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
Common Cold
-rhinovirus most common
-set of symptoms we experience, but many viruses are cause
Viral Sinusitis
-infection of the upper airways
-inflammation and congestion of the sinuses
Respiratory Syncytial Viruse (RSV)
-fusion of adjacent infected cells into a syncytium, a giant cell containing many nuclei
-transmitted Person to person(mucous membrane of eye, mouth, nose, inhalation of droplets
-Young are most vulnerable
Influenza Type A
cause of epidemica and pandeics
-can infect a variety of animals as well as people
-is constantly changing
-does antigenic shift unlike B and C
-pathogenicity depend on 3 proteins: HA,NA,M2
Influenza Type B
-found primarily in humans and usually results in milder illness
-does not cause pandemics
-pathogenicity depend on 3 proteins: HA,NA,M2
Influenza Type C
-Causes only mild disease
-Does not case epidemics or pandemics
-pathogenicity depend on 3 proteins: HA,NA,M2
Covid 19
-SARS-CoV-2
-lower respiratory tract infection
-single stranded, positive- sense, enveloped (came from host) RNA Virus
-emergerd December 2019
-Symptoms= cough, fever, shortness of breath, severe cases include a cytokine storm, many cases are asymptomatic
What was SARS like before 2003
-only caused the common cold
Croup
-aka LTB
-lower respiratory Tract Infection
-infects lower larynx
-spreads to the trachea and even bronchi
-children 6 mths-5years
-Symptoms: Barking cough, runny nose, fever
-parainfluenza viruses type 1 and 2 are the most common cause of croup
-treatment depends on severity of symptoms(maybe steroid)
Otis Media
-upper respiratory infection(midle ear infection)
-caused by viruses and gram+ or gram - bacteria(Streptococcus pneumonia, haemophiles Influenzae, or Moraxella Catarrhalis)
upper respiratory tract infections are anticedent of what?
AOM
Why is Otis Media more common in kids?
-eustachian tube is horizontal causing the causing agent to get trapped
Stretococcus Pheumoniae
-gram postitive
-have capsule
-alpha hemolytic
-facultative Anaerobe
-can cause otis media
Haemophilus Influenzae
-6 sterotypes
-polysaccharide on capsule
-can cause otis media
Moraxella Catarrhalis
-can cause otis media
Bacterial Sinusitis
-upper reparatory tract infection
-inflammation in sinuses
-foul smelling nasal discharge
-antibiotic is the usual course of treatment
Stetococcal Pharyngitis
-sore throat
-strep throat
-vary contagious
-spread via direct contact or indirect contact vie fomites
-treated with antibiotics
-Symptoms: soar throat exudat on tonsils [protein and cell fluid oozing from tissue due to inflamation]
S. Pyogenes produce exotoxins
-SPE
-can cause fever, red rash called scarlet fever, and strawberry tongue
Stretococcal Sequele
-caused by immune response to the bacteria
-antibodies cross react with host cells in an autoimmine reaction, resulting in serious sequalae
-w/ S, Pyogenes uses M protein to attach to host cells (mimicry b/c similar to cardiac cells or kidney cells)
-Can be an acute Rheumetic Fever=damages heart, joint, kidneys, ect.
