Micro Final Flashcards
rhinovirus
- causes common cold
-nonenveloped single stranded positive sense RNA virus - antibodies that neutralize one strain of rhinovirus will not neutralize a different strain
-100 known serotype
serotype
different antigenic structure
Influenza
-not rhinovirus
-single stranded negative sense segmented RNA Genome
-undergoes antigenic shift
antigenic variation
-variation of antigens on the envelope/ capsid protein
-associated with rhinovirus immune avoidance
antigenic shift
- 2 strains of influenza virus infect the same cell and the genomes get mixed
-makes it dramatically different
-associated with influenza immune avoidance
Antigenic drift
-random mutation that can occur within the cell that a virus infects, creating small changes in virus proteins
error prone polymerase
-really bad at making copies of itself
-viruses are error prone polymerases
HPV
-DNA Viruse
-60 types
-can cause warts
HPV division
-has viral protein E7
-chaperones human protein pRb toward degradation (stamps it with ubiquitin)
-causes ubiquitination
Human Herpes Viruse and Latency
- after primary infection it replicates in epithelial cells
-eventually becomes latent in host cells in 2 ways:
1. DNA circularizes and exists as an episome
2. DNA integrates into host cell genome
Latent Virus reemerging
- after years of latency can cause a new active infection
MicroRNA’s
-small RNA’s made by the herpes virus interfere with the host cell’s apoptosis program
-not proteins, so they can’t be recognized by the immune system
antigenic masking
some protozoans coat themselves in host antigens to avoid detection by immune system
antigenic variation
- it can vary the antigens on the cell envelope of capsid protein
2 types of protozoa pathogenesis immune avoidance
1.antigenic masking
2.antigenic variation
What does plasmodium use?
antigenic masking
Types of skin rash spread
-exanthem and enanthem
What is a skin rash
-change in color and texture of the skin
-caused by an infectious agent
exanthem
-widespread skin rash accompanied by systemic symptoms (fever, malaise, headache)
enanthem
-rash on mucous membrane
Types of skin rash
1.Macular
2.Papular
3.Pustular
4.Maculopapular
5.Vesicular
Measles
-rubeola
-negative senses, single stranded RNA virus
-vary contagious (8-10 day incubation)
- portal of entry is respiratory or conjunctiva
-replicates in the lungs(moves to regional lymph nodes and produces a viremia that spreads throughout the body)
-prodromal period starts with cold/ flu symptoms
-high fever (40/ 104 degrees Celsius)
-koplik’s spots (whites spots on buccal mucosa on inner cheeks)
viremia
-pathogen enters bloodstream
pathognomic
-definitive indicator of a disease
-measles= koplick spots
Why is Measles Serious
-killed 146,000 people less than 15 years in 2018
-can cause complications in immunocomprimised
-can causes acute disseminated encephalomyelitus and subacute sclerosing panencephalitis in normal individuals
what does acute disseminated encephalomyelitis do?
