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microbiology final exam (lecture)
Terms in this set (209)
study of when and where diseases occur and how they are transmitted
person can catch the disease
diseases are not contagious
number of NEW cases in a population in a time period
TOTAL number of cases in a population
Endemic: constantly present
Epidemic: large part of the population in a particular region
Pandemic: multiple continents
(the study of the causes of disease) and investigation of disease transmission (mechanisms by which a disease is spread).
in a population can be expressed in a few different ways. Morbidity or total morbidity is expressed in numbers of individuals without reference to the size of the population. The morbidity rate can be expressed as the number of diseased individuals out of a standard number of individuals in the population, such as 100,000, or as a percent of the population.
is the number, or proportion, of individuals with a particular illness in a given population at a point in time.
is the number or proportion of new cases in a period of time.
An epidemic that occurs on a worldwide scale
emerging infectious disease
is either new to the human population or has shown an increase in prevalence in the previous twenty years. Whether the disease is new or conditions have changed to cause an increase in frequency, its status as emerging implies the need to apply resources to understand and control its growing impact.
reemerging infectious disease
is a disease that is increasing in frequency after a previous period of decline. Its reemergence may be a result of changing conditions or old prevention regimes that are no longer working. Examples of such diseases are drug-resistant forms of tuberculosis, bacterial pneumonia, and malaria.
any condition in which the normal structure or functions of the body are damaged or impaired
disease caused by colonization of a host by a pathogen
disease causing microbe
organism infected by pathogen
cause of disease
ability to cause disease
degree of pathogenicity
* rhinovirus and ebolavirus are both
pathogenic, but ebolavirus is much more virulent!
Ex: temperature, blood pressure
Ex: pain, nausea
Subclinical Infection: no noticeable symptoms (asymptomatic)
Opportunistic infection: infection by normally harmless microbe
Or gain entry to body through wounds
regular infection by a microbe
infection that occurs during treatment of a primary infection
pathologic changes occur over a relatively short time
pathologic changes can occur over longer time spans
the causal pathogen goes dormant for extended periods of time with no active replication
The ability of a microbial agent to cause disease
Virulence: the degree
to which an organism is pathogenic is
primary pathogen: can cause
disease in a host regardless of the host's resident microbiota or immune system.
opportunistic pathogen : by contrast, can only
cause disease in situations that compromise the host's defenses, such as the body's protective barriers, immune system, or normal microbiota.
Explain the role of the World Health Organization in monitoring infectious disease
In addition to monitoring and reporting on infectious disease, WHO also develops and implements strategies for their control and prevention. WHO has had a number of successful international public health campaigns.
WHO continues to be involved in infectious disease control, primarily in the developing world, with programs targeting malaria, HIV/AIDS, and tuberculosis, among others. It also runs programs to reduce illness and mortality that occur as a result of violence, accidents, lifestyle-associated illnesses such as diabetes, and poor health-care infrastructure.
maintains a global alert and response system that coordinates information from member nations. In the event of a public health emergency or epidemic, it provides logistical support and coordinates international response to the emergency. The United States contributes to this effort through the CDC. The CDC carries out international monitoring and public health efforts, mainly in the service of protecting US public health in an increasingly connected world. Similarly, the European Union maintains a Health Security Committee that monitors disease outbreaks within its member countries and internationally, coordinating with WHO.
Describe the chain of infection
Reservoir (living organism or non living site) → portal of exit (body fluids, feces, broken skin, contact) → transmission (contact: direct [person to person] vertically pregnancy, horizontally, droplet (< 3 feet) ; indirect (fomites)) , (vehicle: air (< 3 feet), food, water), (vector: mechanical, biological,
oes*) → portal of entry (respiratory, digestive, reproductive tracts, eyes, ears, broken skin) → susceptible individual (immune system, health, behavior, age, gender)
Explain the utility of the Mortality and Morbidity Weekly Report
which provides physicians and health-care workers with updates on public health issues and the latest data pertaining to notifiable diseases.
Koch's postulates (step 1)
Suspected pathogen found in sick hosts, but not healthy host
Healthy mouse (no pathogen) vs unhealthy mouse (suspected pathogen)
Looked under a microscope → slide w/ red blood cells: (pathogens → red blood cells have other cells) → growth is pathogenic, and single colonies can be found using the T-streak
Koch's postulates (step 2)
pathogen can be isolated and grown
Inject the growth from the pathogenic slide into healthy mouse → turns into sick host
Koch's postulates (step 3)
healthy host has the same signs and symptoms as the original host, when infected with the isolate pathogen
Koch's postulates (step 4)
pathogen can be re-isolated from new host
Koch's postulates limitations
The first relates to postulate 1, which assumes that pathogens are only found in diseased, not healthy, individuals. This is not true for many pathogens
Koch's second faulty assumption was that all healthy test subjects are equally susceptible to disease. We now know that individuals are not equally susceptible to disease.
Koch also assumed that all pathogens are microorganisms that can be grown in pure culture (postulate 2) and that animals could serve as reliable models for human disease. However, we now know that not all pathogens can be grown in pure culture, and many human diseases cannot be reliably replicated in animal hosts.
Molecular Koch's postulates
Look for suspected gene rather then suspected pathogen
is not in the ability to isolate a particular pathogen but rather to identify a gene that may cause the organism to be pathogenic
1) The phenotype (sign or symptom of disease) should be associated only with pathogenic strains of a species.
2) Inactivation of the suspected gene(s) associated with pathogenicity should result in a measurable loss of pathogenicity.
