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final exam micro
ch 19-24
| Question | Answer |
|---|---|
| functions of skin | prevent excessive water loss, important to temp regulation, assists in formation of vitamin d, involved in sensory phenomena, barrier against microbial invaders |
| outermost layer of skin | flattened, dead, dry, keratinized; covered w salt and sebum, contains antimicrobial chemicals; sloughing of skin removes microbes |
| microbiome of skin | members of microbiome compete w potential pathogens for nutrients and space, and produce chemicals that interfere w growth of other microbes |
| microbes cannot be completely removed thru cleansing | they typically grow in small clusters in moist areas (waste products produce body odor) |
| prominent members of microbiome of skin | malassezia, staphylococcus, micrococcus, diphtheroids (gram pos rods) |
| folliculitis is caused by | genus staphylococcus (anaerobic, gram pos cocci in clusters) |
| folliculitits is tolerant of | salt, drying, solar radiation, heat |
| staphylococcus epidermis | 90% of bacteria on skin, major member of microbiome (deals w folliculitis) |
| staphylococcus aureus | more virulent than epidermis, often grows in nasal passages, produces variety of disease conditions and symptoms (folliculitis) |
| two species of staph | staphylococcus epidermis and aureus |
| follicutlitis has 3 categories of virulence factors | enzymes, structual defenses against phagocytosis, and toxins |
| enzymes in folliculitis | coagulase, hyaluronidase, staphylokinase, lipase, B-lactamase |
| role of coagulase | immunological disguise |
| role of hyaluronidase and staphylokinase | promotes spread |
| role of lipase | provide source of nutrition on surface of skin |
| role of B-lactamase | resistance to some antibiotics |
| structural defenses against phagocytosis | slime layer, protein A |
| role of slime layer | inhibits chemotaxis of and phagocytosis by wbc; facilitates attachment of biofilms to artificial surfaces |
| role of protein A | inhibits opsonization and complement cascade |
| toxins in folliculitis | cytolytic toxins, leukocidin, epidermal cell differentiation inhibitor, exfoliative toxin, toxic shock syndrome toxin |
| role of cytolytic toxins | damage cytoplasmic membranes |
| role of leukocidin | kills leukocytes |
| role of epidermal cell differentiation inhibitor | induces holes in the linings of blood vessels; invasion into tissues |
| role of exfoliative toxin | dissolution of epidermal desmosomes (promotes spread) |
| role of toxic shock syndrome toxin | causes over-activation of t cells and results in overabundance of cytokines that produce vast array of signs and symptoms |
| folliculitis is transmitted | among humans via direct contact and via fomites; organism grows into hair follicles and invades sebaceous glands; inflammation and fever |
| follicle enlarges and fills w pus | may spread into hypodermis to form furuncle or into neighboring hair follicles to form a carbuncle |
| s. aureus can cause bacteremia and be carried around body w folliculitis | endocarditis, pneumonia, osteomyelitis |
| folliculitis | base of follicle becomes red, swollen, and pus filled (pimple) |
| signs and symptoms of folliculitis | sty, furuncle, carbuncle, fever |
| sty | pimple at base of eyelid |
| furuncle | nodular extension of folliculitis into surrounding tissues |
| carbuncle | when several furuncles join together |
| s. epidermis is ubiquitous on human skin | seldom causes disease bc lacks virulence factors, can be opportunistic pathogen |
| s. aures not permanent resident but grows on skin and mucous membranes (nostrils) at some point in most people's lives | s. aures most oten transferred from face to other locations on body, 20% carry the bacterium for >1 yr w no symptoms |
| diagnosis of folliculitis | detection of gram pos bacteria in grapelike arrangements isolated from pus; positive coagulase test for s. aureus; coagulase-negative staphylococci usually s. epidermis not indicative of staphylococcal infection |
| treatment of folliculitis | treated w topical mupirocin (cream), critical to clean and drain abscesses of pus before topical therapy, drug resistant s. aureus is problem (mrsa and vrsa) |
| prevention of folliculitis | those w staph lesions should refrain from working w food, patients w open wounds, immunocompromised patients and women in labor; and should not work in nurseries or operating rooms; aseptic techniques (hand antisepsis) |
| rocky mountain spotted fever caused by | rickettsia rickettsii (small, aerobic, gram-neg, intracellular) |
| rocky mountain spotted fever requires | vector for transmission (hard ticks of genus dermacentor) |
| rocky mountain spotted fever is dormant in salivary glands of tick | it becomes active and infective only when tick feeds for 6-10hrs; rare cases= human is infected following exposure to tick feces or tissues and fluids from crushed ticks |
| rocky mountain spotted fever organisms travel into mammalian host's cirulatory system where they infect cells lining small blood vessels | stimulates endocytosis, but lyse the endosome prior to endosome/lysosome fusion; released into host cell's cytosol |
| no toxins are produced in rocky mountain spotted fever and it is not due to immune response | damage to blood vessels allowing blood to leak into tissues, low blood pressure, insufficient nutrient and oxygen delivery to body's organs |
| signs/symptoms of rocky mountain spotted fever | one week after infection-->fever, headache, chills, muscle pain, nausea, vomiting; 90% develop non-itchy/spotted rash on trunk and appendages (palms/soles); of 50% have rash develop into petechiae (subcutaneous hemorrhages); encephalitis can occur, |
| severe cases of rocky mountain spotted fever have | respiratory, cns, gi and renal system failure |
| signs/symptoms of rocky mountain spotted fever 2 | 5% die w treatment, patients recovering from life-threatening acute rmsf may experience leg paralysis, hearing loss, and gangrenous secndary infections that require amputation |
| encephalitis | language disorders, delirium, convulsions, coma, and death |
| rocky mountain spotted fever epidemiology | hard ticks in genus dermacentor transmit organisms among humans and rodents(reservoirs/zoonosis);male ticks infect female ticks during mating and females transmit the bacteria to eggs forming in their ovaries(transovarian transmission;direct contact) |
| rocky mountain spotted fever most common in | north carolina, oklahoma, arkansas, tennessee, and missouri; highest among makes, american indians and >40; if do not receive treatment, will have inc risk of death |
| diagnosis of rocky mountain spotted fever | based on rash on soles or palms, sudden fever and headache following exposure to hard ticks; serological tests confirm initial diagnoses; early treatment makes difference bw recovery and death |
| treatment of rocky mountain spotted fever | doxycycline or chloramphenicol; if initiated w/in first 4-5 days, fever subsides within 24-72 hrs |
| prevention of rocky mountain spotted fever | no effective vaccine, wear tight-fitting clothing (light colors), tick repellants (permethrin and DEET), body checks and remove attached ticks; avoid tick infested areas (especially spring and summer) |
| chickenpox/singles caused by | varicella zoster virus (herpesvirus); icosachedral, enveloped, dna virus |
| chickenpox begins in mucous membrane of respiratory tract | it spreads to liver, spleen, lymph nodes via blood and lymph; second wave of viruses spreads via blood thruout body and skin 2 weeks later |
| chickenpox infects cells of dermis, producing rash (fever and malaise) | viruses are shed before and during symptoms thru respiratory droplets and fluid in lesions (direct contact) |
| virus becomes latent in nerve ganglia and can reactivate in adults (shingles) | virus travels down the nerve to cause shingles lesions in the band of skin innervated by the infected nerve |
| signs and symptoms of chickenpox | highly infectious, 2-3 weeks after infection, patient develops slight fever and skin lesions on back and trunk->spread to face, neck ad limbs |
| chickenpox lesions begin as macules | progress in 1-2 days to papules, become thin-walled, fluid-filled vesicles on red bases (teardrops on rose petals); successive crops of lesions appear over 3-5 day period; not life-threatening but may be to newborns |
