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Ch 21 Microbial Diseases of the Skin and Eyes Part 1 — Transcript

by Dr. T.Lopez · 2,463 words · 482 segments · language en · Watch on YouTube

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0:00chapter 21 covers microbial diseases
0:03of the skin and eyes
0:06in this chapter you're going to
0:07understand the composition of the skin
0:09and normal microbiota that colonizes it
0:12you're going to know the types of
0:13staphylococcal and streptococcal
0:15infections and symptoms
0:16as well as their virulence factors
0:18you're going to be able to recognize
0:20pseudomonas infections
0:21know the three types of acne know the
0:24types of viral skin infections and
0:26symptoms
0:27understand viral latency reactivation
0:29and symptoms
0:30and no types of fungal skin infections
0:34before discussing the normal microbiota
0:36that inhabits the skin
0:38let's take a quick look at the structure
0:39of human skin you can see that the
0:41superficial layer here is the epidermis
0:43followed by the dermis
0:45within the dermis is going to be the
0:47hair follicle which is going to be
0:48responsible for the growth of the hairs
0:50as well as a sebum gland that produces
0:53oil
0:54and sweat glands now these perspiration
0:57or sweat glands and sebum glands are all
0:59contain
1:00nutrients and these nutrients are
1:02actually going to support both the
1:04skin as well as be nutrients for
1:07some microbiota salt does inhibit
1:10most microbes or non-salt tolerant
1:13microbes
1:14there will also be the presence of
1:16lysozymes which is that enzyme that's
1:18going to hydrolyze the peptidoglycan
1:21recall that the lysozyme is produced in
1:24the
1:24sweat glands and so that's going to
1:26inhibit and prevent pathogenic microbio
1:28microbes from inhabiting the skin
1:31there's also fatty acids
1:33that's going to be secreted here from
1:35sebum glands that are going to inhibit
1:37some pathogens so in addition to the
1:40skin and an extension to the skin we're
1:42going to be taking a look at some body
1:44cavities
1:44such as a nasal cavity now body cavities
1:48are going to be lined with mucous
1:49membranes
1:50mucous membranes are going to contain
1:52cells which have goblet cells that
1:54produce mucin
1:56and this mucin secretes mucus on top of
1:59these cells will be the presence of
2:00cilia which are responsible for
2:02moving the mucus around the purpose of
2:05that mucus is actually going to be to
2:06trap particles and prevent any
2:09pathogenic bacteria or prevent any
2:11foreign particles from entering into the
2:13body
2:15normal microbiota of the skin will
2:17contain several gram-positive
2:19salt tolerant bacteria which include
2:22staphylococci
2:23micrococci and some diptheroids and
2:26these are non-pathogenic dip
2:28thyroids now so the staphylococci that
2:31inhabits the skin ninety percent of that
2:33is gonna be staphylococcus
2:35staphylococcus epidermidis and it's also
2:38important to note that these bacteria
2:40are non-hemolytic
2:41so they do not lyse red blood cells and
2:43they're coagulase
2:44negative so they do not coagulate blood
2:47you also have the presence of some fungi
2:50present in skin folds
2:54in addition to salt tolerant bacteria
2:56there are other microorganisms that will
2:58grow
2:59on specific regions of the skin there
3:02are some microorganisms that can
3:04easily grow on oils and there's also
3:06others that have very specific
3:08oxygen requirements those microorganisms
3:11that grow on the surface of the
3:12epidermidis
3:13are a-robes which means they require
3:16oxygen for growth
3:17an example bacteria is corny bacterium
3:19cirrhosis
3:21there are some bacteria that can grow
3:22deep inside of hair follicles
3:24where there's not the presence of oxygen
3:27is not prevalent
3:28and so those will be anaerobe bacteria
3:32an example of an anaerobic bacteria is
3:34propionibacterium acnes
3:36as the name implies you can suspect what
3:39this bacteria does cause
3:41we'll get into this further in a later
3:43slide
3:44now there's also the presence of yeast
3:46that likes to grow on
3:48oily secretions this yeast is malassezia
3:51furfer
3:52and it is associated with dandruff and