-myelin sheath stripped from nerve cells= no rapid fire
German Measles (rubella)(3 day measles)(third disease)
-rash similar to measles
-pronounced eliminated from the united states in 2004
-still endemic in many parts of the world
-single stranded postive RNA viruse
-acquired by inhalation of aerosolized respiratory particles
-Replication in the cytoplasm of cells lining in the nasopharynx and nearby lymph nodes
-viremia ensues during the 12-13 day incubation
viremia
spread through out body via bloodstream
Rash of Ruebella
-pinpoint maculopapular pink rash
-appears on head and spreads to the body and extremities
-immmune-related
-does not darken or scab over
-spreads fast
-short duration 1-3 days
-causes low grade fever
-enlargement of head and neck lymph nodes
-mild,subclinical, and self limiting (resolves on it’s own)–> harder on adulats and can give joint pain, bacterial superinfection, birth defects
Birth Defect of Ruebella
-passes through the placenta
-vertical transmission
-causes hearing loss, intellectual disabilities
Erythema Infectiosum (5th disease) (b19)
-portal of entry=respiratory tract
-viral attachment to and replication in erythrocyte progenitor cells
-viremia with in 7-10 days
-binds P antigen, globoside, on surface of RBCs and their progenitors
-the body responds by producing antibodies and cytokines such as TNF-alpha, IFN-y, and interleukins 2-6(inflammatory response)
Inflammatory response of Erythema Infectiosum
-prodromal symptoms coincide with viremia –>mild fever, flu-like symptoms, sometimes arthralgia (joint stiffness)
-initital rash is pathognomic
-described as slap cheek rash
-rash is followed by appearance of a red or gray papular enanthem on the palate or throat
-The third stage is a maculopapular rash that forms on the body and limbs
Roseola Infantum (6th disease)(pseudo ruebella)
-caused by human herpes virus 6 or 7
-double stranded DNA virus
-young children usually under 3 years
-transmitted via respiratory secretion of saliva
-3-5 days of very high fever
-fever followed by sudden mascular or maculopapular red rash
-blanches (turn white) when touched
-laten (hidden in most people)
Chickenpox
-caused by 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
How do you get chickenpox
-inhaling 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(followed by a secondary viremia 14-16 days postinfection)
-VZV invades capillary endothelial cells and the deepest layer of the epidermis
-produces fluid accumulation and vesicle formation
Children and chicken pox
-do not usually have prodromal symptoms and first come down with itchy rash on the face, back, and belly that includes maculopapular, vesicles, pustules, and scabs (releases viral particles)
Life Threatening Aspects of Chicken Pox
-can be life threatening in immunocompromised patients
latency:
-established when viral DNA circulates and forms episome
-can last for decades
-virus infects the nerve endings of the skin
-travel along nerves to ganglia where they lie…
Chicken Pox Treatment
-treated with antihistamines, oatmeal bath, and calamine lotion(reduce itch)
-acyclovir is used to treat shingles (nucleoside analos)
-Varicella Vaccination
-60+ vaccinated with the zoster vaccine to prevent shingles
Herpes (cold Snores and Genital Herpes)
-herpes simplex viruses 1 & 2 (HSV-1 [cold sore]and HSV-2[genital sores])
-Infect skin and mucous membranes( able to infect the central nervous system)(Occasionally can infect the visceral Organs)
-Transmitted by direct contact and replicates and mucosal surfaces or epidermis (final destination is neuronal cell in the ganglia, where the virus becomes latent)
-Primary Infection may be subclinical or symptomatic
-Reactivation of the latent virus always results in symptoms
-reoccurrence dicatated by immune system
HSV1 and 2 Structure
-SS DNA
-linear
-enveloped
-related to Vericella
Herpes Primary Infection
-fever, sore throat, muscle aches, and cervical lymphadenopathy along with vesicular lesions…
Herpes Appearance
- in children and some health care professionals, abrasions, of the skin
Herpes on Skin of Finger
herpetic whitlow
Herpes Gladiatorum
herpes on neck, face, and arms
Herpes Keratitis
herpes in cornea
How to Treat Cold Sores
-antiviral medication
How is HSV2 Spread Primarily
-sexually transmitted
Warts
-Caused by HPV
-tranmitted by contact
-viral proteins (E7) interfere with cell proliferation controls(infected cells replicate uncontrollably
-double stranded DNA Viruse
-Treatments= freezing, burning, and surgical removal
-is tissue specific
What warts can cause genital warts?
