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