Diebel - Bacteiral Skin Infections Flashcards

1
Q

What bacteria causes acne? What are some characteristics of the bacteria?

A

P. acnes – gram (+) rod, aerotolerant. Resident in low levels on the skin – not transmissible.

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2
Q

What is impetigo?

A

superficial bacterial infection that causes the skin to flake or peel off. Usually not serious but is highly contagious. Most common in children. Can be caused by Staphylococcus aureus and/or Streptococcus pyogenes.

S. Pyogenes initiates the lesion and in some cases S. aureus takes over. S. aureus kills off S. pyogenes so sometime S. pyogenes is missed in culture-based diagnosis.

The lesions look like peeling skin, crusty and flaky scabs, or honey-colored crusts. Usually found around mouth or face and extremities (can occur anywhere). Presentation is the same for both Staphylococcus and Streptococcus

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3
Q

What are some characteristics of staphalococcus aureus?

A

Gram + cocci.
catalase +
coagulase +
Common and severe human pathogen. Can cause pneumonia, food poisoning, bloodstream infections, bone infections, toxic shock syndrome, and meningitis. Non-motile bacteria that causes destruction due to the production of superantigens. Grows best at 37C. Facultative anaerobe. Can grow in high salt and low pH.

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4
Q

How does Staph. Auerus colonize the skin and avoid host defense?

A

The bacteria will secrete Protein A which will then bind to constant region of an antibody (the Fc portion). This essentially flips the antibody around so that the variable region of the antibody can’t bind to the bacteria and lead to compliment activation

also

coagulase (forms fibrin coat around the organism)
hemolysins and leukocidins (destroy RBCs and WBCs)

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5
Q

What are virulence factors of Staph. Auereus?

A

Hyaluronidase (breaks down connective tissue)
Staphylokinase (lyses formed clots)
Lipase (breaks down fat)

leads to Toxic shock syndrome and Scalded skin syndrome

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6
Q

What is toxic shock syndrome?

A

Toxic shock syndrome = toxic shock syndrome toxin-1 (TSST-1), diffuses systemically, superantigen (promotes excessive cytokine release (IL-1, TNF)). Results in acute fever, rash, desquamation on palms and soles, hypotensive shock, organ dysfunction, possible death

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7
Q

What is scalded skin syndrome?

A

Scalded skin syndrome = most often effects children, exfoliative toxins ET-A and ET-B, diffuse systemically, epidermis separates and skin sloughs off, fluid loss, secondary infection, possible death (50% mortality rate in adults, Ritter’s syndrome severe in neonates (umbilical cord infection)).

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8
Q

Characteristics of Streptococcus pyogenes?

A
Gram + cocci.
 Catalase – 
beta-hemolytic
bacitracin sensitive.
 May be normal flora of the skin.

Localized skin/subcutaneous infection = impetigo, erysipelas, cellulitis

Toxin-mediated = Toxic shock syndrome, necrotizing fasciitis

Also causes strep throat, scarlet fever, pneumonia, puerperal fever, nectrotizing faciitis, bloodstream infections, rheumatic fever, glomerulonephritis.

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9
Q

Virulence factors of Strep. Pyogenes?

A

Streptokinase (converts plasminogen to plasmin)
M protein (resists phagocytosis)
Hyaluronidase (breaks down connective tissue)
DNase (digests DNA)
Streptolysin O (destroys RBCs)
Streptolysin S (destroys WBCs)

leads to Toxic shock syndrome and Necrotizing fasciitis

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10
Q

What is nectrotizing fascitis?

A

Necrotizing fasciitis = trauma allows for deep seated infection -> release of exotoxin B (protease) -> rapid necrosis along fascial planes with no damage to muscles

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11
Q

What is the catalase test?

A

Aerobic and facultative anaerobic organisms produce reactive oxygen species during normal metabolism, hydrogen peroxide (H2O2) and superoxideradical (O2−). These bacteria have multiple enzymes that detoxify the products of normal metabolism. One of these enzymes, catalase, is capable of converting hydrogen peroxide to water and oxygen. The presence of the catalase is possible by putting a small inoculum of bacteria into hydrogen peroxide. With catalase present there is a rapid release of oxygen bubbles. The lack of catalase is evident by a lack of or weak bubble production.

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12
Q

How can catalase test be used to differentiate between micrococcus, streptococcus, and staphalococcus?

A

Test differentiates between catalase-positive micrococcal and staphylococcal species from catalase-negative streptococcal species.

Micrococcus are rarely implicated in infections but can be differentiated from Staph by aerobic growth requirement, lack of sugar fermentation (glucose/lactose), and they are sensitive to bacitracin.

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13
Q

What is the coagulase test?

A

S. aureus produces two forms of coagulase, bound and free. Bound coagulase, or “clumping
factor,” is bound to the bacterial cell wall and reacts directly with fibrinogen. This results in
precipitation of fibrinogen on the staphylococcal cell, causing the cells to clump when a bacterial suspension is mixed with plasma.

S. Aureus is the only coagulase + staph.

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14
Q

How does coagulase test differentiate between staph infections?

A

Used to differentiate between Staphylococcus aureus (positive) from coagulase-negative staphylococci (negative). Common coagulase-negative staph– are: S. Epidermidis, and S.Saprophyticus

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15
Q

How to differentiate between a coagulase - Staph?

or how to differentiate between S. Epidermidis, and S.Saprophyticus?

A

You can tell difference by using Novobiocin sensitivity.
Novobiocin inhibits bacterial DNA gyrase in susceptible microorganisms.

so this test is used to differentiate between Staphylococcus saprophyticus (resistant) from Staphylococcus epidermidis (sensitive).