- HPV 6, 11, 16, and 18
-vaccines can be administered before sexually active
Small Pox to Variants
- Variola
- Variola Minor
Morphology of Small Pox
-amorphous
Small Pox
-Transmitted via direct or indirect contact(aerozilized particles or fomite)
-replicates
Small Pox Enanthem
-small spots on the oral mucosa
Small Pox Exanthem
small pox pustules on skin
Small Pox Treatment
-no FDA approved treatment for small pox
we no longer vaccinate against smallpox
Staphylococcal Skin Infections from
-S. Aureus and epidrmidis can infect cut
S. Aureus
- Bacterial infection
-has enzymes (VF) that contribute to disease
-coagulates coats the bacteria with fibrin and walls off the infection from the immune system and antibiotics, promoting abscess formation
-requires surgical drainage and antibiotic therapy
-Can cause Toxic Shock syndrome and scalded skin syndrome
Folliculitis
-superficial S. Aureus infection
Boil or Furuncle
- deep S. Aureus Infection
Carbuncle
-2 boils together
-can be from S. Aureus
MRSA
-Resistant to abx methicillin= not beta lactamase
-vancomycin=treatment
-changes target of antibiotic
-first appeared nosocomial(from hospitals)
Impetigo
-S. Aureus and Group A Strep
- 2 Main Types:
1.Bollous
2. Nonbollous
Nonbullous Impetigo
-starts as a superficial bump that becomes a papule and vesicle before it reforms the characteristic pustules on erythematous skin
-honeycomb appearance
-pustules leak fluid
Bolous Impetigo
-large and fluid filled
-vesicle grow larger and become bullae that are full of clear yellow fluid
Necrotizing Fascitis
-flesh eating Steptococcus Pyogenes
-enters in through lesion of cut
-2 Types:
1. Polymicrobial
2. 1 Microorganism
-Treat with ABx
S. Pyrogenes Virulence Possible Factors
- Capsule
- Pilus like M Protein (binds complement regulatory protein)(protects from opsonization)
- Lipoteichoic Acid(cell wall component that facilitates adherence to host cells)
4.streptolysins(lyse blood cells) - Enzymes that degrade
- Peptidoglycan
7.Exotoxins (SPEs)
8.Hemolysin(Lyses RBCs)(these are subclassified from 1-O according to cell wall antigen
Stretococcal Pyogenic Exotoxins
-superantigens
-massive amounts oc cytokines released in response to SPEs can produce hihg level of inflamation and lead to otoxic shock
S. Pyogenes is in what group
A
Cellulitis
-common
-uncomplicated, non-necrotizing inflammation of the dermis related to acute infection
-Characterized by pain, swelling, tenderness, erythema, and warmth
-develops slowly and involved deeper levels of the dermis including subcutaneous fat and connective tissue
-often complication of a wound infection
-Most frequently caused by S. Pyogenes can cause this infection, but a number of other bacterial species can cause this infection
Acnes Vulgaris
-affects 60-70% of Americans at some point
-20% will have severe acne
-caused by blocked hair follicles or pores called comedones (open=white head & closed= black head)
-causes inflamatory acne or cystic and nodular acnea
What % of the body needs to be covered with a burn to put them at risk of developing a serious infection
10%
How does burn alter immune system?
-T cells activety declines
-inflammatory cytokine levels …
Burns
-initially sterile
-deep will colonize with stachylococci
-5-7 days later, gram- negative and gram positive bacteria colonize wound (from gi tract, respiratory tract, hospital environment
-can cause Cellulitis, necrotizing fasciitis, MRSA(most common), and even sepsis
Pseudomonas Aeruginosa
-major cause of serious wound infection
-high level of antibiotic resistance
-virulence factors(Exotoxin A and S [ADP-ribosomyltransfereases that inactivate host protein synthesis and interferes with host signaling pathways, respectively])
Gas Gangrene
-only in dead tissue
-2 types: dry and wet
Dry Gangrene
-when blood supply to tissue is cut off
-affect fingers and toes
seen in severe frostbite cases
-can occur in people with diabetes or certain autoimmune diseases
Wet Gangrene
-occurs due to an infection
-occurs during an internal or external part of the body
-Anaerobic infections affecting the genital area(Fournier’s gangrene)
-clostridium species that produce large amounts of gas
Clostridium Perfringens
-gangrene type
-highly fermentative
-only on dead tisue(saprophyte)
- produces foul smelling gas
-produces toxins