3) Reversion of the inactive gene should restore the disease phenotype.
pathogen can be transmitted , make contact w/host ( layered host cells in body → pathogens enter from outside of the body
growth on the surface tissue
Invasion: squeezing in between cells or going into cells , goes past this first layer of cells deeper into the body
The term adhesion refers to the capability of pathogenic microbes to attach to the cells of the body using adhesion factors, and different pathogens use various mechanisms to adhere to the cells of host tissues.
kill/damage host cells , toxins , hyper inflammation
Evade immune system:
(phagocytes, antibodies, chemical defenses, cytotoxic T cells)
Kill phagocytes: cytolytic toxins
Avoid phagocytes: capsules
Survive inside phagocytes
some molecular structure on the outside of the pathogen will bind to a molecular structure on the surface of the host (pili, capsule , spike , attach to specific host cell receptor)
Biofilm growth can also act as an adhesion factor
A biofilm is a community of bacteria that produce a glycocalyx, known as extra polymeric substance (EPS), that allows the biofilm to attach to a surface.
live in environment , control host cells for replication
endocytosis, fission, enzymes to degrade or damage cells
Explain different ways pathogens evade the immune system
Avoid antibodies: hide in host cells
Viruses: avoid antibodies by direct cell-to-cell transmission
Avoid antibodies: antigenic variation
Avoid antibodies: mimic host antigen
Viruses: block infereron gene transcription
Viruses: determine when host cell dies
Explain the role of virulence factors in pathogenicity
What make "bad bugs" bad
Properties of infectious agents that allow them to cause disease
Allow infection establishment : adhere, colonize (invade) , grow, damage host, avoid host defenses
Collagenase, made of bacteria, it breaks down collagen which is the material found in connective tissue , used to penetrate lumen of the blood vessel
Enzyme that breaks down DNA, enzyme can be useful, for degrading DNA after host cell lysis, DNA that is released by lysing cells, can trap bacterial cells, break DNA into pieces
Break down membranes, various enzymes are used to penetrate host cells cause cells to lyse
Enzymes that break down glycosides (sugars that have been chemically modified)
Enzyme that breaks down hyaluronic acid (hyaluronidases that break the breaking so that bacteria can get through cells)
Same as a lipopolysaccharide
Outer membrane of gram-negative bacteria
Does not act as an endotoxin while attached to a living bacterium
Releases from cell into bloodstream or tissues → endotoxin
Lipid on end = toxic , triggers hyperinflation, lipid is extremely inflammatory , triggers the inflammatory response itself
Causes extreme damage to the body
Septic shock : life-threatening decrease in blood pressure
Exotoxin - " released from pathogens"
Degrade the host cell membrane
Ex: staphylococcal d-toxin (dysregulation of membrane traffic, leads to cell death)
Exotoxin - " released from pathogens"
Over stimulates immune cells, leading to hyperinflammation
APC detects antigen by Tcell (CD4+) → appropriate T cell activation → superantigen binds to both mhc2 and t cell receptor holding them together → cd4+ becomes activated in the absence of antigen sends out cytokines → activate immune cells → create hyperinflammation
B subunit binds to the host cell. A subunit enters/damages the host cell.
b subunit enabled (outside cell membrane) the a subunit taken up into the cell (inside cell membrane) → a subunit inside; going to affect translation of proteins binds to elongation factor that is involved in translation and prevents it from functioning without being able to make new proteins eventually die
which is made by the bacterium toxin cause what's called flaccid paralysis where the muscles cannot contract and so the body becomes limp and the muscles can't contract breathing in the heartbeat → regulated inside muscle cells
stops uncontrollable muscle contraction →
" any toxin infecting the enteric system "
upper respiratory system
is in direct contact with the external environment. The nares (or nostrils) are the external openings of the nose that lead back into the nasal cavity, a large air-filled space behind the nares.
is part of the upper throat extending from the posterior nasal cavity.
The palatine tonsils, which consist of lymphoid tissue, are located within the oropharynx
Air inhaled through the mouth does not pass through the nasopharynx; it proceeds first through the
the last portion of the pharynx, connects to the larynx, which contains the vocal fold
The nasopharynx carries air inhaled through the nose. The middle ear is connected to the nasopharynx through the
lower respiratory system
begins below the epiglottis in the larynx or voice box
in the larynx or voice box
, or windpipe, is a cartilaginous tube extending from the larynx that provides an unobstructed path for air to reach the lungs.
The trachea bifurcates into the left and right bronchi as it reaches the lungs
These paths branch repeatedly to form smaller and more extensive networks of tubes, the
The terminal bronchioles formed in this tree-like network end in cul-de-sacs called the
within the respiratory epithelium secrete a layer of sticky mucus. The viscosity and acidity of this secretion inhibits microbial attachment to the underlying cells.
The beating cilia dislodge and propel the mucus, and any trapped microbes, upward to the epiglottis, where they will be swallowed. Elimination of microbes in this manner is referred to as the
effect and is an important mechanism that prevents inhaled microorganisms from migrating further into the lower respiratory tract.