Diptheria
-reemerging Reparatory Tract Infections
-gram positive rod
-corynebacterium diptheriae (2 varieities
vaccinated by DTap
-sore throat and skin lesions and can cause cardiac events
Corynebacterium Diptheriae Types
- Lysogenized=exo toxins
- Non lysogenized
Whooping Cough
-gram negative bacillus
-transmitted by inhailing aerosolized droplets
-incubation period of 7-21 days
-Virulence Factor= filamentous hemagglutinin (adhesion) adeylyl cyclase is turned on –> increase cAMP–> Cl leaves –> builds up of fluid in lungs
Stages of Whooping Cough
1.Catarrhal= symptoms of upper repiratory infection
2.Paroxysmal= violent cough, followed by struggle to breath
3.Convalescent=paroxysms gradually disapear during the next 2-3 weeks as patient recovers
Bronchitis
-lower respiratory tract infection
-inflammation of the bronchi
-acute and self-limiting(aka resolves on it’s own)
-multiple viral and bacterial etiologies
-productive cough is generally the only presenting symptom –> acute bronchitis is suspected when the patient’s couch persists for more than 5 days
-can be caused by mycopkema, chlamydophia, or bordetella
-can be caused by smoking b/c mucus builds up in lungs
Community Acquired Pneumonia
-lower respiratory infection
-pneumonia= an infection that causes inflamation in the lungs
-can be typical or atypical
- bacteria that can cause= s. pneumoniae (slippery capsule), mycoplasma pneumoniae, legionella, and chlamydophila
-common in winter months and nursing homes (10-30% mortality rate)
-their is vaccine that protects against 23 serotypes
Atypical Pneumonia
-it effects multiple organ systems, not just lungs
Mycoplasma Pneumoniae
-lower respiratory infection
-no cell wall
-exsists in a filamentous form
-VF= adhesion (specialized tip protein)
-smalles known species of bacteria
-in atypical pneumonia
-causes: headache, malaise, progression to a nonproductive cough
-possible low grade fever
-chills
-more common in school aged children and college age adults
-spread via person to person contact
-pathology is not known
-immunopathological
Hospital Acquired Pneumonia
-acquired when receiving health care treatment for other conditions
-P. Aeruginosa is most common bacteria (opportunistic, gram -, large # of VF, major contributor to pneumonia and mortality in patients with cystic Fibrosis)
Other Bacteria: gram - (e. Coli, Klevsiella pneumoniae) and gram + S. Aureus and streptobacter, MRSA)
Tuberculosis
-lower respiratory Bacteria Infection
-mycobacterium tuberculosis=acid fast
- cases are on the rise in developed nations due to HIV and a growing indigent population
-can disseminat and produce absesses in organs
-person to person contact
multidrug resistant (MDR) Tuberculosis
-produces rapid onset and fatal disease among HIV patients
-from person to person
Tuberculosis Pathogenesis
-enter lungs
-phagocytized by macrophage and survives sheltered modified phagolysosome
-a delayed hypersensitivity reaction develops ( causes tubercules with caseous leasions with cheese like consistency and calcify)
-Latent= bacilli contained by immune system and not infectious
Primary TB
-characterized by a productive cough that generates sputum, fever, night sweats, and weight loss
-they have active TB
Secondary TB
-when bacteria reinfect by entering blood stream and infecting other organs
Fungal infections Overall
-portal of entry= respiratory tract
-infection is usually associated with occupation and recreational activities in wooded areas along waterways, where there is moist soil and spores
-are acquired from environment and not person to person
Coccidioidomycosis
-fungal infection
-from coccidioides immities
-endemic in the united states (west)
Histoplasmosis
-from histoplasma capsulatum
-flu-like illness, erythema nodosum, arthritis, arthralgia
-in the U.S>, found most in Ohio and MIssissippi river valleys
-dimorphic
dimorphic
fungi with 2 forms
Blastocycosis
-blastomyces dermatidis
-dimorphic
-disseminates to skin, bone, and genitourinary tract
-found in ohio, mississippi river valleys and eastern U.S.
Cryptococcosis
-fungi
-cryptococcus neoformans
-Eastern U.S.