| chickenpox becomes latent in sensory nerves, stress aging, or immune suppression cause virus to reactivate in 15-20% of infected individuals | travel down nerve they inhabit, produce extremely painful skin rash near distal end of nerve, lesions localized and on same side of body as nerve (accompanied by burning, numbness, itchiness, pain); scabs fall off and no further symptoms; |
| chickenpox more seen in children, more severe in adults | much of tissue damage results from immune response; shingles usually after 45; 4% develop second case shingles |
| shingles person can spread virus to | person who never had chickenpox |
| diagnosis of chickenpox/ | appearance of lesions; antibody tests available |
| diagnosis of shingles | more difficult, localization w/in band of skin on one side of body |
| treatment of chickenpox | self-limint; no treatment required; acyclovir may reduce severity and duration of chickenpox |
| treatment of shingles | management of symptoms, bedrest, and oral acyclovir; loose-fitting clothing and non adherent dressings; acyclovir provides relief but not cure |
| prevention of chickenpox | difficult to prevent exposure to virus (carriers); attenuated vaccine protects against chickenpox (varivax)-12-18months old and again before starting school |
| prevention of shingles | recmbinant vaccine that protects against shingles (shingrix, rzv); 2 dose series in 50+, >90% efficacy; elicits specific response against glyocprotein E; contains novel adjuvant; approved by fda |
| measles virus (rubeola) | more contagious and serious childhood diseases; genome of nonsegmented, ssRNA; helical nucleocapsid surrounded by envelope; humans only natural hosts |
| virulence factors of measles | adhesion proteins= attachment to host cell; fusion protein= enter into and spread bw cells by promoting direct membrane fusion |
| measles is highly contagious | droplet and airborne transmission, infects cells in respiratory tract, spreads thruout body via blood and lymph; ctls kill infected cells, cause most of symptoms |
| bacterial secondary infections inc seriousness of measles | infacts, pregnant women, immunocompromised (compromised cell-mediated immunity) and malnourished patients @ greater risk of developing complications and experience more severe illness |
| measles signs and symptoms | incubation period 8-12 days; fever, sore throat, headache, dry cough, and conjunctivitis appear initially; 2-3 days later, koplik spots develop on mucous membranes of mouth; on 4th day raised lesions appear on head and spread over body (rash lasts 3-5 day |
| koplik spots | described as crystals of salt surrounded by red halo, provide definitive diagnosis of measles |
| 80% of non-vaccinated people exposed to the virus will develop sings and symptoms | only infects humans (dense population of susceptible people must be present for virus to spread); patients are infectious from onset of prodromal symptoms until 2-4 days after rash development (higher before rash appearance) |
| measles can be serious and even fatal for small children | disease kills more than 100,000 people a year, most under 5 |
| diagnosis of measles | kopliks spots; serological testing confirms persence of measles antigen |
| treatment of measles | supportive therapy, administration of vitamin a, antibodies against measles virus, and ribavirin |
| measles prevention | live, attenuated vaccine introduced in 1963 and part of MMR vacine given @ 12 months and ~4yrs |
| elimination of measles | requires 2-dose immunization coverage of at leasat 90-95% of population; choosing not to vaccinate children or opting for an alternate vaccination schedule is leading to the current epidemic in the US; |
| measles immunization can be given up to 72 hrs post-exposure to prevent measles in unvaccinated individuals | passive immunization w measles immunoglobulin bw 72 hrs and 6 days following exposure or in persons who cannot take this vaccine can be given to prevent or dec the severity of disease |
| Nervous system | central and peripheral |
| defenses that protect nervous system | brain encased w/in bony skull, spinal cord protected by vertebrae, both by meninges; |
| csf (cerebral spinal fluid) circulates around the brain and spinal cord bw the layers of meninges | csf adds to the protection bc it absorbs some of the shock of an injury; protected against chemical injury by the blood-brain barrier |
| cns is an axenic environment | has no normal microbiota |
| pathogens can access the cns by | breaking in bones and meninges, medical procedures, traveling in peripheral neurons to cns, carried by blood or lymph and break blood-brain barrier, circulation of cerebrospinal fluid |
| bacterial meningitis caused by >50 species (some opportunitstic); main 5 that cause 90% are | neisseria meningitidis, streptococcus pneumoniae, haemophilus influenzae, listeria monocytogenes, streptococcus agalactiae |
| meningococcal meningitis caused by | neisseria meningitidis; gram neg diplococcus; 12 serogroups (6 are a,b,c,w,x,y) that can cause epidemics; known as meningococcus; nonmotile |
| meningococcal meningitis virulence factors | polysaccharide capsule, lipooligosaccharaide; enable bactera to attach to human cells; avirulent strains lack fimbriae, capsule, and lipooligosaccharide |
| meningococcal meningitis polysaccharide capsule | organisms survive, reproduce, and are carried thru/o body w/in neutrophils and macrophages |
| meningococcal meningitis lipooligosaccharide (LOS=cell wall antigen) | composed of lipid a and sugars; blebbing-released from outer membrane and triggers fever, vasodilation, inflammation, shock, and blood clotting |
| bacterial meningitis pathogenesis 1 | humans inhale organisms in respiratory droplets from infected individuals (droplet transmission) who may be asymptomatic (carriers); metabolize glucose in CSF |
| bacterial meningitis pathogenesis 2 | bacteria spreads to meninges from infections of lungs, sinuses, or inner ear via blood; somewhat protected by capsules in phagocytosis; |
| bacterial meningitis signs and symptoms 1 | inc # of wbc in csf, sudden high fever, intense meningeal inflammation; inflamed cranial meninges produces severe headache, nausea, vomiting, pain, loss of brain functions leading to drowsiness, confusion, fretfulness, or irritability |
| bacterial meningitis signs and symptoms 2 | inflamed spinal meninges produces stiff neck and affects sensory input and muscular control; encephalitis occurs when brain becomes affected (deafness, blindness, behavioral changes, coma or death) |
| bacterial meningitis signs and symptoms 3 | signs and symptoms develop swiftly, can kill w/in 6 hrs; dramatic inc in wbc in csf (milky white in color); differentiated y other types by rapdily spreading petechial rash (occasionally occur in meningitis caused by other bacteria) |
| bacterial meningitis epidemiology | spready via respiratory droplets to those who have prolonged contact w patient; humans are reservoirs; carriage rates higher in older children/young adults; only type that becomes epidemic (military personnel in barracks, dorms) |
| morality rate of meningococcal meningitis | 100% if untreated, 8-15% if treated early and adequately |
| diagnosis of bacterial meningitis | symptoms always seirous, consult physician immediately; culturing bacteria from csf following spinal tap; serological tests can demonstrate presence of antibodies |
| treatment of bacterial meningitis | potentially fatal and should always be viewed as medical emergency; variety of IV administered antimicrobial drugs |
| prevention of meningococcal meningitis 1 | meningococcal polysaccharide vaccine (MPSV4)- menomune; strains a,c,y and w135; only humoral immunity, licensed for use in people>2; discontinued, so recommendation is to receive menactra or menveo |
| prevention of meningococcal meningitis 2 | meningococcal conjugate vaccine (MCV4)-menveo, menactra; strains a,c,y, w135; polysaccharides conjugated to diphtheria toxoid (CRM197); humoral or cell-mediated immunity; menveo-2 mths/55 yrs; menactra-9mths/55yrs; recomennded 11-18 and inc risk of diseas |
| mpsv4 and mcv4 are | 90% effective |
| close or prolonged contact w patient should receive | prophylactic antibiotics for meningococcal meningitisis |
| prevention of meningococcal meningitis 3 | MenB vaccine (bexsero and trumenba)=recombinant protein vaccines |
