MicroBio Quiz 5 - Part one ( Chapter 17 and 19)

hypersensitivity

inappropriate immune

response that results in host damage

~20 percent of population suffers from allergies to a wide variety of agents.

Stages of Type I hypersensitivity

• Overreaction to a foreign antigen and cause more damage than

the antigen alone might cause

• Immediate and severe: anaphylaxis - a severe and potentially life-

  threatening allergic reaction that can affect multiple organs in the

  body

   Can be mild and localized

  • Hay fever

  – Rhinitis, watery itchy eyes, and sneezing

   Systemic response

  • Swelling (edema), low blood pressure, cardiovascular collapse,

  breathing difficulties, suffocation

Allergen

Antigen triggers overreaction of immune response

Determining the cause of type 1

• Allergens are delivered locally to the skin to determine if there

  is an inflammatory reaction.

  • This skin test is useful in identifying the antigen to which a

  patient is allergic.

Antihistamines

counters histamines (Benadryl, Claritin, Allegra)

At later phase of anaphylaxis, antihistamines have little effect so one needs to use….

Steroids  minimize inflammation

• Bronchodilators (e.g., albuterol) to widen bronchioles and facilitate

breathing

• Severe asthma attack – Epinephrine (adrenaline) opens airways to

ease breathing

Prevention of sensitization:

omalizumab (Xolair) for allergic asthma. It

is monoclonal antibody that bind to IgE antibody and prevent IgE from

binding to mast cells. Used to treat patients who don’t show

improvements with steroids.

Desensitization (allergy vaccination):

done thru injecting small but increasing doses of allergen over months  production of antibody that binds to allergen before they bind to mast cells. But results vary and success is not guaranteed.

ABO blood group system

Four major groups are A, B, AB, and O

• Incompatibility occurs

– Specific antibodies in serum bind

to antigen on foreign red blood

cells (RBCs)

Blood incompatibility example

Individual with B blood type

– Carries anti-A antibodies

– Anti-A antibodies attack

transfused RBCs with A antigen

– Cell lysis

Immunodeficiency

Animals (humans included)

– B cell deficiencies -> prone to bacterial infections

– T cell deficiencies -> prone to viral infections and cancers

SCID

Severe combined immune deficiency syndrome

• congenital deficiency of both B and T cells.

– restricted life, limit exposure to pathogens (“Boy in the Bubble” syndrome)

• No T cells are made.

• By 6 months of age, most SCID infants develop recurrent infections.

• Treatment is bone marrow transplant or intravenous immunoglobulin (IVIG).

AIDS

Acquired Immunodeficiency syndrome

• caused by HIV infection -> kills CD4+ T cells.

– No T cell help -> opportunistic infections and cancer

Primary immunodeficiencies

have a genetic basis and usually manifest in early childhood

Secondary immunodeficiencies

can be acquired at any age.

• Infection (HIV)

• Immunosuppressive drugs

• Radiation therapy

DiGeorge syndrome

Caused by mutations in several genes

• Results in incomplete development or absence of thymus

and parathyroid glands

– Immunodeficiency includes T-cell deficiency.

• Treatment involves thymus transplant.

Cancer, or a neoplasm

defined as new growth of abnormal cells.

Tumors

masses of abnormal cells that occur in tissues

Benign tumors

slow growing and self-contained.

Malignant tumors

grow rapidly and can spread to other tissues.

Immune surveillance

The immune system functions to detect and eliminate cancer cells as they arise

• Dysregulation of the immune system can result in a variety of

  cancers.

Lymphoid

tissue responsible for producing lymphocytes and antibodies

Lymphocytes

T cells, B cells, natural killer cells

Lymphoma

a solid mass in a lymphoid organ

Leukemia

malignant lymphoid cells found in circulation or bone marrow

Plasmocytoma

cancerous plasma cells that are found in a single site

Multiple myeloma

cancerous plasma cells at multiple sites, mainly throughout the bone

Lymphoid cancers

start in the immune system and tend to affect the whole body early on, while other cancers start in specific organs or tissues and usually cause localized tumors before spreading.