-can involve skin, lungs, prostate gland, urinary tract, eyes, bones, and joints
-the most prevalent clinical form is meningoencephalitis in AIDS patients
systemic Infection
-starts in one location and moves to another via blood stream and lymph system
Epstein-Barr Virus
-95% of people have it
-herpes virus family (HHV4)
-shed in saliva
-fever, sore throat, enlarged lymph nodes (proliferation of B and T cells), fatigue
-Virus infects and replicate
-B cells are misshapen and spread didsease through body
-humans= only reservoir (have virus for life)
Cytomegalovirus(CMV)
-herpes virus family, human herpesvirus 5
-Double Stranded
-episome which can cause latent infection
-Asymptomatic (sheds virus in body fluids)(can be vertical transmission)(starts in salivary glands–>lymphocytes and monocytes, & kidneys)
-cell mediated immunity typically occurs
-Reinfection can occur
-Immune compromised are at higher risk for reactivation
episome
-you have it= you have it for life
cell mediated immunity
stops reinfection of the latent virus
What are the problems of cytomegalovirus being transplacental
-can cause low birth weight, microcephaly, siezures, rash, enlarged liver, most common=deafness
-leading cuase in intellectula disease
Dengue Fever
-endemic in the tropics
-causes joint and muscle pain= controtions
-transmitted by mosquito= vector
Ebola
-acute rapid fever, muscle pain, and bleeding from multiple orifices
-50-60% mortallity rate
-transmitted via contact with fluids
Chikungunya Virus
-causes debilitating muscle pain
-prevalent in the are around the Indian Ocean, Europe, and recently the U.S.
Bacteremia
-bacteria in bloodstream
-cut or getting teeth clean
Sepsis
infection of the bloodstream
Septicemia
-pathogen replicates to high numbers, overcomes the innate immune system
-can lead to medical emergency
Systemic Inflammation Response Syndrome(SIRS)
-medical emergency characterized by rapid heart rate, and abnormal white blood cell count
-can be infectious or noninfectious(trauma)
-Septicemia
Septic Shock
-Catastrophic drop in blood pressure due to severe sepsis
-superantigens or MAMPs
-a septicemia
MAMPs
-LPS or teichoic acid=T cells trigger inflammation= inflammation=vasodilation and coagulation= clotting in small BVs= disseminated intravascular coagulation=death
Plaque
caused by yersinia pestis
-transmitted by rodents via fleas
-humans not normally part of cycle
-zoonotic disease
Bubonic Plague
-organisms move site to lymph nodes, forming bubeos
-not tranmissable
-step 1
Septicemic Plague
-step 2
- pathogen enters bloodstream
-nottranmissable
-massive amount of LPS in blood
Pneumonic Plague
-Step 3
-pathogen infects lungs
-transmissible, easily spread through populations
Lyme Disease
-the most common vector-borne illness in U.S.
-B. burgdorferi
-linear chromosome
-transmitted by tick bite(when tick feeds it regurgitates)
-spirochete
-intracellualr pathogen
Lyme Disease Treatment
-antibiotic treatment is most effective in ealier stages
-doxycycline
VF of Lymes disease
-proteins and adhesions facilitate colonization
-has enzymes that cleave proteoglycan(found in connective Tissue)
Lymes Disease days 3-30 days
-bull’s eye rash, fever, muscle pain, joint pain, headache
-ring in rash is from bacteria moving away from bite
Lymes Disease Stage 2
-after a month
-spread from blood to organs
-neurological and cardiac involvement
-inflammation causing joint pain thought to be autoimmune
Stage 3 Lymes Disease
-months to years
-neuropathy and encephalopathy
-affects memory, mood, sleep
Typhoid Fever
-salmonella enterica
-lives in macrophages in gastrointestinal tract
-infects a variety of organ systems
-bacteria are continuously shed during infection; can be transmitted via fecal-oral route
-typhoid Mary (organisms can infect gall bladder, and bile contains typhi)
-humans are only resevoir
-intracellular pathogen
Rocky Mountain Spotted Fever
-Rickettsia rickettsii
-transmitted by ticks and lice
-rash begins on the wrist and ankles and spreads to the center of the body
-induces phagocytosis to get into the cell
-escapes the phagosome (fate 3)(infected cells burst)
-intracellular pathogen
Malaria
-transmitted by 4 species of plasmodium(a protist)
-parasite
