Microbiology Exam 4

the new material on the final exam

pathogenesis

the process by which a pathogen causes disease

steps of pathogenesis

entry into host, attachment colonization, avoidance of immune system, cause damage to host, exit from host

virulence factors

various features which help pathogen accomplish the goals of causing disease

genomic island

a region of a bacterial chromosome that was acquired recently through horizontal gene transfer. it possesses a GC content that is different from the rest of the genome

pathogenicity island

a genomic island that contains virulence factors. absent in closely related non-pathogens

entry and colonization

pathogens must bind to specific target tissues to avoid clearance. several mechanisms have evolved to achieve this goal

pili (fimbriae)

a protein extension made up of the subunit pilin. the tip of the pilus is an adhesion protein that binds to host cell receptors. the pili tip is assembled first, and then extended away from the cell by sequential addition of pilin monomers at the bottom of the stalk

type I pili

static hair-like appendages only used for attachment

type IV pili

can extend and retract. used for twitching motility

non-pili adhesions

other molecules that can attach to surfaces but are not composed of pilin. a mixture of protein, carbohydrate, and lipid molecules

biofilm

can help organisms adhere to surfaces. the matrix sticks to surfaces and protects bacteria from harmful chemicals. are difficult to remove from surfaces which is a contributing issue for hospital-acquired infections

immune system avoidance

pathogens can sense conditions present with the host, and express virulence factors when these conditions are met. these factors help hide the pathogen.

virulence factors for immune system avoidance

capsule prevents phagocytosis, vary surface antigen structure to evade detection, bind antibodies, secrete fake cytokines, manipulate cytokine production

intracellular pathogens

some pathogens grow within host cells to avoid the immune system.

facultative intracellular pathogen

can survive inside or outside of host cells. ex. Salmonella

obligate intracellular pathogen

can only reproduce inside of host cells. ex. Rickettsia

intracellular pathogens in phagosomes

some species replicate within this kind of vesicle since they possess enzymes that neutralize digestive enzymes. some species breakout of these vesicles. some species prevent digestive enzymes contained in lysosomes from fusing with this type of vesicle.

host damage and manipulation

many pathogens can directly damage cells through production of toxin molecules

immunopathology

damage to host tissue caused by the immune response

exotoxins

secreted molecules that have a wide variety of effects on target cells. are proteins that can have a variety of functions

exotoxin potential functions

can disrupt plasma membrane, lysing cells, disrupt protein synthesis, disrupt cell cycle, block exocytosis, redirect vesicle traffic, disrupt cell-cell adhesion, disrupt signal transduction

Alpha toxin (Staphlyococcus)

forms pores in the cell membrane and causes cell to lyse

E. coli, S. enterica, S. flexneri

induced diarrhea (disrupting signal transduction)

AB toxin

an exotoxin composed of two distinct protein molecules

structure of AB toxin

the A subunit is toxic, the B subunit delivers subunit A into target cell. most AB toxins have five B subunits arranged around one A subunit. the A subunit transfers an ADP-ribosyl group (from NAD) to target proteins, which inactivates them

Anthrax toxin (Bacillus anthracis)

has two separate A subunits, the edema factor and the lethal factor

B antigen of Anthrax toxin

called the protective antigen

edema factor subunit

causes fluid loss from target cells

lethal factor subunit

cripples the immune system

toxin secretion

many delivery systems evolved from proteins originally involved in locomotion

type II secretion system

evolved from type IV pili (twitching motility), toxin molecule is loaded into the system, which then acts like a piston to push the molecule out of the cell

type III secretion system

syringe system used to directly inject toxin into host cells. Salmonella uses this system to disrupt intestinal epithelial cell ion regulation

type IV secretion system

evolved from conjugation system, tube that allows toxin to diffuse out of the cell from the cytoplasm

endotoxins

lipopolysaccharides part of the outer membrane of Gram-negative cells. released upon cell death

functions of endotoxins

induce fever, activate clotting factors, vasodilation, shock and death may occur if endotoxins enter blood

viral pathogenesis

viruses use resource in host cells to make more viral particles. viruses have evolved numerous ways to subvert the immune system

different viral pathogen systems

alter cytokine production, interfere with MHC-I presentation, inhibit apoptosis, increase host cell division, enter latency to hide from immune system, infect immune cells directly

rhinovirus

naked ssRNA+, pathogen that causes colds. there are >100 different serotypes, which are distinct antigens compared to other serotypes. have antigen variation

antigen variation

immunity to one serotype does not grant immunity to others (antibody will not bind)

influenza virus

enveloped ssRNA-, segmented genome. genome is 8 discrete pieces of RNA. pathogen that causes influenza, different strains can infect various mammals and birds. have antigenic drift AND antigenic shift

antigenic drift

random mutations during genome replication result in small changes in virus proteins that add up overtime. viruses mutate much faster than cells because they lack repair enzymes

antigenic shift

unique to influenza, arises due to genetic reassortment. different strains of the virus can co-infect the same cell because there is eight pieces of RNA instead of one single molecule. When new virions are packaged, the eight pieces can be assembled from multiple sources leading to a completely new strain. Pigs are a common location for this to occur, because they can be infected by mammalian and avian influenza viruses.