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16
Q

How to tell from micrococcus from staphalococcus?

A

Micrococcus are rarely implicated in infections but can be differentiated from Staph by aerobic growth requirement, lack of sugar fermentation (glucose/lactose), and they are sensitive to bacitracin.

17
Q

What is cellulitis?

A

It is a fast-spreading infection in the dermis and in the subcutaneous tissues. It causes pain, tenderness, swelling, and warmth. Fever and swelling of the lymph nodes draining the area may also occur. Cellulitis generally follows introduction of bacteria or fungi into the dermis. Symptoms take several days to develop. The most common causes of the condition in healthy people are Staphylococcus aureus and Streptococcus pyogenes.

Mild cellulitis responds well to oral antibiotics chosen to be effective against both S. aureus and S. pyogenes. More involved infections and infections in immunocompromised people require intravenous antibiotics. If there are extensive areas of tissue damage, surgical debridement is warranted.

18
Q

Staphylococcal Scalded Skin Syndrome

A

It affects mostly newborns and babies, although children and adults can experience the infection. Newborns are susceptible when sharing a nursery with another newborn who is colonized with S. aureus. Transmission may occur when caregivers carry the bacterium from one baby to another
it is an exotoxin-mediated disease (systemic form). ET-A and ET-B.
Toxins gain access to the bloodstream. Lose dead skin layer all over the body = susceptible to secondary bacterial infections.

It is more systemic than impetigo. It does use the same toxins as impetigo though.

19
Q

Gas gangrene

A

caused by Clostridium perfringens (gram + rod which can produce sports - which also can cause cellulitis)

Toxins produced in large muscles, such as the thigh, shoulder, and buttocks, diffuse into nearby healthy tissue and cause local necrosis there. This damaged tissue then serves as a focus for continued clostridial growth, toxin formation, and gas production. The disease can quickly progress through an entire limb or body area, destroying tissues as it goes. Initial symptoms of pain, edema, and a bloody exudate in the lesion are followed by fever, tachycardia, and blackened necrotic tissue filled with bubbles of gas

Clostridia are not highly invasive, infection requires damaged or dead tissue, which supplies growth factors, and an anaerobic environment. The low-oxygen environment results from an interrupted blood supply and the presence of aerobic bacteria, which deplete oxygen. Such conditions stimulate spore germination, rapid vegetative growth in the dead tissue, and release of exotoxins. C. perfringens produces several active exotoxins; the most potent one, alpha toxin, causes red blood cell rupture, edema, and tissue destruction.

Treatment includes immediate and rigorous cleansing and surgical repair of deep wounds, decubitus ulcers (bedsores), compound fractures, and infected incisions. Debridement of diseased tissue eliminates the conditions that promote the spread of gangrenous infection. Penicillin and clindamycin can be used for antibiotic therpapy.

20
Q

Clostridium perfringens

A

Obligate anaerobe, they can’t survive even in low oxygen conditions.
Pathologies: Cellulitis, gas gangrene (myonecrosis with crepitus), food poisoning.
Treat: Surgical removal of infected areas. Hyperbaric oxygen to kill anaerobic organisms. Penicillin or clindamycin (effective only in local, weak infections).

21
Q

Describe pathologies of Clostridium perfinges

A

Cellulitis: pick up the bacteria from the soil where the bacteria infect the anaerobic environment of a necrotic skin wound. The bacteria release degradative enzymes which results is a slow, painless infection with gas production. Forms collections of gas under the skin that crackle when touched (crepitus).

Gas gangrene: pick up spores from the soil where they get introduced into deep muscle lacerations (military wounds, auto accidents, etc). Spores germinate and bacteria grow in the anaerobic environment releasing toxins and degradative enzymes that degrade muscle tissue and form gas. Black fluid may leak from the skin. Shock is possible.

22
Q

Pseudomonas aeruginosa

A

Gram – bacili
Lactose non-fermenter
Oxidase +
Glucose non-fermenter

Occasional cause of bacterial skin infections. “Hot tub folliculitis”
Burn wound infection (cellulitis) and folliculitis (hot tub infection)
Inhabits many environments such as the soil, water, and large intestine. Infection arises by breach of host defense barriers.

23
Q

Lyme Disease

A

Causative agent = Borrelia burgdorferi. Carried in small mammals such as mice -> Ixodes tick transmits from mice to humans -> spirochetes disseminate systemically.

Three stages Stage 1 (10 days after bite)
Erythema chronicum migrans

Stage 2 (weeks later)
CNS involvement – Bell’s palsy, aseptic meningitis, peripheral neuropathy
CV – carditis, AV nodal block
Skin – secondary annular lesions
Joints – migratory myalgias, transient arthritis

Stage 3 (month to years later)
Chronic arthritis, encephalopathy, acrodermatitis chronicum atrophicans
24
Q

Rocky Mountain Spotted Fever

A

Causative agent: Rickettsia rickettsii
Clinical Presentation: Rash, fever, headache

Carried in dogs, rodents -> bite of the Dermacentor wood or dog tick transmits to humans -> organism infects and proliferates in endothelial cells -> inflammation of endothelial lining of small blood vessels -> maculopapular rash on palms and soles SPREADING TO THE TRUNK -> widespread vasculitis -> headache and CNS changes, renal damage -> may lead to death if left untreated

25
Q

What are some characteristics of Rickettsia Ricketsii?

A

Obligate intracellular parasites that need host ATP = Chlamydiae and Rickettsiae (can’t make its own ATP).