Describe respiratory anatomy (upper)
Upper respiratory tract: cavity by the nose (nasal cavity) + (oral cavity) as air is breathed in and out through the (nasal cavity) it will also pass through the sinuses where the air gets warmed and moistened before it travels down to the pharynx (tube that goes down behind the cavities and the pharynx can be divided into sections called the nasopharynx, the oropharynx, and the laryngopharynx)
describe respiratory system (upper pt.2)
→ tonsil collect the fluids that are draining off the tissues and checking any pathogen it's an important part of immune defense → connecting the nasopharynx to the ear is called eustachian tube → cut off for the upper respiratory tract is at epiglottis (flap so that food doesn't travel to the lungs →
Describe respiratory anatomy (middle)
larynx + trachea = voice box → air travels down trachea to lungs and enters various branches → bronch 1: bronchi branch into bronchioles → alveoli and bronchioles tiny sacs are covered with blood vessels → gas is exchanged with the environment in blood →
Describe respiratory anatomy (middle pt.2)
blood will release CO2 into the air that is breathed in and out → take in O2 from the air that is breathed in → respiratory mucosa: which is primarily made of epithelial cells + goblet cells , goblet cells secrete mucus , e cells are covered in cilia , hellp push mucus up and out → below are deeper tissues called submucosa
Rhinitis = nasal cavity
is an inflammation of the nasal cavities, often characteristic of the common cold. Rhinitis may also be associated with hay fever allergies or other irritants.
Otitis media = inflammation in the ear
is an inflammation of the middle ear.
A variety of microbes can cause pharyngitis, commonly known as a sore throat.
An inflammation of the larynx is called
Chronic cases of tonsillitis may be treated surgically with tonsillectomy. More rarely, the epiglottis can be infected, a condition called
In the lower respiratory system, the inflammation of the bronchial tubes results in
Most serious of all is pneumonia, in which the alveoli in the lungs are infected and become inflamed.
Valley Fever or coccicidio mycosis
Pathogen: coccidioides immitis or fungus
Pathogenesis: spores enter bronchi → spore forms spherical → spherical fills up with endospores release and disseminated through the body → travels to all different places → form sporules
Spheircal damage tissues and are too big for phagocytosis
Prevention/Treatment: avoid area, antifungal drugs
Pathogen: streptococcus pyogenes (Group A Strep), gram + coccus
Pathogenesis: numerous exoenzyme and exotoxins damage the upper respiratory mucosa. Toxin may disseminate systematically
Prevention/Treatment: B-lactin drugs, antibiotics
Pathogen: several different viruses; rhinovirus, coronavirus, adenovirus
Pathogenesis: reproduce in upper respiratory mucosa (mostly used in cavity), damaging host cells
Pathogen: numerous viruses; bacteria & fungi , respiratory syncity viruses, streptococcus pneumoniae, hemophilus influenzae
Pathogenesis: damage to alevoli results in accumulation of phs/fluid. Can lead to suffocation
Prevention/Treatment: some vaccines + antibacterial drugs
Pathogen: Influenza virus
Pathogenesis: damage to the lower respiratory tract from viral replication. Hyperimmune response levels leads to cytokinstom → shock → death
Capsid → RNA genome inside → envelope around capid w/hemmaglutin on it (entry) + neuraminidase (exit)
Group A: severest disease (+++) , antigenic drift: Y, animals: Y
Group B: severse disease (++), antigenic drift: N, animals: N
Group C: severse disease (+), antigenic drift: N, animals: N
Influenza (pt. 2)
Antigenic Drift: virus 1 → mutation on RNA genome → slightly different antigens
Antigenic Shift: host cell → viruses enter, intermixing of RNA genomes → new virus exits with a mix of genomes →
Prevention/Treatment: yearly vaccine , antiviral drugs , block neurominidase (an enzyme, present in many pathogenic or symbiotic microorganisms, that catalyzes the breakdown of glycosides containing neuraminic acid.)
Pathogenesis: Damage to respiratory tissue from viral replication. Hyper inflammation can damage lunga, heart, kidneys
Prevention/Treatment: vaccine is close and bamlanivimab (Human immunoglobulin that binds to SARS-CoV-2 spike protein, preventing entry to cells. FDA has approved emergency use authorization for mild-to-moderate disease in people over the age of 12) and rendesvir (Blocks viral replication by acting as a nucleoside analog. Studies unclear on effectiveness. FDA approved for use.)
Pathogen: mycobacterium tuberculosis , acid fast , rod
Pathogenesis: survive inside macrophages, tubercles form and chronic inflammation damages respiratory tissues. Tubercle rupture leads to dissemination. Sequestered bacteria persist for life/years without treatment.
Sequale: tuberculosis meinigitis or pneoumia
Prevention/Treatment: Vaccine (not use 100%), isoniazid & other drugs given months/years, directly observed treatment short-course (DOTS)
Pathogen: corynebacterium diptheriae, gram positive , rod
Pathogensis: stains that have undergone lysogenic conversion produce diphtheria toxin, an AB toxin that blocks host cell protein synthesis, leading to respiratory tissue death
Prevention/Treatment: vaccine, antibacerial drugs, anti toxin
carry out the urinary system's primary functions of filtering the blood and maintaining water and electrolyte balance.
Urine that collects in each kidney empties through a
Urine is released from the bladder to the...which transports it to be excreted from the body through the urinary meatus, the opening of the urethra.
The kidneys are composed of millions of filtration units called
Each nephron is in intimate contact with blood through a specialized capillary bed
Fluids, electrolytes, and molecules from the blood pass from the glomerulus into the nephron, creating the filtrate that becomes
The testes are responsible for the production of sperm.
is a coiled tube that collects sperm from the testes and passes it on to the vas deferens. The epididymis is also the site of sperm maturation after they leave the testes.
The seminal vesicles and prostate are accessory glands that produce fluid that supports sperm.