3:55the scaling skin condition
3:56shampoos for treating dandruff actually
3:59can contain
4:00an antibiotic ketoconazole as well as
4:03zinc pyrothrium
4:04or selenium sulfide all of which are
4:06active against yeast
4:10now that you understand the normal
4:12microbiota that makes up the skin
4:14let's discuss some pathogenic bacteria
4:16that is responsible for
4:18skin diseases and so one of the most
4:20pathogenic of the staphylococci
4:22is a resident of nasal passages which is
4:25present in about 20 percent of the
4:26population and that's staphylococcus
4:28aureus
4:30staph aureus does have several virulence
4:32factors which help it evade host
4:34defenses
4:35and is also known to be multi-drug
4:37antibiotic resistant
4:39in fact you probably are familiar with
4:41two of the strains
4:42and here on this is going to be a
4:44confluent plate
4:46and there is going to be these
4:47antibiotic discs but i'm going to
4:49draw your attention to this m right here
4:51which actually stands for methicillin
4:53you can see that there's bacteria that's
4:55growing around it and so this is mrsa
4:57or methicillin-resistant staphylococcus
4:59aureus
5:00in the next few slides i'm going to be
5:02discussing some of these virulence
5:04factors that are responsible
5:06for causing uh skin diseases
5:10let's take a look at the effects of
5:11staphylococcus aureus staph aureus
5:14can release two different types of
5:16toxins and that's going to result
5:18in different syndromes toxin a is going
5:20to cause impedigo
5:22whereas toxin b can cause scalded skin
5:24syndrome
5:25what you are observing here this is
5:27actually scalded skin syndrome
5:29and it's actually a characteristic of
5:30the late stages of toxic shock syndrome
5:33so symptoms are going to include this
5:35red in skin and the skin is an appeal
5:38off in sheets so this toxin b is
5:41actually going to be due to an
5:42exfoliative toxin
5:44here you can see the normal skin and
5:46normal skin is actually held together by
5:48desmosomes
5:50in between cells and so an exfoliative
5:52toxin
5:53are actually going to be a type of
5:55serine protease
5:57that's going to selectively recognize
5:59and hydrolyze
6:00desmop desmosomal proteins that are in
6:03the skin
6:04and that's going to cause a skin to fall
6:05off in these sheets and peel off in
6:07sheets
6:08secondary infections too exfoliative
6:11toxins can be pseudomonas and candida
6:14in terms of epidemiology you'll notice
6:16that it's most common newborns
6:18or any individuals who are immune
6:20compromised
6:25moving on to other infections caused by
6:27the staphylococcus aureus bacteria
6:30there can be the penetration and
6:31infections of hair follicles
6:33so that's going to lead to folliculitis
6:35otherwise known as the pimple
6:36as you can see this is actually an
6:38infection of a hair follicle and
6:39accumulation of white blood cells that
6:41are trying to phagocytose that staph
6:43aureus infection
6:44a stye is going to be the same thing
6:46except on an eyelash
6:48a fur uncle will result in an abscess
6:51and the pus is going to be surrounded by
6:54inflamed
6:55tissue now a fur uncle can progress
6:58to neighboring tissues and also infect
7:00other
7:01hair follicles resulting in what's
7:03called a carbuncle
7:05and that's going to be an inflammation
7:06now of multiple
7:08uh hair follicles and the surrounding
7:10tissues
7:12an impenetrable is going to be a highly
7:15contagious
7:16skin infections that's going to
7:17typically infect children about two to
7:19five years of age
7:20this is where crusting or non-bola sores
7:22are gonna
7:23be present and this the spread of
7:26impetigo is caused by direct
7:28contact
7:31now you'll be able to recognize these
7:33staphylococcal skin infections visually
7:35beginning with folliculitis which is
7:37that infection of a single hair follicle
7:40and then here is a fur uncle this is
7:42going to result in
7:43inflammation and the surrounding tissues
7:46a fur uncle can lead to a carbuncle as
7:49you can see here there's
7:50multiple hair follicles that have been
7:52infected
7:54a stye is going to be a folliculitis but
7:56on the eyelash
7:58and then this is going to be impedigo
8:00once again caused by staphylococcus