-complex life cycle (asexual erythrocytic cycle in intermediate host/ the human)(sexual cycle in the definitive host/mosquitoe)
- treatment includes chloroquine
Malaria Lifecycle
1.Infected Mosquito bites person and injects plasmodium into blood stream (sporozite form)
2.Plasmodium goes to liver where asexual fission takes place
3.Infects RBC= consume hemoglobin causing it to become a trophozoite form rapidly multiplying nuclei
4. Cell bursts and releases schizont
babesiosis
-caused by babesia microtu (protist)
- tranmitted by ticks
-maltese cross formation/tetrad arrangement
-mild in immunocompetent
-fatal in elderly or patients w/ out spleen
Toxoplasmosis
-Toxoplasma Gondii (protozoan)
-forms spore
-obligate intercellular pathogen
-from cats (definitive host)( other animal is intermediate)
-2 Stages: feline and mamal stage
Toxoplasmosis Symptoms
- Mild for peeps with good immune system
-Hard on immunocompromised
-causes congenital disease= organism can cross placenta(can cause hydrocephaly)
Toxoplasmosis Life Cycle
1.Cat sheds oocytes in feces
2. Animal Eat cat feces (humans get from fecal oral, meat, or blood transfusion)(schizophrenia maybe)
3.Stomach acidity dissolves the wall of cyst releasing spores in intermediate host(alters brain chemistry, so animal seeks cats)
Tooth decay
-infection of oral cavity
-from many organisms( especially lactobacilli and streptococci)
-dental plaque (biofilm that produces acid causing tooth decay)
-eventually penetrates to the nerve
-brush, floss, lower sugar, drink fluoride treated water
Gingivitis
-inflammation of the gums
-b/c of tarter build up below the gumline
Periodontal Disease
-advanced inflammation causing the gums to bleed and pull away from teeth
-aggregatibacter, actinomycetemcomitans, porphyromonas gingivalis, and bacteroides for sythos
-necrotising Infection( trench mouth= serouse with ged gums, gray film, crater like canker sores= treatment = remove dead tissue and use hydrogen peroxide mouth wash
-can cause bacteremia, possibly cancer, and pneumonia
Thrush
-white coating resembling cottage cheese
- caused by yeast candida albicans
-common in new borns, patients taking antibiotics, and immunocompromised
Osmotic Diarrhea
-intestinal osmolarity is higher than internal osmolarity causing water to leave cells
-pathogens that prevent nutrients absorption can cause it
Secretory Diarrhea
-increased ion secretion causes electrolytes to leave to imbalance
-pathogens that cause ion secretion cause secretory diarrhea
Inflammatory Diahrea
-inflammatory cytokines damage mucosal cells and prevent absorption of nutrients and water
-shigella and salmonella are common causes of inflammatory diarrhea
Motility- Related Diarhrea
-food moves too quickly through the intestinal tract and nutrients are not absorbed
-often caused by enterotoxins and rotavirus
Gastris
inflamation of the stomach
Gastroenteritis
inflammation on GI Tract
Enteritis
-inflammation mainly of the small intestine
Enterocolitis
inflammation of the colon and small intestine
Colitis
-inflammation of the colon
Rotavirus
-fecal-oral
-nonenveloped, segmented, dsRNA
-enterotoxin (stimulates vagus nerve) that causes hypermotility of the intestinal tract
vaccines prevent severe disease
-all get it 6months-24months (all by age 5)
-symptoms= nausea, vomiting, dark green diarrhea from bile
-virus destroys epithelial cells= osmotic dirhea
What causes most GI issues?
viruses
Norovirus
Fecal-oral
-nonenveloped, positive sense, SSRNA
-causes sudden symptoms: fever, headache, malaise (like stomach flu)
-Outbreak common on cruise ships
Hepatitis
-inflamation of the liver
-caused by viral infection, too much alcohol, toxic chemicals, or autoimmune reactions
Hepatitiis A
-single starnde RNA
-postive sense
-fecal Oral
-food borne
-self limiting
-asymptomatic or liver disease
Hep B
-DNA
-positive sense
-exchange of blood or body fluids
-often no symptoms are displayed
-liver damage in 30% and 1% liver failure
Hep c
-SSRNA
-positive sense
-exchange of blood or body fluids
-mild initially
-70% progress to chronic infection
-risk of liver failure and cancer
Hep D
-ssRNA
-positive sense
-only causes disease if occurs with hep
Hep E
-ssRNA
-positive sense
…..
