diarrhea
E.Coli most common, toxin destroys RNA, prevents cells from reproducing, bloody.
Common causes of secretory diarrhea
v.cholerae
Watery.
Common causes of inflammatory diarrhea
Mucus-y
Salmonella, Shigella
During inflammation we get these common effects
Vasodilation
Swelling
F
W
P
P
R
S
Fever is caused by
IL-1, systemic proinflammatory mediator
Warmth in inflammation is caused by
Vasodilation increasing blood flow
Redness is caused by
Vasodilation increasing blood flow
Swelling is caused by
Vasodilation increasing capillary permeability, allowing antibodies, compliment and white blood cells to cross the endothelium and reach the site of injury.
How does the pH change during inflammation?
The pH is lowered
Why is the pH lowered in inflammation?
It creates an inhospitable environment for invading microbes.
Why do we get vasodilation in inflammation?
Vasodilation helps increase blood flow to the area which helps deliver the proteins needed for clotting, inflammation, healing and remodeling.
Neutropenia
Low Neutrophils, <1000cells/microliter
These 3 types of cells are phagocytic
Macrophages, Neutrophils, Monocytes
Low neutrophils increases chance of what
infection
Extreme neutropenia is defined as
<500cells/liter
Chediak-higashi syndrome:
Autosomal recessive, neutrophils have a profound defect in the formation of intracellular granules.
In this syndrome, neutrophils have a lack of intracellular granules
Chediak-higashi
In this syndrome neutrophils intracellular granules cannot fuse with phagosomes and form phagolysosomes.
Chediak-higashi
Myeloperoxidase deficiency
Most common neutrophil disorder
In this syndrome phagocytosis, chemotaxis and degranulation are nrormal, but metabolic pathways are impaired.
Myeloperoxidase deficiency
Most patients with this neutrophil disorder are asymptomatic
Myeloperoxidase deficiency
Chronic granulomatous disease
genetically heterogeneous group if disorders characterized by the failure of phagocytic cells to produce superoxides.
Osler lesions
ouchy on hands and feet
Janeway lesions
Just on hands and feet, no ouchy
What do we believe causes osler lesions and janeway lesions?
Depositions of immune complexes
Pathogenic bacteria like s pneumonia and n meningitidis secrete:
IgA protease that inactivates host antibody and facilitates mucosal attachment
Two theories for passing blood brain barrier
Trojan horse, tight junction opening from cytokine
Bacteria have this that let them survive in the CSF
Large capsules
IL-1, IL-6, Metalloproteinases and tumor necrosis factor are thought to be:
Inflammatory mediators for meningitis
Types of cerebral edema
Vasogenic
Cytotoxic
Interstitial
Vasogenic cerebral edema is caused by :
Increase in the blood brain barrier, dilation of the blood vessels
Cytotoxic cerebral edema is caused by
Toxic factors released b bacteria or neutrophils
Interstitial cerebral edema is caused by
Obstruction in the flow of CSF
Mast cells produce these two inflammatory mediators
Histamine and LeukotrinesL
Hitamines and Leukotrines mediate
vasodilation in inflammation
Stages of inflammation
Vascular response
Leukocyte recruitment
Phagocytosis
Vascular response in inflammation
Starts with vasoconstriction, turns into vasodilation
Leukocyte recruitment consists of
Neutrophils being guided to the area through chemotaxis
Phagocytosis
nom nom nom
Aside from histamine and leuktrines, these are key players in inflammation
Prostaglandin
Cell membranes, phospholipids, when inflammation takes place, this phospholipid can be converted into arachadonic acid which is split into
Leukotrines or prostaglandins
The enzyme that is required for leukotrine production is
Lipogenase
The enzyme required to convert arachadonic acid into prostaglandins is
COX
COX
Cyclooxygenase
Term for wbc leaking into tissues
fenestration
How is skin different from mucosa?
skin is distinct from mucosa in that it contains adnexal structures such as the eccrine units that exude sweat and the folliculosebaceous apocrine units that produce hairs and oils