During ejaculation, the vas deferens releases this mixture of fluid and sperm, called semen, into the urethra, which extends to the end of the penis.
The external genitalia (vulva) in females open to the vagina, a muscular passageway that connects to the cervix.
The cervix is the lower part of the uterus (the organ where a fertilized egg will implant and develop). The cervix is a common site of infection, especially for viruses that may lead to cervical cancer.
The uterus leads to the fallopian tubes and eventually to the ovaries. Ovaries are the site of ova (egg) production, as well as the site of estrogen and progesterone production that are involved in maturation and maintenance of reproductive organs, preparation of the uterus for pregnancy, and regulation of the menstrual cycle
Infections of the urinary tract most commonly cause inflammation of the bladder (cystitis) or of the urethra (urethritis).
Urethritis can be associated with cystitis, but can also be caused by sexually transmitted infections. Symptoms of urethritis in men include burning sensation while urinating, discharge from the penis, and blood in the semen or the urine. In women, urethritis is associated with painful and frequent urination, vaginal discharge, fever, chills, and abdominal pain.
The symptoms of cystitis are similar to those of urethritis. When urethritis is caused by a sexually transmitted pathogen, additional symptoms involving the genitalia can occur. These can include painful vesicles (blisters), warts, and ulcers. Ureteritis, a rare infection of the ureter, can also occur with cystitis.
Pyelonephritis and glomerulonephritis are infections of the kidney that are potentially serious.
Pyelonephritis is an infection of one or both of the kidneys and may develop from a lower urinary tract infection; the upper urinary tract, including the ureters, is often affected. Signs and symptoms of pyelonephritis include fever, chills, nausea, vomiting, lower back pain, and frequent painful urination. Pyelonephritis usually only becomes chronic in individuals who have malformations in or damage to the kidneys.
Infections occurring within the reproductive structures of males include epididymitis, orchitis, and prostatitis.
Bacterial infections may cause inflammation of the epididymis, called epididymitis. This inflammation causes pain in the scrotum, testicles, and groin; swelling, redness, and warm skin in these areas may also be observed. Inflammation of the testicle, called orchitis, is usually caused by a bacterial infection spreading from the epididymis, but it can also be a complication of mumps, a viral disease.
Because of its proximity to the exterior, the vagina is a common site for infections in women. The general term for any inflammation of the vagina is vaginitis.
Vaginitis often develops as a result of an overgrowth of bacteria or fungi that normally reside in the vaginal microbiota, although it can also result from infections by transient pathogens. Bacterial infections of the vagina are called bacterial vaginosis, whereas fungal infections (typically involving Candida spp.) are called yeast infections.
Pelvic inflammatory disease (PID) is an infection of the female reproductive organs including the uterus, cervix, fallopian tubes, and ovaries.
The two most common pathogens are the sexually transmitted bacterial pathogens Neisseria gonorrhoeae and Chlamydia trachomatis. Inflammation of the fallopian tubes, called salpingitis, is the most serious form of PID. Symptoms of PID can vary between women and include pain in the lower abdomen, vaginal discharge, fever, chills, nausea, diarrhea, vomiting, and painful urination.
Hair → epidermis → sebaceous gland (attached to the hair) → sweat gland (produce sweat and release it through the pore on the top of the epidermis) → nerves + touch receptors → blood vessels → lymph vessels → everything underneath the epidermis = dermis → fatty tissue or hypo-dermis
dermatitis: inflammation of the skin
Folliculitis: inflammation of the hair follicle
Cyst: enclosed sac filled with fluid
Ulcer: break in skin or open sac
Wheel: swollen, inflamed skin
Abscess: localized collection of pus
Conjuctiva: surface of eyeball and inner eyelids
Lacrinal gland on top of eyelid
Lacrinal puncta in the inner corner of the eyes → lacrimal ducts → lacrimal sac →
Flow of tears: lacrimal gland → through the conjunction → through the lacrimal puncta → then through the lacrimal sac → through the nasal cavity → travels down to to the nasiocrimal duct → excess (swallowed to the stomach, spit out of the oral cavity)
conjuctivitis : inflammation of the conjunctiva
Blephanritis: inflammation of the eyelids
Kidneys → tubes connected to kidneys called ureters → bladder → urethra → renal veins ( kidneys to urethra) → renal arteries bring blood to each kidney so the the blood is filtered and excess salt + water can be removed from the blood
Inside (kidney) → lobes w/nephron (tiny tube) → glomerulus (where the blood is filtered) → enters the nephron comes through the arteoile, it branches off the renal artery → excess salts + water secrete through tubule down to ureter
Most common infection: bladder or kidneys
Cystitis = bladder
Pyelonephritis = kidneys
Urinary tract: urinary bladder → clitoris → urethra → labia minora → labia major → labia majot + minor = vulva → above labia major is the vagina → cervix is above the vagina → then the uterus → fallopian tube → ovary
Urinary tract → urethra → below the urinary bladder, urinary prostate → bulbourethra gland → seminal vesicle → vas deferns → epididymis → testis →
Reproductive System: (not involved in sexual reproduction)
Rectum → anus
Pathogen: measles virus
Portal of entry: respiratory
Enters bloodstream & spreads throughout body
encephalitis (brain inflammation) ; brain damage, death, pneumonia (in lungs); death, rash (skin)
Suppresses immune system (susceptible to secondary infections) ; death
Rash: skin cell mhc1 → tcr cytotoxic cell which causes the cells to kill the skin cells, this kill creates the measles rash
Pathogensis: enters through rep. System & spreads. Infects many cell types, including respiratory, skin, immune cells + brain cells. Cytotoxic T cells attack skin cells, causing rash. Pneumonia encephilitis & secondary infections from decreased immune function may occur.