8:01aureus bacteria
8:03and can be transported or transferred to
8:05another
8:06by direct contact
8:09another virulence factor of
8:11staphylococcal bacteria
8:12is going to be the ability to form
8:14biofilms
8:16biofilms are going to allow for the
8:17attachment onto certain certain surfaces
8:20for example they're actually a common
8:22cause
8:23of nosocomial infections because they
8:25accumulate on catheters
8:27as you can see in these images
8:31while on the topic of nosocomial
8:33infections we can now take a look at
8:34these staphylococcal wound infections
8:37causative agent staph aureus symptoms
8:40will be rather obvious and i'll show you
8:41that on the next slide
8:43pathogenesis is because of the ability
8:45to have this coagulase
8:47enzyme and as well as being able to
8:50evade
8:51host defenses and thereby then producing
8:55toxins that's going to cause us
8:56inflammation now how does a wound
8:58infection come about
8:59that could be from improper wound
9:01cleanliness as well as the transfer
9:04of staphylococcus aureus because of a
9:07source such as from nasal carriers from
9:09other
9:09patients or physicians or as well as
9:13displacing the staphylococcus aureus
9:15from one region
9:16to the next because of surgery
9:20here's a sternal wound infection from
9:23heart surgery that is caused by
9:24staphylococcus aureus
9:26you can see inflammation so this redness
9:29as well as destruction of some tissues
9:33this chart summarizes the virulence
9:35factors of staphylococcus aureus
9:37you'll notice that from these virulence
9:39factors how
9:40it can evade the host defenses produce
9:43toxins
9:44and also destroy tissues and so you can
9:47see one of the variance factors here is
9:49a capsule
9:50inhibits phagocytosis it's coagulased
9:52positive so it produces clots to inhibit
9:56white blood cells to really get to that
9:57site of infection it also can produce
9:59that exfoliative toxin
10:01causing scalded skin syndrome that's
10:03what separates the layers of the
10:05epidermis
10:06it also can produce hyaluronidase to
10:08dissolve connective tissues and
10:10penetrate to deeper tissues
10:12it can produce leukocytes which lyse
10:15white blood cells and also can produce
10:17hemolysins
10:18which lyse red blood cells it does have
10:21the presence of a lipase which degrades
10:24lipids
10:25proteases which breaks down proteins
10:27protein a which is actually going to
10:29inhibit phagocytosis
10:31and produced toxic shock syndrome
10:34toxin which is a super antigen
10:38the next type of bacteria that causes
10:40skin infections is going to be
10:41streptococcus pyogenes
10:44and you can see that from the genus this
10:46is a chain like
10:47coccy morphology bacteria beta-hemolytic
10:51streptococci
10:52is going to be the one that's associated
10:54with human diseases
10:56beta-hemolytic strep is going to be
10:57further classified according to
11:00different serological groups designated
11:03a through t
11:04and this is dependent on the antigenic
11:06carbohydrates of the cell
11:08wall group a strep is the most common
11:12and pathogenic of the streps and that's
11:14going to include streptococcus pyogenes
11:17during growth there will be the
11:18production of enzymes and other
11:20virulence factors
11:21that are responsible for local tissue
11:24destruction
11:25and possible sepsis on the right you
11:27will actually
11:28see here this is an irisy palace which
11:30is responsible
11:31or streptococci is responsible for the
11:33formation
11:34of the ceresi pellets otherwise known as
11:36holy fire you'll notice that there is no
11:38inflammation as also
11:39no pus formation
11:43group a streptococci or gas as it's
11:46abbreviated
11:47will have an m protein found on
11:50external cell wall on a fuzzy layer of
11:53fibrils
11:54you can actually see on the right here
11:55this is going to be fibrils that
11:57lack that m protein and on this side
12:00this is actually group a streptococci
12:02with the m protein and the purpose of
12:04this m protein is to evade the immune
12:06system
12:07and it will actually prevent the
12:08activation of complement and allows the
12:11microbe to evade phagocytosis
12:15in addition to erecipellas group a strep