B-cell and plasma cell neoplasms

Activation of oncogenes (gene that has the potential to cause cancer) can cause proliferation of B cells and plasma cells leading to a number of cancers.

– Burkitt’s lymphoma

– Chronic lymphocytic leukemia

– Hodgkin’s lymphoma

– Non-Hodgkin’s lymphoma

Autoimmunity: self-tolerance

B and T cells learn not to

react with self antigens.

o T cells

• Deleted in the thymus

o B cells

• Undergo apoptosis in bone marrow

Autoimmunity: loss of self-tolerance

Autoimmune disease

o Results in tissue damage

Type 1 Diabetes (1.3 Mill in US)

Cannot make insulin (allows glucose to go from blood to cells)

 Excessive glucose in blood, hungry, frequent urination, very thirsty

• Autoimmune disease prevents insulin production (bodies own T-cells

  attack insulin-producing cells in pancreas)

   4 – 6 year old kids

Type 2 Diabetes (37 Mill in US)

insulin resistance: Body makes insulin, but does not respond to it:

Adults mostly (becoming more common in kids and teens), mostly for

people 20% over target body weight

Type 1 diabetes how it occurs

pancreas makes a hormone called insulin using special cells

called beta cells

• Insulin helps sugar (glucose) move from your blood into your

body’s cells for energy  This keeps your blood sugar level

normal.

• In Type 1 diabetes, your immune system attacks your own

beta cells by mistake — as if they were germs.

• This destroys the cells that make insulin. Without insulin,

sugar can’t get into your cells, so it stays in your blood and

builds up

Type 1 diabetes - symptoms and treatments

Symptoms: high blood sugar, feeling tired, thirsty, frequent

urination

• Treatment: insulin injection/pump, blood sugar monitoring

superficial layer of skin (epidermis)

Five layers

• Dead keratinocytes (epidermal cells)

– Keratin (hair, feathers, hoofs, claws)

Deep layer (dermis)

Connective tissue

• Cells

• Blood vessels, nerves, hair

follicles, sweat glands

Exanthem

widespread skin rash accompanied by systemic symptoms (fever, malaise, headache)

Enanthem

rash on mucous membranes

A rash is cause by an infectious agent

A reaction to a toxin produced by

o the organism

o damage to the skin by the organism

o an immune response

Macular Rash

flat and red, less than 1 cm in diameter. A macule is a flat lesion that cannot be palpated, like a freckle.

Papular rash

small, solid, and elevated. A papule is a raised lesion resulting from the accumulation of material, infectious or otherwise, in the dermis.

Pustular rash

a papule filled with pus. A pus-filled raised lesion on the skin is called a pustule. It is usually the result of a buildup of the cellular debris of inflammatory cells, with or without microorganisms, under the epidermis

maculopapular rash

a papule that is reddened

vesicular rash

Small blisters are formed. A vesicle forms from the accumulation of fluid under the epidermis. <5 mm, Blister > 5mm

Mucous membranes (called mucosae; singular, mucosa)

Epithelial

• Serve as barrier (protection)

• Line the inside of the body

• Continuous with the skin in several places

Measles (rubeola)

Negative-sense, single-stranded RNA virus

• Very contagious (8‒10 day incubation period)

• Portal of entry is respiratory or conjunctiva

• Replicates in the lungs

– Moves to regional lymph nodes

– Produces a viremia (presence of virus in

bloodstreams) that spreads throughout the body

• Prodromal period (initial symptom to full

development) starts with cold/flu-like symptoms.

• High fever (40°C/104°F)

• Koplik’s spots

– White spots on the buccal mucosa (lining of the inner

cheeks)

Immunocompromised patients can develop serious

complications

– Death

– Blindness (ulceration of the cornea)

– Myocarditis (inflammation of the heart muscle) or pericarditis

(inflammation of the pericardium)

– Variety of GI maladies

• Serious complications include

– Acute disseminated encephalomyelitis (ADEM)

– A delayed complication called subacute sclerosing

panencephalitis (SSPE)

Chickenpox

Herpesviridae family

• Varicella-Zoster virus (VZV)

• Initial exposure = chickenpox

– Virus remains latent in the dorsal root ganglia.