| pneumococcal meningitis caused by | streptococcus pneumoniae, gram pos coccus; ususally in pairs (pneumococcus); >93 strains known to infect humans; leading cause of meningitis in children <5 and old adults |
| normal microbiome of throat that opportunistically grow in lungs, sinuses and middle ear and mvoe from these locations via blood into meninges | pneumococcal meningitis microbiome |
| virulence factors for pneumococcal meningitis | polysaccharide capsule, secretory IgA protease, pneumolysin, phosphorylcholine |
| polysaccharide capsule pneumococcal meningitis | protection from digestion following phagocytosis |
| secretory IgA protease pneumococcal meningitis | destorys IgA |
| pneumolysin pneumococcal meningitis | cholesterol-dependent cytolysin |
| phosphorylcholine pneumococcal meningitis | cell wall adhesion that binds to receptors on cells in lungs, meninges, and blood vessel walls; stimulates target cells to endocytose them; organisms can then cross from these cells into the blood and brain |
| pneumococcal meningitis present in mouths and throats of 75% of humans w/o causing harm | organism becomes bloodborne in some patients and invades meninges (children/elderly); mortality rate of pneumococcal meningitis and L. monocytogenes menigitis >2x that of meningitis caused by other organisms |
| pneumococcal meningitis prevention 1 | pneumococcal polysaccharide vaccine (PPSV23)-pneumovax (23 valent formulation that represents 85-90% of strains cause invasive disease;t-independent antigens dont produce secondary response and may not be long lasting;efficacy 60%;cant be given to kids <2 |
| who should receive PPSV23 | anyone 2+ w certain medical conditions; adults >65 |
| pneumococcal meningitis prevention 2 | pneumococcal conjugate vaccine (PCV15 (vaxneuvance)and PCV20 (prevnar 20); 15 or 20 valent formulation conjugated to nontoxic mutant diphtheria toxin (carrier protein CRM197); t dependent b cell response-memory |
| who should receive PCV15 or PCV20 | all adults>65 and younger people @high risk for pneumococcal disease; if person has received pcv13 or pcv15, they should receive PPSV23 6-12 months later; if person received PPSV23, they should receive one of new PCVs at least a year after PPSV23 |
| viral diseases of nervous system | most common form of meningitis, viruses cross blood-brain barrier, more frequent than bacterial and fungal infections, attack other body systems can also affect the brain |
| viral meningitis virulence factors | 90% of cases caused by members of genus Enterovirus of the family Picornaviridae (very small, nonenveloped, rna viruses |
| viral meningitis pathogenesis 1 | often spread from person to person via fecal contamination of food, water, or hands; can also be spread via respiratory secretions; replicates in GI or lungs and kills target cells; gains access to bloodstream (primary viremia) |
| viral meningitis pathogenesis 2 | spreads to liver, spleen, lymph nodes; secondary viremia occurs=thought to be responsible for seeding the cns; cells in meninges killed, incubation period 3-7 days and patients recover completely after another 7-10 days |
| signs/symptoms viral meningitis | more mild disease than bacterial meningitis, similar to bacterial meningitis; fever, stiff neck, severe headache, drowsiness, confusion, nausea, and vomiting (worst headache of my life); skin rash, sore throat colds; death rare |
| viral meningitis epidemiology 1 | enteroviruses are very common and very contagious (result in infection resembling a cold; meningitis rare); spread in summer and early fall; stable in environment and survive in chlorinated swimming pools |
| viral meningitis epidemiology 2 | contagious from onset of signs and symptoms up to 10 days; neonates at greatest risk w most significant risk of morbidity and mortality; |
| risk factors viral meningitis | exposure to someone w recent viral infection, children in daycare facility, or having suppressed immune system |
| diagnosis of viral meningitis | signs and symptoms of meningitis without presence of bacteria in CSF |
| treatment of viral meningitis | no specific treatment; bed rest, plenty of fluids, and medication to relieve fever and headache |
| viral meningitis prevention | hard to prevent, frequent hand washing, avoidance of crowded swimming pools, and refraining from touching mouth, nose, or eyes w contaminated hands |
| cardiovascular system | heart, blood, blood vessels; capillaries carry blood to the surrounding tissues and also leak fluid that is picked up by the lymphatic vessels |
| defenses that protect the cardiovascular system | closed system, mechanical defenses |
| normal micrbiota of cardiovascular system | blood normally does not contain microbes (breaks in skin or mucous membranes provide entry route), blood and lymph may spread microbes throughout body |
| lyme disease caused by | borrelia burgdorferi (rarely B. mayoni)= gram neg spirochete that has endoflagella w/in the periplasmic space, burrows into tissues |
| lyme disease lacks iron-containing enzymes and molecules | changes outer surface proteins (OSPs), antigenic variation; called he great imitator bc its symptoms mimic many other diseases |
| lyme disease transmits by | vector bite-hard ticks of genus Ixodes (deer ticks in northeastern and north-central US); western black-legged tick in pacific coastal US |
| lyme disease pathogenesis | white-footed mouse, chipmunks, short-tailed and masked shrews and eastern gray squirrels serve as hosts; NYMPHS transmission into large animal hosts |
| lyme disease transmission | transmitted thru bite of tick and infection occurs 12-24 hrs; organisms move from site of infection thru blood/lymph; accumulate in joints and can subsequently trigger arthritis; remain dormant in human host for long periods |
| lyme disease signs/symptoms | mimics other diseases and highly variable in its presentation, vast array of signs and symptoms bc organism can infect several parts of the body at the same time; typically 3 phases in untreated patients |
| early signs of lyme disease | 3-30 days after tick bite, expanding red rash resembling bull's eye that may appear @ site of tick bite (erythema migrans- EM) w/in 3-14 days of infection and lasts 2-4 wks, appears in 70-80% of cases |
| other early signs of lyme disease | malaise, headaches, dizziness, stiff neck, severe fatigue, fever, chills, muscle and joint pain, infected lymph nodes |
| disseminated lyme signs/symptoms | days to months after tick bite, multiple secondary ringed rashes on areas of body, flu-like symptoms; |
| cardiac manifestations lyme disease | heart arrythmia, myocarditis and pericarditis |
| rheumatologic manifestations lyme disease | arthritis, pain in tendon, bursae, muscle, and bones |
| neurologic manifestations lyme disease | bell's palsy, meningitis, subtle cognitive difficulties |
| PTLDS (chronic lyme) signs/symptoms | occurs if disease is not diagnosed and treated early and appears weeks, months, or even years later; severe fatigue, sleep impairment, joint pain, depression, headaches |
| inc incidence rate of lyme disease | discovered 1975, humans moving into woodland areas, deer population protected; even encouraged to feed in suburban yards; foxes which reduce mouse populations have been displaced by coyotes (~476,000 new cases annually) |
| diagnosis of lyme disease based on | signs and symptoms of diseases and history of possible exposure to infected Ixodes ticks |
| diagnosis of lyme disease | confirmed by demonstrating presence of antibodies against Borrelia; neg test doesnt mean that dont have disease, not enough time for antibodies to develop (>4-6 wks), suppressed immune system, infection=causing strain not measured by test |
| treatment of lyme disease | antimicrobial drugs like doxycycline or amoxicillin, or cefuroxime axeti can cure if disease is in first phase; prolonged treatment w large doeses may be required if neurological or cardiac forms are present; treatment of later phase is difficult |
| prevention of lyme disease 1 | prevent contact w ticks in summer when nymphs are feeding, wear long-sleeved shirts and long, tight-fitting pants and tuck pants cuff into socks; repellents using DEET (N,N-diethyl-m-toluamide); |
| prevention of lyme disease 2 | examine body for ticks or bites; remove attached ticks using forceps; vaccine available until march 2022 |