Prevention/Treatment: vaccine (mmr)
Chicken Pox or Shingles
Pathogen: varicella - zoster virus
Pathogenesis: Transmitted by inhalation or direct contract. Replicates in many cells; including skin and nerve cells. Initiated infection causes chicken pox: pasteur rash. Stays latent in neurons and can re-emerge causing a painful rash called shingles
Pathogen: hemophilus influenzae, adenovirus or others
Pathogensis: inflammation of conjuctivia due to viral or bacterial replication and damage to the tissues
Prevention/Treatment: antibacterial drugs to treat bacterial conjuctivitis
Pathogen: staphylococcus and streptococcus
Pathogensis: grow and damage host cells with exotoxins and exoenzymes
Leukcoidins kills WBC's → pus
SSSS may be caused by straph toxin
Neocrotizing fascitiies: strep penetrates to connective tissue
Skin → fascia → muscle
Prevention/Treatment: antibacterial drugs, staph may be drug resistant
Epidermis → dermis → hypodermis
Cells in epidermis → nucleus blue (HPV genomes) infect the nucleus → genome maintenance in lower layers → HPV virions released in upper layers
Evade immune system → prevent antigen presentation + recruit T regulatory cells to decrease immune cells
Disease: warts, cancer
Pathogenesis: Primarily replicates in epidermis. May integrate into the host genome.
Lower layers: genome maintenance
Upper layers: virions release
Immune evasion: black antigen presentation & recruit T regulatory cells
Viral proteins may dysregulated cell cycle
Prevention/Treatment: often self-limiting , vaccine for cancer-causing stains , wart removal
Tineas: e.g ringworm, athlete's foot, jock itch
Pathogen: various dermatophytes, fungus
Pathogenesis: Cause superficial infections of skin, hair, or nails. Fungi consume Keratin protein
Prevention/Treatment: antifungal drugs
Pathogen: Loa Loa , helminth
Pathogenesis: transmitted by deer flies. Adult worms infect the hypodermis and can migrate through eye conjunction.
Prevention/Treatment: Antihelminthic drugs , eye worms may be surgically removed
Pathogen: myxobacteria, e. Coli, gram (-) rod
Pathogenesis: attach to and damage urinary epithelial cells (inner lining of urinary tract)
Prevention/Treatment: antibacterial drugs
Pathogen: chlamydia trachomatis , gram (-), coccobacillus , no peptidoglycan
Pathogenesis: obligate intracellular replication in reproductive epithelial cells. Infections form: elementary body. Replicative form: reticulate body. Survives inside the endosome. Cell lysis until ready for release.
Prevention/Treatment: antibacterial drugs
Elementary body (endocytosis) → elementary body is inside the endosome inside the host reproductive epithelial cell → reticulate body (binary fission) → inclusion → elementary bodies reproduce, inclusion takes up the entire cell → elementary bodies are released → host cell lysis or extension
Disease: cold sores, genital herpes
Pathogenesis: Initially infects epidermal cells, then moves into neurons. Retrograde transport of virla genome begin latency. T cells maintain latency, HSV blocks cell lysis. Stress/ immunosuppression lead to reactivation and antergrade transport of virion subunits
Prevention/Treatment: antiviral medication e.g. acyclovir
Epidermis → dermis → hypodermis
Virions infect nucleus of cells in epidermis → neuron extends through all three layers and gets to the nervous system → infect the neuron and send copies of the genome up to the cell body of the neuron → retrograde transport of viral genome → In neuron cell body (stable, circulaized viral genome) latent infection → cytotoxic T cells maintian latency but can't quite kill the infected cell → HSV supresses host cell lysis → stress suppresses immune functions, including cytotoxic T cells (reactivation of the cell in the neuron cell body) , starts the viral replication again → anterograde transport of virions
Pathogen: neisseria gonorrhea, gram (-), cocci
Pathogenesis: attach to and damage reproductive epithethal cells from exoenzymes. No immunity; reinfection can occur (mimics host antigen, prevents T cell proliferation , does antigenic variation)
Prevention/Treatment: antibacterial drugs
Pathogen: candida albicans, fungus
Pathogenesis: commensal organism but can be opportunistic , overgrowth biofilm forms on vagina epithethal cells and damage host cells
Prevention/Treatment: antifungal drugs
Pathogen: Trichomonas vaginalis , protozoan
Pathogenesis: overgrowth causes damage through mechanical trauma and hydrogen gas production
Circulatory Anatomy (pt. 1)
Center: heart → lungs are on either side of the heart → vessels coming out of the heart → low oxygen blood: coming from lower extremities + back from upper extremities → Upper right = right atrium → then to lower right chamber of heart here the right ventricle → right ventricle where heart pumps blood → muscles of the heart squeeze tight, squeeze blood out of the right ventricle into blood vessels (pulmonary arteries) → lungs where blood becomes oxygenated →
Circulatory Anatomy (pt. 2)
blood vessels on lungs turn into tiny capillaries that surround the alveoli and oxygen carbon dioxide → oxygen carbon dioxide is exchanged such that the blood is coming back to the heart from the lungs (OXYGENATED BLOOD) → high oxygen blood return through the pulmonary veins entering the upper left chamber of the heart → left atrium move into the lower left chamber of the heart → left ventricle here and where the heart squeezes out again →
Circulatory Anatomy (pt. 3)
Muscles on the left ventricle are going to squeeze that blood out of the heart through the aorta (major blood vessel) → leaving the heart and traveling to the rest of the body there are branches coming off → sending oxygen rich blood to the upper extremities
Circulatory Anatomy (pt. 4)
Aorta curls around down behind the heart to send the blood to the lower extermemities → oxgenated rich blood travels through the capillaries in body → deliver that oxygen to all of the cells of the body → aerobic respiration takes place → providing ATP to cells →
Circulatory Anatomy Infection
Septicemia: bacteria dividing in blood
Sepsis: hyperinflammatory response that is systemic level can lead to septic shock (decrease blood pressure + organ failure + death)
Circulatory Anatomy (infectious agents)
Infectious agents: maybe extracellular or intracellular
If intracellular they maybe infecting red blood cells or various types of white blood cells
Central Nervous System (CNS)
brain and spinal cord
peripheral nervous system
→ network of nerves outside of PNS
Blood barrier → limited permeability between blood vessels and brain
Protects cerebrospinal fluid from infection → restricts drug access: small, lipid-soluble drugs pass through the best
Intracellular entry (pathogen) → Transcellular entry → Leukocyte facilitated → pathogen inside of leukocyte → pathogen flow through the neuron (nonhomogeneous entry) →
Nervous Anatomy (infection)
Meningitis: inflammation of meninges
Encephalitis: inflammation of brain
send sensory and motor information to / from the brain / body.