– Re-emerges later in life in about 20% of patients, which causes

shingles

• Shingles occurs more frequently in older individuals.

– Cell-mediated immunity decreases.

• Chickenpox and shingles are usually diagnosed clinically, but

antibody and DNA tests can also be used to detect the virus.

Inhalation of infected particles from skin lesions

– Virus replicates in the nasopharynx and infects the regional

lymph nodes, leading to viremia.

– Second round of viral replication takes place in the liver and

spleen.

o Followed by a secondary viremia 14–16 days postinfection

• VZV invades capillary endothelial cells and the deepest layer of

the epidermis.

• Children do not usually have prodromal symptoms and first

come down with itchy rash on the face, back, chest, and

belly that includes maculopapules, vesicles, pustules, and

scabs.

Can be life-threatening in immunocompromised patients

• Latency

– Established when viral DNA integrates into host DNA

– Can last for decades

– Virus infects the nerve endings of the skin.

– Travel along nerves to ganglia where they lie in a dormant state

– Latent virus reactivation

o Virus particles travel along the sensory nerves of the skin to produce

a localized, painful, dermatomal rash known as shingles.

Chickenpox treatment

Treated with antihistamines, oatmeal baths, and calamine

lotion

– Goal is to reduce and control the intense itching and use

acetaminophen to reduce pain and fever.

• Acyclovir is used to treat shingles.

– Used only for severe or complicated cases of chickenpox

• Varicella vaccination

– Routine childhood immunization schedule

– Varicella vaccine is a live, attenuated form of VZV.

• Persons 60 years and older should be vaccinated with the

zoster vaccine to prevent shingles.

Warts

• Caused by human papilloma virus (HPV) of the family

  Papillomaviridae

  • Transmitted by contact

  • Enters cell via an endosome by a receptor-

  mediated mechanism

  • HPV DNA leaves the endosome, enters the

  nucleus.

  • Viral proteins interfere with cell proliferation

  controls.

  – Infected cell replicates uncontrollably, producing warts.

  • Treatments include freezing, burning, and

  surgical removal.

Warts treatment/prevention

HPV-6 and HPV-11 infect the mucous membranes of the ano-

genital region.

– Cause 90% of genital warts (condyloma acuminata)

• HPV subtypes 16 and 18 have more serious consequences.

– Linked to 70% of human cervical cancers

• Vaccines are available.

– Must be administered before the recipient (male or female) is

sexually active to ensure effectiveness

Staphylococci associated with skin infections include

• Staphylococcus epidermidis

• Staphylococcus aureus

– Normal inhabitant of the nares (nose)

– Can infect a cut and gain access to the dermis via a hair follicle

S. aureus

possesses enzymes that contribute to disease.

• Coagulase coats the bacteria with fibrin and walls off the

infection from the immune system and antibiotics, promoting

abscess (pustular) formation.

 Staph infections routinely require surgical drainage and

antibiotic therapy.

 Exotoxins damage host tissue and weaken host defenses.

Toxic shock syndrome toxin (TSST)

Superantigen causes toxic shock syndrome.

Exfoliative toxin

Superantigen causes a blistering condition in children called scalded-skin syndrome

Staphylococcal skin infections

S. aureus infection of hair follicles can be superficial or deep

resulting in:

– Folliculitis (superficial)

– Boil or furuncle (deep)

o Carbuncles are boils joined together.

Methicillin-resistant S. aureus (MRSA)

Strain that has emerged over the past decade

• Resistant to the antibiotic methicillin

– Interfering with cell wall synthesis

• S. aureus strains (~60%) have now evolved to resist methicillin.

 Vancomycin is the treatment of choice.

 First appeared as nosocomial (originating in a hospital) infections

 Today, MRSA is no longer confined to the hospital.

• Individuals who have not been in a hospital are being infected with

MRSA in what are being called “community acquired infections”

at an epidemic rate in the United States.

Streptococcus pyogenes

The human nasopharynx and parts of the skin are the natural

reservoir for S. pyogenes.