| infetious mononucleosis caused by | human herpes virus 4 (HHV-4= epstein-barr virus (EBV); enveloped ds DNA virus, latent w/in cells, resulting in lifelong infection, EBV causes infected b lymphocytes to become immortal which are source of cancers (additional factors) |
| ebv plays role in | chronic fatigue syndrome, b cell lymphomas, oral hairy leukoplakia |
| ebv is transmitted thru saliva (direct/indirect contact) | kissing, coughing, sneezing, sharing drinking glass or eating utensils; humans only known reservoir but the virus is not very contagious |
| ebv infects epithelial cells of the throat and parotid salivary glands | lytic replication cycle associated w release of virions into bloodstream (viremia); virus then invades b lymphocytes which then spread the infection thru/o body; ctls kill infected b cells (signs/symptoms) |
| mono signs/symptoms | appear 4-6 wks after infection; initial symptoms=severe sore throat, fever, weakness; swollen lymph nodes in neck and armpits, enlarged spleen, fatigue, nausea, loss of appetite, headache, skin rash; resolve in 1-2 months; can last 6+months |
| in children <6, ebv caused milk illness that resembles respiratory infections | cell immune system immature, typically occurs in countries w poor sanitation and inadequate standards of hygiene |
| where living standards are higher, childhood ebv infection less likely and infection doesnt occur until adolescence or later | more vigorous cell-mediated immune response that produces signs and symptoms |
| 95% of adults worldwide have | been infected w ebv |
| peak incidence in US of ebv is | 15-24 yrs; cell immune system active and produces vigorous response |
| diganosis of mono | large, lobed b lymphocytes w atypical nuclei and neutropenia; atypical lymphocytes account for up to 30% of wbcs; can test for antibodies to viral capsid antigen (vca), early antigen (ea), ebv nuclear antigen (ebna) |
| treatment of mono | relief of symptoms, most recover w/o treatment w/in 2-4 wks, avoid contact sports to reduce risk of rupturing enlarged spleen |
| prevention of mono | no vaccine, do not donate blood for at least 6 months after onset of infection; transmitted regularly in saliva and widespread so prevention hard |
| malaria caused by | 5 species of plasmodium |
| virulence factors of malaria | reproductive cycle occurs w/in rbcs (no mhc i); genetic/antigenic variation; adesins; plasmodium |
| adhesins in malaria | adherence to cell receptors in mosquito and human; plasmodium engage host and invaginated the membrane to form parasitophorous vacuole where the replicates; mediate adherence of infected erythrocytes w/in host |
| change in vertebrae for malaria | plasmodium can change the attractiveness of vertebrae hosts to Anopheles vectors,leading to greater # of vector-host contacts & inc transmission;aldehydes heptanal,octanal,nonanal produced in inc amounts by infected individuals&detected by mosquito antena |
| 3 stages of life cycle of malaria | exoeryhtrocytic cycle, erythrocytic cycle, sporogonic cycle |
| exoerythrocytic cycle | infected female mosquito of genus Anopheles bites host, infective forms injected along w anticoagulant, sporozites reach liver via bloodstream and reproduce over next 7-10 dys, livre cells rupture and organisms released into bloodstream |
| erythrocytic cycle | organisms invade rbcs and feed on hemoglobin, ring stage is diagnostic; reproduce w/in and lyse rbc; lysis of rbc occusr simultaneously cyclically every 48-72 hrs (symptoms in synchrony w rupture of infected rbcs) |
| sporogonic cycle | female mosquito feeds on infected human and ingests organisms, organisms undergo replication cycle w/in mosquito; mosquito transmits organisms to new host during blood meal |
| asymptomatic malaria | patient has circulating parasites but no symptoms |
| uncomplicated malaria | non-specific symptoms like fever, moderate-severe shaking chills, sweating, headache, nausea, vomiting, diarhhea, and anemia; no organ dysfunction |
| severe malaria (P. falciparum) | complications include severe anemai and organ damage, coma, pulmonary complications, and acute kidney injury; cerebral malaria |
| genetic traist that inc resistance | large structural variants in human glycophorin genes are protective, sickle cell trait, hemoglobin c, gemetic deficiency of glucose-6-phosphate dehydrogenase, lack of duffy blood group antigens prevent infection |
| large structural variants in human glycophorin genes protective for malaria | glycophorins are among the many receptors that are recognized by P. falciparum |
| sickle cell trait for malaria | heterozygous for the abnormal hemoglobin gene HbS; are relatively protected from severe and uncomplicated malaria |
| hemoglobin c for malaria | provides protection against severe malaria by a poorly understood mechanism |
| genetic protection of glucose-6-phosphate dehydrogenase for malaria | in rbcs, provides protection against uncomplicated malaria by an unknown mechanism |
| signs/symptoms of malaria 1 | associated w immune response against organisms, cell debris, toxins after erythrocyte lysis; two weeks after that cycle=fever, chills, diarrhea, headache, pulmonary/cardiac dysfunction; loss of erythrocytes leads to anemia, weakness, fatigue |
| signs/symptoms of malaria 2 | inability for liver to process the large amounts of hemoglobin released from ruptured erythrocytes results in jaundice; if victim survives the acute stages, immunity gradually develops |
| humans are reservoir for human malaria (other forms that infect animals) | endemic in 109 cuntries; half world propulation live in areas of malaria transmission; 1.2 mill die each year (70%<5 yrs and 93% subsahara africa) |
| climactic factors such as | temp, humidity, rainfall affect where malaria is found |
| movement of infected individuals and mosquitos continue to expand beyond endemic areas | transfusion-transmitted malaria |
| malaria diagnosis | easily identifed and distinguished in blood smears so microscopy; look like ringlike forms w/in erythrocytes; demonstration of antibodies against plasmodium can be used for differntial diagnosis; case history, travel history |
| malaria treatment varies by | species, area where infected, clincal status of patient, any accompanying illness or condition, pregnancy, drug allergies, other meds taken |
| malaria treatment | chloroquine, malarone (uncomlicated), coartem, mefloquine, quinine, antibiotics combined w quinine; antifever medication and blood transfusions may be required |
| malaria prevention | limit contact w mosquitos, widespread use of insecticides let to insecticide-resistant strains;drainage of wetlands and removal of standing water;use of repellants containing 30-35% DEET,mosquito netting and protective clothing;prophylactice drug malarone |
| function of respiratory system | exchange of gases bw atmosphere and blood |
| respiratory system divided into 2 parts | upp-->collects air, filters contaminants from air, and delivers it to the lower respiratory organs; lower |
| upper respiratory system | aggregates of lymphoid tissue (tonsils or adenoids), contains cells and chemicals to combat microbes; mucus contains defensins, lactoferrin, lyzosome, secretory IgA; normal microbiome limits infection and disease by microbial antagonism |
| lower respiratory system | ciliated mucous membrane lines trachea, bronchi and bronchioles; alveolar macrophages, secretory IgA in tears, saliva, mucus; lysozyme in mucus; microorganisms typically not present |
| upper respiratory system colonized by many types of microorganisms | 33% of healthy people carry s. aureus in nose (can be opportunist); many organisms colonize upper regions of throat, can move from here to infect lungs, middle ears, and sinuses |
| streptococcal respiratory diseases caused by | genus streptococcus, gram pos, facultatively anaerobic cocci in chains or pairs; differentiated by Lancefield grouping |
| lancefield group a-s. pyogenes | major cause of bacterial phayngitis and scarlet and rheumatic fevers; causes a # of diseases, depending on site of infection, strain of bacteria, and immune responses of patient |
| M protein | inhibition of C3b, interferes w opsonization and MAC formulation |
| Hyaluronic acid capsule | acts as immunologic disguise |
| virulence factors for streptococcal respiratory diseases | m protein, hyaluronic acid capsule, streptokinases, C5a peptidase, pyrogenic (erythrogenic) toxins, streptolysins |