12:18can also result in necrotizing fasciitis
12:21otherwise known as the flesh eating
12:23bacteria and this is from getting into
12:25minor breaks in the skin
12:27and causing these tissue destruction
12:30a group a strep will also have the
12:31presence of an exotoxin a that's going
12:33to act as a super antigen
12:35resulting in that massive cytokine storm
12:38and that's going to lead to
12:39streptococcal toxic shock syndrome
12:42of which there's only an 80 percent
12:44mortality rate from
12:48group a beta hemolytic streptococcus
12:50pyogenes is going to be the most common
12:52and pathogenic of the streptococci
12:54you can see that it contains several
12:56virulence factors
12:57with one of the more more notable
12:59factors is going to be this m
13:01protein that's going to prevent
13:02activation of the complement
13:04and inhibit phagocytosis in addition
13:08when it's shed from the bacteria it's
13:09going to form a complex with fibrinogen
13:12that's going to activate neutrophils
13:13leading to that streptococcal
13:15uh toxic shock syndrome as you saw with
13:17the necrotizing fasciitis in addition to
13:20this
13:20it does have the presence of an exotoxin
13:23exotoxin a
13:24that is going to result in the super
13:26antigen further leading to
13:27toxic shock syndrome another bacteria
13:31that can cause significant skin
13:33infections
13:34are the pseudomonads and you may be
13:36familiar with pseudomonas aeruginosa as
13:38we have covered this one in lab
13:40it is a gram-negative aerobic bacillus
13:43bacteria
13:45and it does produce this green
13:47coloration
13:48or blue green coloration that's an
13:50extracellular pigmentation
13:52pseudomonas ruganosa is common in water
13:55and
13:55soil and it's highly resistant to many
13:57antibiotics
13:58and disinfectants
14:02pseudomonas can be found in water and
14:05thrive
14:05in some dilute disinfectants it can be
14:08present in chlorinated pools and waters
14:10an infection from these areas will
14:13result in
14:14pseudomonas dermatitis a self-limiting
14:16rash that can resolve within two weeks
14:19another type of infection is swimmer's
14:21ear that's going to result in this
14:23inflammation of the external ear called
14:25otitis externa
14:27in addition to this immunocompromised
14:31individuals can be susceptible to this
14:34infection
14:35so this bacteria is highly opportunistic
14:38and can impair wound healing
14:40particularly for
14:42post-burn infections and individuals who
14:44had suffered second and third degree
14:46burns
14:50the next type of skin infection i'm
14:51going to discuss is acne
14:53and there are three types the first type
14:55you see here is called comodonal
14:57acne in normal situations there are
15:00cells that are shed
15:01and they can fall into these channels
15:04most of the time they are pushed out
15:06in comadonal acne this the shed cells in
15:10combination with sebum are going to
15:12cause a blockage of these channels
15:15treatments for comadonal acne can be
15:17exfoliating facial washes
15:19salicylic acid preparations and more
15:21rarely retinoids
15:23also note that comedonal acne is not
15:26caused by any bacterial infections
15:30the second type of acne is inflammatory
15:33acne
15:33and this is the result of an infection
15:36by bacterium
15:37the bacterium that causes inflammatory
15:39acne is propionibacterium acnes
15:42recall that this bacteria is present in
15:44hair follicles
15:46and is highly anaerobic treatments for
15:49inflammatory acne because this is a
15:51bacteria
15:52can be antibiotics such as tetracycline
15:57the third type of acne is nodular cystic
16:00acne
16:00this is the result of propiono bacterium
16:04acnes
16:05in which there is a prolonged bacterial
16:07infection
16:08causing an inflammatory response and
16:10eventually a formation of a large
16:12abscess or nodular cyst treatments for
16:15nodular cystic acne can be
16:17more intensive one such treatment is
16:20accutane or isotretinoin but before
16:23taking
16:23accutane an individual does need to sign
16:26an i pledge
16:27contract or and understand the i pledge
16:30program
16:31as accutane can result in the loss of
16:34pregnancy

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