HIV

enveloped, ssRNA + . is a retrovirus, infects T_H cells by binding to CD4 and CCR-5 receptors

retrovirus

converts RNA to a DNA molecule which integrates into host genome

Human Papillomavirus (HPV)

naked dsDNA, common cause of genital warts, viral protein E7 inhibits regulation of mitosis, which can lead to cancer. most common cause of cervical cancers

Herpes simplex virus (HSV-1 and 2)

enveloped, dsDNA. cause of cold sores or genital herpes. during a primary infection, can become latent in host neurons or white blood cells.

HSV-1

cause of cold sores, fluid filled blisters on the skin. enters nerves of jaw and goes dormant. can reactivate due to stress/ trauma.

HSV-2

cause of genital herpes

primary infection of HSV

can become latent in host neurons or white blood cells. DNA circularizes and becomes an episome. can reemerge after years of latency and begin a new infection cycle. ~50% of humans have a latent HSV infection

protozoan pathogenesis

pathogens of this group also exhibit antigen variation, with different life cycle stages of the same pathogen often presenting different antigens. others coat themselves in host antigens to evade immune detection. others induce secretion of anti-inflammatory cytokines to reduce the effectiveness of the host immune response

integumentary system

skin, nails, hair, cutaneous glands

skin regions

two parts: epidermis and dermis

epidermis

superficial, avascular, multiple layers of keratinocytes, some immune cells

dermis

deep thick area containing accessory organs

antimicrobial defenses of skin

keratin is durable and difficult to damage, excessive salt, antimicrobial chemicals, and sebum’s acidity

skin microbiome

varies depending on location, inhibits pathogen binding by taking up space. some members (S. aureus) are opportunistic pathogens

rash

many skin infections result in a change in color and texture of the skin

exanthem

widespread skin rash accompanied by systemic symptoms

enanthem

rash on mucous membranes

macular rash

flat and red rash

papular rash

small, solid, and elevated

pustular rash

a papule filled with pus

maculopapular rash

a reddened popular rash

vesicular rash

formation of small blisters

acne pathogen

Cultibacterium acnes

acne

an immune response to the presence of Cultibacterium acnes, excessive oil production, and hormones (most common during adolescence when hormone production is high). blockage of hair follicles and sweat/oil glands results in black/whiteheads

staphylococcal skin diseases pathogens

various Staphylococcus spp. but most commonly S. aureus

Staphylococcal skin diseases

various lesions or boils form as immune cells attack pathogens that have invaded areas of the dermis. either through pores/ hair follicles or damaged areas of the skin

abscess

confined, pus-filled skin lesion

folliculitis

lesion at the base of a hair follicle

furuncle

larger, painful boil

carbuncle

multiple connected furuncle

impetigo and scalded skin syndrome

diseases caused by the toxins produced by S. aureus

impetigo

superficial blisters, highly contagious

scalded skin syndrome

most common in children < 5, toxins cause desquamation

desquamation

shedding of outer layer of skin, superficially looks like 2nd degree burns

toxic shock syndrome

a systemic disease which occurs when S. aureus toxins enter the blood stream. massive inflammatory response causes fever, vomiting, diarrhea, aches, sunburn rash, sudden low blood pressure, and heart failure. prompt treatment is essential for survival. can also be a staphylococcus disease

streptococcus skin diseases pathogen

various Streptococcus spp.

cellulitis

Streptococcus disease, severe, fast spreading infection of dermis and subcutaneous tissue

erysipelas

streptococcus disease, superficial cellulitis (upper dermis)

necrotizing fasciitis

streptococcus disease. destruction of muscle, fat, and soft tissue by strep toxins. amputation may be required to prevent spread

gas gangrene pathogen

Clostridium perfringens

gas gangrene

acquired from soil contaminating wound, multiple toxins cause tissue death, gas production by microbes produce foul smell

herpes simplex pathogens

viruses in the family Herpesviridae, dsDNA viruses

chicken pox

varicella-zoster virus, vesicular rash with blisters filled with fluid

shingles

reactivation of VZV in adults, icepick pains and vesicular rash encircling trunk, can cause long term pain (years) if virus enters nerves

measles pathogen

measles virus (Paramyxoviridae family - sense RNA)

measles symptoms

hacking cough, runny nose, high fever, Kolpik spots in mouth, full body rash

measles

highly contagious through respiratory droplets, capable of destroying immune memory cells, erasing adaptive immunity

rubella (german measles) pathogen

rubella virus (+ sense RNA)

rubella (german measles)

fever, runny nose, swollen lymph nodes, full body rash. can induce miscarriage or birth defects in pregnant women

fifth disease (erythema infectiosum) pathogen

human parvovirus B19

fifth disease (erythema infectiosum)

replicates within erythrocyte progenitor cells, then spreads via blood. slapped cheek rash is followed by popular rash on the throat or palate. maculopapular rash forms on body and limbs (lace rash)

roseola infantum pathogen

HHV-6, HHV-7

roseola infantum

transmitted via saliva or respiratory secretions, symptoms in children < 3 years old

roseola infantum symptoms

high fever followed by maculopapular rash that blanches when touched, many people carry latent infection

warts pathogen

various, HPV-1 and HPV-2 most common (human papillomavirus dsDNA)

warts

growths form at infected skin

warts treatment

area is typically frozen, and dead cells physically removed

smallpox pathogen

variola virus