| streptokinases | lyse blood clots and allow for spreading |
| C5a peptidase | dec movement of wbc to infection site |
| pyrogenic (erythrogenic) toxins | stimulate leukocytes to release cytokines that stimulate fever, widespread rash, and shock |
| streptolysins | lyse erythrocytes, leukocytes, and platelets |
| s. pyogenes frequently infects throat, but disease is usually temporary | w/in one week the immune responses against bacterial antigens (m protein and streptolysins) clear the organisms |
| strep throat and streptiococcal bronchitis typically occur when | normal micobiota are missing, large inoculum is introduced, or adaptive immunity is impaired |
| s. pyogenes can invade | deeper tissues and organs through a break in mucous membranes |
| streptococcal respiratory diseases signs/symptoms | back of pharynx red, swollen lymph nodes, purulent abscesses over tonsils, pain during swallowing, fever, malaise, headache, bacteria can spread from throat to larynx and bronchi to cause laryngitis and bronchitis; scarlet fever; acute glomerulonephritis |
| scarlet fever (scarlatina) | can develop if pharyngitis caused by strain s. pyrogenes carrying lysogenic phage for pyrogenic toxins; 1-2 dys of pharyngitis; toxins released |
| toxins released in scarlet fever | trigger fever, diffuse rash that begins on neck, underarm, and groin, and spreads across body; tongue becomes strawberry red, rash disappears after one week and skin sloughs off |
| acute glomerulonephritis and rheumatic fever are complications of untreated strep throat | glomerulonephritis (kidneys), rheumatic fever (damage to heart valves and muscle (autoimmune in nature) |
| streptococcal respiratory diseases epidemiology | human adapted pathogen, spread via respiratory droplets, occurs most often in winter and spring among elementary and middle school children (most susceptible); is sensitive to anitmicrobial drugs |
| diagnosis of streptococcal respiratory | some estimate that <50% of patients diagnosed w strep throat actually have it; most have viral pharyngitis (sure diagnosis requires serological testing); immunological strep test gives results in ~10 mins |
| treatment of streptococcal respiratory | oral/intramuscular penicillin g,penicillin v,amoxicillin r effective;despite >100 yr research,GAS vaccine hasnt reached commerical use;all vaccine candidates target m protein;studies suggest that non-m protein antigens protective vs GAS in animal models |
| prevention streptococcal respiratory | antibodies against m protein provide long-term protection (>50 kinds of m proteins), antibiotic intervention precludes development of protective antiboides; keep sick children isolated/home 24h after initiation of antibiotics; should be treatd immediately |
| tuberculosis caused by | myobacterium tuberculosis and mycolic acid |
| myobacterium tuberculosis | non-endospore forming, gram pos rod w cell walls containing mycolic acid (acid fast positive) |
| mycolic acid directly responsible for unique characteristics of pathogen | slow growth, protected from destruction following phagocytosis, intracellular growth, resistant to gram staining, detergents, many common antimicrobial drugs and desiccation |
| virulent strains of tuberculosis produce cord factor | cell wall glycolipd causes daughter cells to remain attached to one another in parallel alignments;prevents fusion phagosomes w lysosomes;inc production of cytokines4 granuloma formation;mutant mycobacteria unable synthesize cord factor dont cause disease |
| primary tuberculosis pathogenesis 1 | inhalation of respiratory droplets, macrophages in alveoli phagocytize organisms but cannot digest them, bacteria replicate freely w/in macrophages, gradually killing them; cycle repeats itself (asymptomatic/mild fever) |
| primary tuberculosis pathogenesis 2 | t cells produce lymphokines that attract and activate more macrophages and trigger inflammation (granuloma forms over 2-3 month period); collagen fibers enclose granuloma |
| primary tuberculosis | immune system reaches stalemate--> prevents further spread of pathogen and stop progression of disease, cant rid body of all mycobacteria |
| secondary (reactivated) tuberculosis pathogenesis | occurs when organisms break stalemate, organisms rupture granuloma and reestablish active infection, bacteria spread thru lungs via bronchioles; occurs in ~10% of patients |
| disseminated tuberculosis pathogenesis | macrophages carry pathogen via blood and lymph to variety of sites=bone marrow, spleen, kidneys, spinal cord, brain; consumption; signs/symptoms correspond to complications arising @various sites involved |
| tuberculosis sign/symptoms | not always initially apparent and may limited to minor cough and mild fever; as disease progresses patients develop breathing difficulties, fatigue, malaise, chest pain, wheezing, and cough up blood |
| uberculosis epidemiology | tb responsible for 2nd highest # of deaths worldwide due to infectious disease; 1.6 mill die from tb worldwide 2021; organism not particularly virulent (5% infected develop disease, kills 55% untreated patients and 15% treated patients) |
| greatest risk of infection for tb | those w lowered immunity; tb is leading killer of hiv-infected patinets; other risks=diabetes, poor nutrition, stress, crowded living conditions, alcohol consumption, drug abuse, and smoking |
| diagnosis of tb | tb skin test (cell wall antigens injected into skin, recheck 24-72h);cell-mediated hypersensitivity rxn (past infection, immunized w m. bovis, active disease, chronic carriers);chest xray reveals of granulomas,check sputum sample 4 acid fast cells/cords |
| treatment of tb 1 | common antimicrobials have little effect (drug cleared from body b4 they have effect on organisms, little impact of bacteria living w/in macrophages, pyrazinamide w inh, rifampin, and streptomycin or ethambutol) |
| treatment of tb 2 | mdr-tb strains (resistant to inh and rifampin); xdr-tb strains (resistant to inh, rifampin and 3+ more other drugs), have emerged in populations w high incidence of hiv; bedaquiline=first anti tb drug in >40 yrs used to treat mdr-tb and xdr-tb; dots |
| tb prevention | antibacterial drugs prophylactically, recent conversion from neg to pos tb skin test, significant exposure to active cases of tb; bcg vaccine (attenuated)=not used for immunocompromised patients bc it can cause disease; |
| in us cost of mass immunizatinon for tb | not warranted due to low prevalence |
| influenza types | a and b (orthomyxoviruses) |
| influenza virion caused by | 8 diff ssRNA molecules as genome; pleomorphic envelope; glycoprotein spikes of neuraminidase and hemagglutinin |
| neuraminidase | hydrolyzes mucus in lungs thereby providing access to pulmonary epithelial cells |
| hemaglutinin | binds to pulmonary epithelial cells and triggers endocytosis |
| influenza infects | upper and lower respiratory tract cells |
| mutations in influenza occur in 2 main processes | antigenic drift and antigenic shift |
| antigenic drift | accumulation of HA and NA mutations w/in single strain in given geographical area, relatively minor variations in spike glycoproteins, results in localized inc in # of infections ab every 2 yrs |
| antigenic shift | reassortment of genomes from diff influenza a strains infecting same host cell, occurs in influenza a every 10 yrs; strains typically arise in asia |
| influenza pathogenesis | droplet,airborne,indirect contact(fomites);viruses remain infective for up to 8 hrs on fomites;epithelial cells in lungs endocytose viruses;lytic replication cycleeliminates lungs 1st line of defense, patients susceptible to secondary bacterial infection |
| symptoms of influenza produced by | cytokines released as part of immune response to virus |
| signs/symptoms of influenza | incubation period 1 dy following infection, sudden fever 102-6; pharyngitis, congestion, dry cough, malaise, headache, myalgia, recovery in 1-2 weeks, more contagious one day b4 disease is manifested and for a week or more after signs begin |
| influenza epidemiology | changing antigens guarantee there will always be susceptible people; some are carriers; millions infected; patients w weak immune systems (very young, elderly, and immunocompromised) vulnerable |
| influenza diagnosis | flu signs/symptoms during community-wide outbreak often sufficient for diagnosis; antiviral therapy must begin w/in 48 hrs infection in order to be effective |