Necrotizing fasciitis, also known as flesh-eating disease

Type 1: polymicrobial

• Type 2: one microorganism, usually S. pyogenes and sometimes S.

aureus. Other organisms that can cause necrotizing fasciitis (fibrous

tissue enclosing muscle or organs) include Clostridium perfringens

and Vibrio vulnificus.

• Therapy includes antibiotics: clindamycin, metronidazole, and

gentamicin

• The incidence of necrotizing fasciitis has risen recently due to an

increase in the use of NSAIDs (ibuprofen, aspirin), which accentuate a

person’s susceptibility to infection by S. pyogenes.

Streptococcal pyogenic exotoxins (SPEs) - an exotoxin: 

superantigens; massive amounts of cytokines released in response to SPEs can produce high levels of inflammation and lead to shock.

• SPEs are associated with scarlet fever, streptococcal toxic shock syndrome, and necrotizing fasciitis.

Hemolysin

Lyses RBCs

• These streptococci are subclassified into groups A–O according to cell wall antigens.

• S. pyogenes is the main pathogen among the group A streptococci (GAS)

Beta-hemolysis appears as a completely clear zone around the

bacterial colonies, while alpha-hemolysis results in a greenish

or brownish discoloration

Acne vulgaris

• Affects 60–70% of Americans at some point

  • 20% will have severe acne

  • Results from blocked hair follicles or pores

  called comedones

  – Can be open (blackheads)

  – Or closed (whiteheads)

  • Inflammatory acne

  – Inflamed macules, papules, pustules,

  and nodules

  • Cystic or nodular acne

  – Most severe

  – Painful fluid-filled cysts or nodules

Fungi

Includes molds and yeasts

• Eukaryotic microbe

• Filamentous or single-celled

Dermatophytes “love” human skin

Cool, moist, keratinized tissues (skin, hair follicles, nails)

• Epidermophyton, Trichophyton, and Microsporum cause the majority

of infections

Tinea capitis

Scalp

Tinea corporis 

body

tinea cruris

jock itch

tinea pedis

foot

tinea unguium

nails

Fungal skin infections are diagnosed via

Clinical appearance

• Microscopic examination of potassium hydroxide (KOH)

preparations of skin flakes or hair

– The KOH destroys the skin cells but not the more resilient walls of

mycelia or spores, which can be seen under a light microscope.

Fungi can also be cultured on a special selective medium called

Sabouraud agar

Antifungal medications are used to treat these diseases.

Imidazole compounds such as clotrimazole are most common and can be purchased over the counter.

Skin is the primary barrier against infection.

When this barrier is damaged, pathogens have a direct route to

infiltrate the body and cause disease

Patients with burns covering more than BLANK are more

likely to develop serious infection

10% of body

Burns alter the immune system

• T-cell activity declines.

• Inflammatory cytokine levels decrease.

• Neutrophil chemotaxis and phagocytosis are diminished.

What happens when a burn occurs

Initially the skin surface is heat sterilized.

 Deep structures

• Contain staphylococci

• Will quickly colonize the wound surface

 5–7 days later, Gram-negative and Gram-positive bacteria

colonize the wound.

• Microbes come from the patient’s GI tract, upper respiratory

tract, or the hospital environment/health care workers.

 Cellulitis, necrotizing fasciitis, and even sepsis (life-threatening

condition that occurs when the body's immune system overreacts

to an infection) can occur.

Methicillin-resistant Staphylococcus aureus (MRSA) is the most

common cause of burn wound infection.

 Gram-negative bacteria and fungi such as Candida and Aspergillus

species can also cause dangerous infections.

 Pseudomonas aeruginosa

• Major cause of serious wound infections

• High level of antibiotic resistance

Conjunctivitis

– “Pink eye”

– Inflammation of the conjunctiva

– Can be due to infection, trauma, or an allergic reaction

keratitis

– Inflammation of the cornea

– Corneal destruction by a bacterial infection

endophthalmitis

– Infection of inner structures

– Uncommon and almost always results from direct spread of a

superficial eye infection or seeding the infection with bacteria

carried by blood

Are you going to fail this quiz?

NOOOOOO believe in yourself!