support function of neurons
Periodontal disease → inflammation of the gums fleshy tissue where the teeth are embedded in the gastrointestinal tract
Result of biofilms formed by many different species of many different microbes → become extremely thick and solidify → the bacteria → biofilms contribute to tooth decay and cavity formation → they do this by fermenting sugars into acids →
Tartar (pt. 2)
acids wear down the enamel on the surface of the tooth which exposes the soft tissue beneath → if protective layer on enamel gets worn through the detin and the pulp can become infected leading to even more severe disease
Streptococcus mutans → bacteria that forms biofilms on the surface of the teeth like this producing acid → also associated with spread to the heart → causes endocarditis can be fatal → preventing dental disease → preserve the teeth of the oral cavity →
Disease: Dental Cavities or Periodontal Disease
Pathogen: many and streptococcus mutans and grant coccus
Pathogenesis: biofilm fermentation on teeth, ferment sugars into acid which damages tooth enamel. Inflammation of gums. Sequelae: endocarditis
Prevention/Treatment: dental hygiene, canies removal, antibacterial drugs
Pathogen: Heliobacteria pylori, gram (-) , spirillum
Lining of stomach, made with epithelial cells → mucous layer (inside of stomach) by the lumen of stomach
where food is
s* → pathogenesis: flagella burrow into the mucosa helps protect it from stomach acid → makes toxins is a cytolytic toxin (VAC) →
Pathogen: Heliobacteria pylori, gram (-) , spirillum (pt.2)
VAC damages host cell causes urea to be released in the stomach → once urea is present in the stomach, secrete enzyme (urease) → urease breaks down urea into carbon dioxide and ammonia → ammonia (base) production helps neutralize acids in stomach → urease breaks down urea producing ammonia and neutralizing the stomach acid →
Pathogen: Heliobacteria pylori, gram (-) , spirillum (pt.3)
h.pylori doesn't do well in an acidic environment , so this is how it alters the environment → other toxins produced by H.pylori (a kag toxin) → kag toxin regulates inflammation , causes hyperinflammatory response → causes damage to the host tissues →
so pathogenesis of h.poly includes: vac + kag (toxin) , urease (toxin) , allows flagella to burrow into the mucous which causes infection of the mucous → leads to ulcers
Pathogen: Heliobacteria pylori, gram (-) , spirillum (pt.5)
Disease: Gastric Ulcers
Flagella: help penetrate mucous
VacA: kills cells/releases urea
Urease: urea → NH3 + CO2, NH3 neutralized
Sequelae: gastric cancer
Triple therapy with 3 antibacterial drugs
Disease: Bacterial Gastroenteritis
Pathogen: clostridium difficile and many others, gram (+), rod
Pathogenesis: Infection or intoxication damages host, C.diff: tcda; enterotoxin damages epithelium + tcbd; cytolytic toxin and kills many cell types
Prevention/Treatment: metronidazole + vancomycin , fecal transplant
Disease: viral gastroenteritis
Pathogen: rotavirus (longer), norovirus(short lived)
Pathogenesis: infect small intestine epithelial cells
prevention/treatment: self-limiting, rotavirus vaccine, oral rehydration therapy
Pathogen: giardia lamblia, protozoan
Pathogenesis: cyst are consumed and develop into trophozoites. Attaches to intestinal epithelium with adhesive disc, blocking nutrient absorption.
Disease: Pinworm Infection
Pathogen: enterobius vermicularis
Pathogenesis: Fecal-oral transmission worms emerge from anus to lay eggs at night, causing itching.
Prevention/Treatment: Anthelmintic Drugs
Pathogen: 5 different viruses (HAV, HBV, HCV, HDV, HEV)
Replicate in liver cells, causing inflammation of the liver.
Chronic inflammation can lead to liver failure or liver cancer
Prevention/Treatment: Vaccine (HAV / HEV / HBV / HDV) and Antiviral drugs for HCV
Pathogen: Epstein Barr Virus
Pathogenesis: Primarily infects B cells. Becomes latent in memory B cells, persists for life.