| treatment of influenza | two drugs=oseltamivir (tamiflu) and zanamivir (relenza); both inhibit neuraminidase which blocks release of virus from infected cells; supportive care to relieve symptoms (antihistamines and pain relievers) |
| influenza prevention | immunization w multivalent vaccine, at least 70% effective, protection lasts 3 yrs/less; culling infected birds, good personal hygiene can reduce spread |
| structures of digestive system divided into 2 groups | gastrointestinal (digestive) tract (GI tract) & accessory digestive organs |
| gi tract | pathway from mouth to anus, most organs of gi tract protected by membranous covering called peritoneum |
| accessory digestive organs | organs involved in grinding food or providing digestive secretions |
| protection of digestive systems 1 | seamless surface of epithelial cells coated w mucus containg secretory IgA and lysozyme; peristalsis in esophagus; stomach acid (~pH 2); microbial antagonism=production of vitamin b12, folic acid, biotin, vitamin k; |
| protection of digestive systems 2 | rapid transport of food thru stomach and duodenum, bile |
| normal microbiota of esophagus, stomach, duodenum | almost free of microbes |
| normal microbiota of tongue, teeth, jejunum, ileum, colon, rectum | mouth/throat=>700 species of microbes in oral biofilms; lower small intestine/colon=bacteroides, lactobacillus, eschericihia, enterbacter, proteus, klebsiella, candida, and entamoeba |
| bacterial gastroenteritis | inflammation of stomach or intestines due to presence of bacteria; most associated w poorly prepared foods, contaminated washing/drinking water and communities w poor living conditions; institutional settings are prone to outbreaks in developed countries |
| features of bacterial gastroenteritis | some asymptomatic/involve mild diarrhea only; most have nausea, vomiting, diarrhea, loss of appetite, abdominal pain, and cramps; some malaise and fever; symptoms disappear w/in hrs or days |
| rare w bacterial gastroenteritis | infection spreads beyond gi tract and causes kidney failure or anemia |
| dysentery w bacterial gastroenteritis | severe and painful type of gastroenteritis in which patients experience diarrhea containing mucus and blood |
| diagnosis of bacterial gastroenteritis | based on signs and symptoms; causative agent can be identified but generally not |
| treatment of bacterial gastroenteritis | fluid and electrolyte replacement; may need anti-nausea meds, iv fluid replacement (rare); antidiarrheal drugs may prolong symptoms |
| prevention of bacterial gastroenteritis involves proper handling, storage, preparation of food | clean food b4 consuming, cooking; cook foods high temp to kill bacteria; keep food <40F or >140F; clean utensils; use only pasteurized milk/juices; good sanitation/personal hygiene; proper handwashing essential |
| shigellosis caused by | shigella dysenteriae, s flexneri, s boydii, and s sonnei; gram neg nonmotile bacilli |
| all sepecies for shigellosis produce | type III secretion systems and enterotoxins |
| type III secretion systems | form channel from bacterium into host cell thru which bacterial proteins are introduced into host cell |
| enterotoxins | bind to epithelial cells lining intestines and trigger loss of electrolytes and water into lumen of intestine |
| s. dysenteriae produce exotoxin | shiga toxin= stops protein synthesis in host's cells |
| shigellosis pathogenesis | initially colonizes cells of small intestine and causes enterotoxin-mediated diarrhea; organism attaches to and invades epithelial cells in large intesine; bacteria multply in cytosol; directrly invade neightboring cells and evade immune system; |
| organisms in shigellosis | kill host cells resulting in abscesses in intestinal mucosa |
| signs/symptoms of shigellosis | fever, abdominal cramps, diarrhea; when bloody diarrhea is present, the syndrome is known as bacillary dysentery |
| shigellosis epidemiology | human reservoirs, people infected by ingesting bacteria on own contaminated hands and by consuming contaminated food (direct contact/foodborne); little affected by stomach acid (infective dose=as few as 100 cells); person-person spread possible; |
| groups @highest risk for shigellosis | children in daycare centers and persons in custodial settings, where personal hygiene is difficult to maintain |
| shigellosis diagnosis | based on symptoms/presence of shigella in stool; nucleic acid test- xTAG gi pathogen panel (xTAG GPP) |
| shigellosis treatment | disese self-limiting; administration. of antimicrobials can shorten the duration of disease and reduce the spread of shigella to close contacts |
| shigellosis prevention | live attenuated vacine recently developed against s flexneri, prevents dysentery, but recipients experienced mild diarrhea and fever as result of immunization; worl continues |
| campylobacter diarrhea caused by | campylobacter jejuni (gram neg slightly curved rod w polar flagella) |
| virulence factor of campylobacter diarrhea | adhesins, cytotoxins, endotoxin that enable colonization and invasion of jejunum, ileum, and colon; nonmotile strains are avirulent; survives inside cells after being endocytosed |
| campylobacteriosis pathogenesis 1 | found in cattle, birds, pigs (nonpathogenic/zoonosis)= chickens colonized soon after birth and most important source for human infection; spreads to humans in contaminated meat <500 cells can cause illness |
| campylobacteriosis pathogenesis 2 | organism produces bleeding lesions and triggers inflammation in jejunum, ileum, colon; in immunocompromised patients, the organism can spread to the bloodstream and cause life-threatening infection |
| campylobacteriosis signs/symptoms | infections commonly produce malaise, fever, abdominal pain, bloody/frequent diarrhea; 10+ bowel movements per day not uncommon |
| campylobacteriosis epidemiology | responsible for more cases of diarrhea that send people to doctors in us than any other bacterium; most due to consumption of raw/undercooked poultry from cross-contamination of other foods by these items; |
| campylobacteriosis-->infants infected by contact w poultry packages in shopping carts; one drop of juice from raw chicken can infect humans | outbreaks associated w unpasteurized milk/contaminated water supplies; estimated infect 1.5 mill people per yr in us; WHO classifies 1/4 key global causes of diarrhea diseases |
| campylobacteriosis diagnosis | based on signs/symptoms and demonstration of organism in stool, xTAG GPP |
| campylobacteriosis treatment | disease self-limiting, bacteria expelled from intestinal tract; severe cases require supportive therapy and antimicrobial drugs |
| campylobacteriosis prevention | no vaccine so preventative practices should focus on minimizing contamination of kitchen surfaces and utensils from raw chicken/turkey; protect drinking water from feces of stockyards, feedlots, slaughterhouses |
| cholera caused by | vibrio cholerae, slightly curved gram neg rod w polar flagella; naturally in estuarine or marine environments worldwide |
| epidemic strains of cholera | O1 El Tor (7 pandemics) and )139 Bengal (arose in India in 1992); environment w/in human body activates genes so more virulent in humans |
| virulence factor of cholera | cholera toxin is encoded on bacteriophage CTXO |
| cholera pathogenesis | reservoir aquatic fauna as copepods; humans infeccted by ingesting contaminated water or raw/undercooked shellfish (high infective dose bc cells die in stomach, use antacids have lower infective dose); colonize small intestine and produce cholera toxin |
| cholera signs/symptoms 1 | asymptomatic/cause mild diarrhea; 10% patients it results in rapid, severe, fatal fluid/electrolyte loss; explosive watery diarrhea/vomiting 2-3 days after infection; stool more watery, colorless, and odorless; rice water stools (flecked w mucus) |
| cholera signs/symptoms 2 | some lose 1L of fluid an hour; dehydration, thirst, metabolic acidosis, hypokalemia, and hypovolemic shock can result; muscle cramping, sunken eyes, irregular heartbeat, kidney failure, coma/death can result; mortality 25-50% in untreated patients |
| cholera epidemiology | 7 cholera pandemic since 1817, 7th pandemic began 1961 reached S America 1991; oct 21, 2010 cholera confirmed in haiti lasted until jan 2019 and killed close to 10,000 people |