Mumps
-paramyxovirus
-ssRNA
-highly infectious
-causses: inflamation in parotid glands & testis–> shed in saliva and spread by sneexing and coughing
- their is vaccine
-can cause meningitis and encephalitis=siezures
Peptic Ulcer
-bacterial infection of GI
-helicobacter pylori
-gram negative
-survive acidic nature
-symptoms= dyspepsia, upper abdominal pain, bloating, belching, nausea
-Treatment= proton pump inhibitors and antibiotics (bad for long time)
-can survive in stomach because it secretes urease
-Urease and LPS produce immune response= inflamtion= ulcer
E. Coli (enterotoxigenic)(ETEC)
-produces labile toxin(AB toxin and ADP ribosyltranferase)
-causes secretory, watery diarrhea
-no animal reservoirs
-fecal oral
Enteroinvasive E. Coli (EIEC)
-causes bloody diarrhea similar to that caused by shigella
-invades epithelial cells
What does it mean tha e coli is a pathovar
-Produces O(LPS) and H (Flagellar) protein
Enterohemorrhagic E. Coli (EHEC)
-shiga toxin
-causes bloody diarrhea
-in severe cases EHEC can lead to hemolytic uremia syndrome and thrombocytopenic purpura
-can survive in stomach acid
-from animal reservoir= intestines of cattle
All E. Coli uses what pili system
-grappling hook like
Shigellosis
-bloody diarrhea
-bacillary dysentary
….
What Fate does shigellosis follow?
fate 3
-the damage it causes to epithelial cells is what causes bloody diarrhea
Salmonellosis
-2 major diseases are typhoid fever and enterocolitis
Typhoid Fever
-no animal reservoir
-associated with food preparation
-intermittent fevers and diarrhea for 1-3 weeks
-abdominal path
-salmon colored rash
Enterocolitis
-indistinguishable from other enteric pathogens
-associated with animal contact= poultry and reptiles
-short term illness lasts 6-48 hours ( no abx)
-not resistant to stomach acid
-uses fate 2
-has risk of sepsis
Cholera
-vibrio cholerae
-gram negative curved rod with a single flagellum
-fecal oral
-rice water stool
-noninvasive( no fever or bloody stool)
-cholera toxin= secretory diarrhea
-Lose 10L-15L of water= dehydration and death
Staphylococcal Food Poisoning
-staphylococcus aureus
-gram positive, cocci
-intoxication= toxin causes disease
-symptoms are seen within 2-6 hours upon ingestion
-toxin is heat stable
Macular Rash
flat and red, less than 1 cm in diameter
Papular Rash
small, solid, and elevated
Pustular Rash
A papule filled with pus
Maculopapular Rash
A papule that is reddened
Vesicular Rash
small blisters are formed
Erysipelas
-caused by S. Pyogenes
-acute infection
-Causes Erysipelas Rash= face and sometimes lower extremities, covers the face and bridge of the nose, and “butterfly” appearance
What Factors contributes to acne development
-genetic predisposition
-hormones
-gram-positive bacteria (Propionibacterium Acnes)
Propionibacterium Acnes
-promotes inflammation by binding to Toll-like receptor 2 on macrophages and neutrophils, which then release proinflammatory cytokines
Chaga Disease
-trypanosoma cruzi
-protozoan
-vector-Reduviid bug
-fever and lymphadenopathy
-systemic symptoms include: enlarged spleen, liver, neurological issues, myocarditis
-Treatment=nifurtimox or benzidazole
-causes death due to heart failure