Sequale: burkitt lymphoma in people with HIV or malaria
Pathogen: Human Immunodeficiency Virus (HIV)
Disease: Acquired immunodeficiency syndrome (AIDS)
Pathogenesis: Infects CD4+ T cells, leading to immunodeficiency. Forms a provirus in the host cell genome, making eradication impossible. Fast mutation due to error-prone reverse transcriptase.
Prevention/Treatment: Combination antiviral drug therapy can increase lifespan by decades
Pathogen: Human Immunodeficiency Virus (HIV) [pt.2]
CD4+ cell → inhibited by antiviral drugs (HIV virion) → entry by fusion → uncoating → reverse transcription (copy viral RNA to DNA) → integration (nucleus + host dna + provirus) → provirus transcribed viral RNA → translated to viral polypeptides → cleaved → creates viral proteins or
Translated → byrons which are released from cell as HIV virion
Pathogen: Human Immunodeficiency Virus (HIV) [pt.3]
Inhibit reverse transcriptase
Inhibit viral protease
Pathogen: Plasmodium Falciparum and Protozoan
Plasmodium Falciparum Life Cycle:
Human → mosquito inject P.Falciparum into blood → Travels to liver and replicates inside of liver cells → enters blood (replicates + makes gametes) → can see P.f as dots/rings under the microscope → mosquito ingests gametes → gametes, fuse forming zygote → divide + develop → migrate to mosquito salivary glands →
Pathogen: Plasmodium Falciparum and Protozoan
Infects liver cells, RBCs, mosquito gut and salivary glands. Hyperinflammatory damage to RBCs leading to hypoxia (low oxygen) , organ failure, death.
Immune evasion: no MHCI, Sticky protein, antigenic variation
Prevention/Treatment: limited anti-protozan drugs, mosquito & nets + pesticides
Pathogen: many microbes
Pathogenesis: Typically enter through blood-brain barrier and cause inflammation, nerve damage and brain swelling
Prevention/Treatment: Viruses mostly self-limiting , Antibacterial drugs
Pathogen: usually viral
Pathogenesis: viral replication in nervous tissue causes brain inflammation. May cause permanent brain damage, coma, or death.
Prevention/Treatment: Vaccine for japanese encephalitis
Pathogen: zika virus
Disease: zika virus infection
Pathogenesis: usually mild respiratory symptoms. Can infect neural progenitar cells, may explain fetal microephaly
Prevention/Treament: no vaccine or treatment
Bite → viral replication of muscle cells → virus moves to neuron, travels to spinal cord → viral replication in neurons → travel to the brain → virus travels to salivary glands
Damage: neuron death, enccephilaits, fatal
Pathogen: rabies virus
Pathogenesis: infects muscle cells then neurons. Induces neurons to produce nitric oxide and reactive oxygen species, damaging and killing neurons.
Prevention/Treatment: vaccine , human rabies immunoglobulin (only effective before symptoms)
mouth → teeth + tongue → glands (produce saliva and digestive enzymes start digesting the food before the tongue swallows the food down through pharynx→ pharynx → esophagus ( long tube that undergoes peristalsis where the muscles squeeze pushing the food down into the stomach) → liver; producing bile , helps breaks down fat→ gallbladder; bile is stored, squirted through the bile duct into the small intestine, the fats are digested in the small intestine then leaving the small intestine →
GI anatomy: (pt.2)
stomach (has acids and enzymes that help digest the proteins in the food ) several layers of muscle ; Stomach muscles → squeeze and pulverize the food until it's a liquid pulp then the food will move from the stomach → pancreas → makes enzymes for digesting fats, proteins, and carbohydrates sends them to small intestine → small intestine; majority of food digestion and absorption makes digestive enzymes , leaving is any food waste that wasn't absorbed in the small intestine moves to large intestine
GI anatomy: (pt. 3)
→ large intestine; travels up and around ends in the rectum, has massive # of bacteria in it that are fed on the food waste that is not consumed and absorbed in the small intestine, absorbs most of the water not the only place where microbiota are found through the entire length of the digestive tract, pathogens can gain hold throughout the length of the digestive tract → rectum + anus;
GI anatomy: DAMGE
Gastrointestinal tract → infection
Intoxication → where the pathogens don't grow inside, they've grown elsewhere and produced toxins consuming those toxins causes damage
Disease inflammation for causing gastrointestinal→ gastritis
Disease inflammation for causing stomach → enteritis
Both are called gastroenteritis inflammation → caused by contaminated food diseases are spread through a fecal oral route
Disease inflammation for causing colon → colitis
Inflammation in the liver → hepatitis
mouth, teeth, tongue
Food enters the digestive tract through the mouth, where mechanical digestion (by chewing) and chemical digestion (by enzymes in saliva) begin. Within the mouth are the tongue, teeth, and salivary glands, including the parotid, sublingual, and submandibular glands
Tooth: (pt. 1)
begins with the visible outer surface, called the crown, which has to be extremely hard to withstand the force of biting and chewing. The crown is covered with enamel, which is the hardest material in the body. Underneath the crown, a layer of relatively hard dentin extends into the root of the tooth around the innermost pulp cavity, which includes the pulp chamber at the top of the tooth and pulp canal, or root canal, located in the root.