| cholera diagnosis | signs/symptoms, rice-water stools |
| cholera treatment | supportive care w fluid and electrolyte replacement, doxycycline reduces production of cholera toxin |
| cholera prevention | adequate sewage and water treatment can limit spread and prevent epidemics, oral vaccine against O1 El Tor strain (protection short lived), infective dose is high, so proper hygiene usually sufficient |
| staphyloccal intoxication | staphylococcus aureus, gram pos cocci in clusters |
| staphylococcal intoxication virulence factors | 5 enterotoxins that stimulate intestinal muscle contractions, trigger nausea, and cause intense vomiting (heat stable) |
| staphylococcal intoxication pathogenesis 1 | contaminate foods w s aureus during cooking, found in unpasteurized milk/cheese products; grow well @ room temp in foods containing high conc of protein (processed meats, custard pastries, potato salad, ice cream); |
| staphylococcal intoxication pathogenesis 2 | must grow @ warm temps for hours before enterotoxins secreted, warming/reheating food doesnt inactivate enterotoxins, although it does kill bacteria; toxin consumed, crosses mucous membranes of intestinal tract; incubation period 1-6 hrs |
| staphylococcal intoxication signs/symptoms | nausea, severe vomiting, diarrhea, headache, sweating, abdominal pain; self-limiting and last ~24hrs but severe cases may last 3 days |
| food intoxication epidemiology | outbreaks w picnics, school cafeterias, large social functions where food stands unrefrigerated or where food prep is less than optimal; number of cases unknown (milk/self-limiting) |
| food intoxication diagnosis | based on history, signs/symptoms |
| food intoxication treatment | fluid/electrolyte replacement |
| food intoxication prevention | good hygiene and proper food handling techniques |
| signs/symtoms of rmse are due to what | damage to blood vessels |
| prior to the development of the chickenpox vaccine, chickenpox was a highly contagious disease tha most school age children contracted. what is the reason? | bc virus was transmitted by respiratory dropletes |
| which of the following statements regarding chickenpox are true | person can acquire chickenpox from a patient w shingles, chickenpox is typically more severe in adults, chickenpox virus can become latent w/in sensory nerves, patients vaccinated w chickenpox vaccine should also receive shingles vaccine |
| you suspect that your patient may have measles. which of the following would hep confirm your suspicion | small white spots on oral mucosa |
| you isolate a microbe from a patient who contracted bacterial meningitis during epidemic in your community. what do you expect to see when you gram stain this microbe? | gram neg diplococci |
| the ppsv pneumonococcal vaccine is a 23-valent formulation that is designed to induce protective immunity against which of the following? | capsular polysaccharides |
| sinus and ear infection for a few days, but became irritable, lethargic, and developed a fever. after examining the patient, you suspect she has meningitis. what do you suspect is the causative agent? | streptococcus pneumoniae |
| how do health care professionals determine the causative agent of an individuals meningitis? | analysis of CSF sample obtained by lumbar puncture |
| what organism causes the type of meningitis that can become epidemic? | N. meningitidis |
| erythema migrans is a characteristic of which of the following diseases? | lyme disease |
| children 4-15 can be infected w EBV, they usually only develop a mild respiratory infection. why dont they develop mononucleosis like 15-17 do when they are infected? | bc cell-mediated branch of immune system is immature |
| woke and are having pain while swallowing, a fever, throat is red and see white pus pockets on tonsils. swab throat and perform gram stain and observe gram pos cocci in chains. what is unofficial diagnosis of illness? | streptococcal pharyngitis |
| virulence of mycobacterium tuberculosis is directly related to production of what? | cord factor |
| patient experiences difficulty breathing, chest pain, and malaise. learn they are recent immigrant from S. Africa and infected w HIV. order tb skin test and xray, examine white areas in regions that should be black. what are these white areas called? | granulomas |
| what must happen for an antigenic shift in influenza virus to occur? | two diff influenza a virus strains must infect the same host cell at same time |
| production of new strains of influenza viruses is due to mutations in genes coding for which of the following? | hemagglutinin and neuraminidase |
| of following, which would put a person at inc risk of contracting bacterial gastroenteritis? | consuming unpasteurized milk from a local source |
| which of the organisms that causes bacterial gastroenteritis is commonly associated w supermarket chicken? | campylobacter jejuni |
| who of following would be most @risk of developing cholera after consuming contaminated water? | person whose body doesnt produce normal amount of stomach acid |
| working w healthcare worker in bangladesh and assisting room of patients w massive diarrhea that resembles rice water. what do you suspect is the causative agent of the patients diarrhea? | vibrio cholera |
| under what conditions are staphylococcal enterotoxins produced in food? | produced when contaminated food sits @ room temp or warmer for several hours |
| kidney functions | remove waste from blood and excrete it in urine; nephrons functional unit |
| nephrons | filter blood to form urine |
| ureters | urine travels via these to urinary bladder |
| urinary bladder | stores urine until it can be eliminated |
| urethra | site of urine excretion |
| female urinary/reproductive systems distinct | ovaries, uterine tubes, uterus, vagina, external genitalia; mirobes enter reproductive tract thru vagina |
| ovaries | site of egg production |
| uterine tubes | eggs travel toward uterus thru uterine tubes |
| uterus | develops blood-rich wall in preparation for pregnancy |
| vagina | unfertilized eggs pass thru vagina during menstruation |
| external genitalia | includes clitoris and labia |
| male urinary/reproductive systems share components | testes, scrotum, systems of ducts, accessory glands, penis; microbes enter reproductive tract thru urethra, skin of penis |
| testes | site of sperm production |
| scrotum | external structure that contains testes |
| systems of ducts | pass sperm to prostate gland |
| accessory glands | prostate gland, add fluid to sperm to form semen |
| penis | semen passes from penis out of body |
| protection of reproductive/urinary systems | flow of urine, acidic pH of urine, mucosall epithelial cell layer, vagina maintains pH ~4.5; urethra of men and women (men ~20cm, women ~4 cm) |
| urethra | supports colonization by some microorganisms; primary species include Lactobacillus, Staphylococcus, and Streptococcus; remainder of urinary organs and urine in them are axenic; can move up to infect kidneys |
| male reproductive system | regions above prostate are sterile |
| female reproductive system | vagina colonized by various microorganisms depending on hormone levels |
| gonorrhea caused by | neisseria gonorrhoeae, gram neg diplococci w adjacent sides flattened |
| virulence factors gonorrhea | fimbriae, polysaccharide capsule, lipooligosaccharide (LOS) containing lipid a, IgA protease; if lack fimbriae, capsule and LOS typically avirulent |
| gonorrhea pathogenesis 1 | as few as 100 pairs can result in disease; gonococci adhere to mucous membranes of genital, urinary,digestive tracts of humans=fimbriae/capsule mediate,cannot attach to cells in vagina;attach to sperm via fimbriae=can result in pelvic inflammatory disease |
| gonorrhea pathogenesis 2 | chronic infections can lead to scarring, resulting in ectopic pregnancies or sterility; infections of urethra in women are common; oral and anal infections can occur (more common in men who have sex w men) |
| gonorrhea pathogenesis 3 | organisms phagocytosed but survive and multiply w/in neutrophils, travel thru/o body, can enter blood and travel to joints, meninges, or heart (arthritis, meningitis, endocarditis); infection during childbirth (ophthalmia neonatorum or blindness) |