The pulp that fills the pulp cavity is rich in blood vessels, lymphatic vessels, connective tissue, and nerves. The root of the tooth and some of the crown are covered with cementum, which works with the periodontal ligament to anchor the tooth in place in the jaw bone. The soft tissues surrounding the teeth and bones are called gums, or gingiva. The gingival space or gingival crevice is located between the gums and teeth.
bacteria and archaea are abundant in the mouth and coat all of the surfaces of the oral cavity. However, different structures, such as the teeth or cheeks, host unique communities of both aerobic and anaerobic microbes. Some factors appear to work against making the mouth hospitable to certain microbes.
Additionally, fluids containing immunoglobulins and phagocytic cells are produced in the gingival spaces. Despite all of these chemical and mechanical activities, the mouth supports a large microbial community.
produce saliva, which lubricates food and contains digestive enzymes.
As food leaves the oral cavity, it travels through the pharynx, or the back of the throat, and moves into the esophagus, which carries the food from the pharynx to the stomach without adding any additional digestive enzymes. The stomach produces mucus to protect its lining, as well as digestive enzymes and acid to break down food.
The environment of most of the GI tract is harsh, which serves two purposes: digestion and immunity. The stomach is an extremely acidic environment (pH 1.5-3.5) due to the gastric juices that break down food and kill many ingested microbes; this helps prevent infection from pathogens
small intestine (pt.1)
Digestion continues in the small intestine, where the majority of nutrients contained in the food are absorbed. Simple columnar epithelial cells called enterocytes line the lumen surface of the small intestinal folds called villi. Each enterocyte has smaller microvilli (cytoplasmic membrane extensions) on the cellular apical surface that increase the surface area to allow more absorption of nutrients to occur
small intestine (pt.2)
Digested food leaves the small intestine and moves into the large intestine, or colon, where there is a more diverse microbiota. Near this junction, there is a small pouch in the large intestine called the cecum, which attaches to the appendix. Further digestion occurs throughout the colon and water is reabsorbed, then waste is excreted through the rectum, the last section of the colon, and out of the body through the anus
small intestine (pt.3)
The environment in the small intestine is less harsh and is able to support microbial communities. Microorganisms present in the small intestine can include lactobacilli, diptherioids and the fungus Candida.
Partially digested food then leaves the stomach through the pyloric sphincter, reaching the first part of the small intestine called the duodenum. Pancreatic juice, which includes enzymes and bicarbonate ions, is released into the small intestine to neutralize the acidic material from the stomach and to assist in digestion
Bile, produced by the liver but stored in the gallbladder, is also released into the small intestine to emulsify fats so that they can travel in the watery environment of the small intestine. Digestion continues in the small intestine, where the majority of nutrients contained in the food are absorbed.
On the other hand, the large intestine (colon) contains a diverse and abundant microbiota that is important for normal function. These microbes include Bacteriodetes (especially the genera Bacteroides and Prevotella) and Firmicutes (especially members of the genus Clostridium). Methanogenic archaea and some fungi are also present, among many other species of bacteria. These microbes all aid in digestion and contribute to the production of feces, the waste excreted from the digestive tract, and flatus, the gas produced from microbial fermentation of undigested food. They can also produce valuable nutrients.
Infections and intoxications of the lower GI tract often
produce symptoms such as nausea, vomiting, diarrhea, aches, and fever. In some cases, vomiting and diarrhea may cause severe dehydration and other complications that can become serious or fatal. Various clinical terms are used to describe gastrointestinal symptoms.
is an inflammation of the stomach lining that results in swelling
refers to inflammation of the intestinal mucosa.
When the inflammation involves both the stomach lining and the intestinal lining, the condition is
Inflammation of the colon, called
commonly occurs in cases of food intoxication. Because an inflamed colon does not reabsorb water as effectively as it normally does, stools become watery, causing diarrhea. Damage to the epithelial cells of the colon can also cause bleeding and excess mucus to appear in watery stools, a condition called dysentery.
Inflammation of the liver is
Ingested food → down the stomach to intestines → bacteria may produce toxins during the infection and then bacteria themselves and or toxins they produce can damage the host
Bacteria produce toxins in food while still in the environment → toxins are ingested → cause gastroenteritis , toxins damage host
Normal gut microbiome member
Can overgrow during antibiotic use (survives by forming endospores)
Common hospital-acquired infection (HAI)
Clostridium Difficile (pt. 2)
Epithelium → intestinal epithelium → lumen side → layer of mucous → starts to overgrow → produces toxins: tcda and tcbd → tcda: enterotoxin that attacks the junctions between epithelial cells has two different effects → tcda makes the intestinal epithelial cells more leaky allow c.diff to invade deeper into the tissues → tcbd cytolytic toxin that kills many cell types can cause intestinal epithelia often forms a pseudo membrane which can decrease the ability of the intestine to perform its functions of water and mineral absorption
If bacteria are reproducing in the blood as they spread, this condition is called
is characterized by the production of excess cytokines that leads to classic signs of inflammation such as fever, vasodilation, and edema
Critical organs such as the heart, lungs, liver, and kidneys become dysfunctional, resulting in increased heart and respiratory rates, and disorientation. If not treated promptly and effectively, patients with sepsis can go into shock and die.
Stage 1: Acute HIV infection: chronic inflammation
Acute HIV syndrome
Wide dissemination of virus
Seeding of lymphoid organs
Stage 2: Clinical latency
Low level replication
Slow increase in amount of virus
Slow decrease in # of T cells
Stage 3: Acquired immunodeficiency syndrome (AIDS)
This drastic decrease in the number of t cells means that the person is now immunocompromised ( not capable of fighting off pathogens)
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