| gonorrhea signs/symptoms men | begin after 2-5day incubation, acute inflammation of urethra; thick, purulent, creamy-yellow discharge from penis and extrememly painful urination; organisms can invade prostate or epididymis (scar tissue can result in infertility) |
| gonorrhea signs/symptoms women | 50-80% asymptomatic, lack of treatment results in infertility or pelvic inflammatory disease (25%); begin after 2-5 incubation; bruning/frequency of urination; yellow or bloody vaginal discharge; mistaken for vaginal yeast infection or bladder infection |
| gonorrhea-->ophthalmia neonatorum | inflammation of conjunctiva in newborns |
| gonorrhea epidemiology 1 | humans only reservoir, transmitted by direct contact w infected host (susceptible to drying/extremes of temp); disparities in rates of reported STIs among some racial minority or hispanic ethnicity groups as compared w nonhispanic whites; |
| gonorrhea epidemiology 2 | msm disproportionally impacted by stis, risk inc w frequency of sexual encounters (women w 50% chance of becoming infected during single sexual encounter w infected man; 20% for men); infection of children strong evidence of sexual abuse |
| gonorrhea diagnosis | presence of gram neg diplococci in pus from inflamed penis from symptomatic male patient is diagnostic, asymptomatic men/women diagnosed by commerically available genetic probes |
| gonorrhea treatment | antimicrobial resistance inc concern and successful treatment more difficult; cdc recommends single dose of 500mg of intramuscular ceftriaxone (previous was 2 antibiotics simultaneously), alternative regimens available when ceftriaxone cannot be used |
| gonorrhea prevention | no long-term specific immunity;reinfection common (surface antigens highly variable); no vaccine available bc many strains; control difficult except in newborns; |
| gonorrhea prevention strategies 1 | latex condoms, when used consistently/correctly, can reduse risk of transmission; abstain fom vaginal, anal, oral sex; monogamous relationships w partner who has been tested and known to be uninfected; |
| gonorrhea prevention strategies 2 | education to change sexual behavior, aggressive detection, and screening of all sexual contacts of those infected |
| chlamydia caused by | chlamydia trachomatis, obligately intracellular-only grow/multiply w/in vesicles in host cells; nonmotile, gram neg |
| 18 diff strains of chlamydia | all but one are pathogens in humans; infect conjunctiva, lungs, urinary tract, or genital tract; >10 stratins cause STIs in humans |
| chlamydia pathogenesis 1 | organism enters body thru scrapes or cuts, infects cells of conjunctiva or cells lining mucous membranes of trachea, bronchi, urethra, uterus, uterine tubes, anus, or rectum; |
| chlamydia pathogenesis 2 | manifestations result from destruction of infected cells at infection site and from inflammatory response the destruction stimulates |
| chlamydia think | lesion @ site of infection but small, painless, heals rapidly (often overlooked); in adolescence inc risk of developing cervical cancer later in life |
| chlamydia signs/symptoms | ~85%women asymptomatic; >75% men infected have discharge from penis/burning w urination, can have burning/itching around opening of penis, can cause epididymitis or orchitis which can lead to sterility |
| chlamydia can be found in | throats of men/women having oral intercourse w infected partner |
| 10-15% women w untreated chlamydia will develop pelvic inflammatory disease | can result in permanent damage to fallopian tubes, uterus, surrounding tissue; chronic pelvic pain, infertility, ectopic pregnancies |
| chlamydia epidemiology | humans are reservoirs, transmission=direct contact; most common sexually transmitted bacterium; most common reportable STD in US (more go unreported annually) |
| chlamydia is most prevalent in | women <20; physiologically more susceptible; cervix not fully matured and more suscetible; women w chlamydia have 3-5 fold inc risk of acquiring HIV if exposed |
| chlamydia diagnosis | demonstration of chlamydial DNA in specimen following PCR amplification of DNA |
| chlamydia treatment | doxycycline for 7 days; alternative regimen (azithromycin (z-pak) or levofloxacine for 7 days |
| chlamydia prevention | absitence or faithful mutual monogamy; condoms can provide some protection some irritation and lubricants can inc likelihood of infection; infections often asymptomatic/frequently occur among populations that have limited access to medical care |
| reticulate bodies in chlamydia | replication |
| elementary bodies in chlamydia | infectious |
| genital warts caused by | familly papillomaviridae, non-enveloped dsDNA viruses of which >100 strains; >40 strains can infect genital tract |
| genital warts virulence factors | replicate excliusively in basal layer of keratinocytes; various straiins infect either cutaneous/mucosal tissues (replicate only in body surface tissues), shed thru release of skin cells (desquamination) to help avoid inflammatory response |
| family papillomaviridae low risk | does not cause cancer, can cause genital warts, strains 6 and 11 linked to 90% of all cases of genital warts |
| familly papillomaviridae high risk | 13 strains integrate into human chromosomes; believed to cause cervical, anal, vaginal, penile, and oral cancers (especially coinfected w herpesvirus); types 16/18 cause 70% of cervical cancers; |
| 80-90% of all cervical cancers in women due to HPV | 72% oropharyngeal cancer in men due to HPV |
| genital warts are very contagious=contracted by direct skin-skin contact during vaginal, anal, (rarely) oral sex w infected partner | ~67% who have sexual contact w infected partner will develop warts, usually w/in 3-4 months; gain access to keratinocytes thru microtraumas in skin; causes infected epithelial cells to proliferate |
| genital warts sign/symptoms | condylomata acuminata or venereal warts most recognized sign-range in size from almost undetectable small bumps to giant, cauliflower like growths; may experience itching, burning, tenderness, pain, or no symptoms at all; |
| genital warts are commonly found | on vulva, in/around anus/vagina, on cervix, penis, thigh, groin, or scrotum; may have hpv infection w/o presence of warts |
| genital warts epidemiology | transmitted via direct contact during vaginal, oral, or anal sex; can be found on fomites, but indirect contact transmission has never been documented; hpv most common sexually transmitted disease in US, mostly young adults (not reportable), |
| ~14mill new cases of hpv infections reported each year in us | ~79 mill americans currently infected w gential hpv (late teens/early 20s); almost everyone sexually active will get hpv at some point in life if they dont get hpv vaccine |
| genital warts diagnosis | observation for abnormal results from pap smear (cancerous/precancerous cells in cervix), dna probes determine exact strain of hpv, ctls eventually recognize/destroy infected cells (warts disappear over time) |
| genital warts treatment | genital warts removed w surgery, freezing, burning, laser or caustic chemicals but viruses may remain in surrounding tissues; laser surgery casues viruses to become airborne; duct tape |
| genital warts prevention | abstinence/mututal monogamy w uninfected partner; condoms may reduce risk of infection (hpv sheds from skin at base of penis or around external genitalia; gardasil 9-prevents infection w hpv strains 6,11,16,18,31,33,45,52,58; |
| gardasil-9 | first vaccine to prevent cervical cancer, precancerous genital lesions, genital warts due to hpv; provides strong protection against new hpv infections, but are not effective @ treating established hpv infections |
| friend having pain w urination, urge to urinate frequently and preesence of bloody urine/creamy discharge from penis. He has no lesion. complete gram stain and what do you expect to see? | gram negative diplococci |
| what are the infectious/transmissible forms of chlamydia trachomatis? | elementary bodies |
| why are certain strains of hpv associated w development of cancers? | bc they trigger the action of oncogenes following integration into the chromosome of human cells |
| all known papillomaviruses have what feature in common? | they all infect the basal layer of keratinocytes |
| although condoms are effective for protecting large # sexual transmitted agents, they are ineffective at preventing transmission of which? | human papillomavirus |
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