Microbio Exam 4 – Flashcards
Unlock all answers in this set
Unlock answers| What are three agents that cause infections of the integument? |
Propionibacterium acnes Staph aureus Strep pyogenes |
| Which agent is the predominant ANAEROBIC member of the normal skin flora? What type of rod is it? |
Propionibacterium acnes
Gram positive diptheroid |
| What are the three normal flora of the skin? |
-Propionibacterium acnes -diphtheroids -coagulase negative staph |
Which class can be described as "short Gram positive bacilli, like 'Chinese letters?'
|
| Diptheroids |
| What is the most common skin disease? |
| Acne Vulgaris |
What population does Acne Vulgaris normally occur in?
What is it initially caused by?*
The overgrowth of which agent causes inflammatory Acne Vulgaris? |
-adolescent population
-alteration in sebaceous physiological processes
-propionibacterium acnes |
In the absence of P. Acnes, what is formed from:
increased sebum production after puberty or follicular canals plugged due to altered physiology? |
| microcomedones |
| In the non-infectious process of acne, what two things can cause canal/duct blockage? |
Keratinization Desquamation |
| What non-inflammatory structure may microcomedones evolve into? |
| Comedones; open or closed surface pores |
| What is not present in the non-inflammatory manifestation of acne? |
| there is no P. Acnes present |
What is a closed comedeone?
What is an open comedone? What is the common misconception about open comedones? |
"White head"
"Black head' -the "black" part is not dirt, rather melanin, which results in pigmentation |
| What are the four main goals of treatment for acne vulgaris? |
-antikeratinizing -inhibit sebum production -anti p. acnes -anti-inflammatory |
| How long may intermittent treatment of Acne vulgaris take? |
| months to years |
| Name 5 treatments for acne vulgaris that inhibit P. Acnes |
Salicylic acid Retinoic Acid Azelaic Acid Benzoyl Peroxide Antibiotics; |
| Which three antibiotics are anti-P acnes? |
erythromycin clindamycin doxycycline |
| Name 4 non-abrasive compounds in medicating cleansing OTC's for acne vulgaris: |
-Topical Vitamin A -Topical Vitamin C -Low does retinol -Alpha hydroxy acid |
| What three treatments can you use for severe acne? |
-systemic antibiotics -corticosteroids -estrogens, anti-androgens, spironolactone |
| What are the four most harmful actions you can do if you have acne? |
-Frequent, non-medicated vigorous cleansing -abrasive cleaning -restricted diet -squeezing pimples (can lead to inflammatory response) |
| Is Acne curable? Is the treatment duration less than or more than 6 months? |
| No; more than 6 months |
Which agent of the integument can be described as Gram-positive cocci forms pairs, short chains, grape-like clusters produces coagulase? |
| Staph Aureus |
| The manifestations of Staph Aureus can be grouped into which two groups? |
| Non-toxin mediated and toxin mediated |
Folliculitis, Furuncles, Carbuncles, and Epidermis impetigo
fall under which classification of manifestations of staph aureus integument infection? |
| Non-toxin mediated diseases |
What is "cured" defined as in HCV?
Because it is so expensive and difficult, what are the three criteria for treatment of HCV? |
-persistent loss of HCV RNA in blood during long-term follow-up
-persistent elevation of aminotransferases, quantitative HCV RNA, severe histologic changes on liver biopsy |
| What are the two transmissions for HAV? Which are the major vehicles? |
-Fecal-oral and person-to-person transmission are possible (fecal-oral is bigger)
-food and water are major vehicles |
| Which immunoglobulin in HAV indicates lifelong immunity? |
| IgG |
| Which immunoglobulin in HAV is generally present 5-10 days before symptoms and last for under 6 months? What can this be useful for? |
| IgM; It can be useful for diagnosing HAV. |
| What are HavRix and Twinrix? Who are they recommended for? |
| Killed vaccine for hepatitis A virus; recommended for children and international travelers |
| Where is HEV common in? |
| -underdeveloped countriess mostly in S.E./central asia |
| Fulminant hepatitis E with liver failure is found very rarely (1%) EXCEPT in which population? |
| Pregnant women in their third trimester (25%) |
| What is the treatment for HEV? |
| Supportive treatment only |
| What "kind" of virus is HIV? What does it have multiple of? |
| it is a retrovirus and has multiple serotypes |
| How long is the incubation period for HIV? |
| 2-4 weeks |
| What does M-tropic strain of HIV infect? |
| Infects macrophages/primary T lymphocytes |
| What does M-tropic strain indicate? |
| Non-progression of AIDS |
| What does the T-tropic strain of HIV indicate? |
| It indicates that the patient will progress to AIDS rapidly and a steep decline in T-helper cells. |
Viral genome for HIV:
RNA -->DNA? or DNA--> RNA? |
| RNA-->DNA |
| In HIV, what 2 things convert ssRNA into ssDNA? |
-reverse transcriptase (66) -ribonuclease H |
| What is an important distinction that occurs when HIV ssRNA is converted to ssDNA? Why does this occur? |
| Many replication (base pair) errors occur because reverse transcriptase has no proofreading. |
| Some drugs that target reverse transcriptase also target what? |
| DNA-dependent polymerase in mitochondria; (big effect on normal replication) |
| Once infected with HIV, how long does a person remain infected? How long must he/she be treated for? |
| A person remains infected for life and treatment must be lifelong. |
| In acute phase of infection, where does HIV primarily replicate? |
| T cells in the GIT |
| After three weeks of infection of HIV, what noticeable endoscopic change will occur? |
| there will be no more T cells in the GIT |
| Where does the human immune system battle HIV virus in the body? What happens with a few years? |
| lymph nodes (T cells and HIV virion die); eventually, the virus overwhelms the immune system and progresses to AIDS |
| After all the T-cells are gone from the gut, what is activiated? |
| a chronic, generalized/systemic immune activation |
| What is one of the strongest predictors for progression from HIV infection to AIDS and which may be the main cause of CD4 depletion? |
| the strong chronic, systemic immune activation |
| What is the CD4 count for AIDS? |
| <200/mm^3 |
| What is defined as a "slowly progressive demyelinating disease with neuronal loss of the CNS?" |
| HAD: HIV-associated dementia |
| What is the worst risk factor for HAD? |
| IV drug abusers |
| What does HIV affect in the CNS? What doesn't HIV affect in the CNS? |
It affects: monocytes, macrophages, and microglia cells. ; It does not affect: neurons or oligodendrocytes; |
| What are the results of HIV infection in the CNS (2) |
-diffuse or focal myelin pallor of white matter (demyelination) -neuronal loss |
| What is defined as: neurocognitive impairment demonstrated by cognitive testing but are asymptomatic in their daily life? |
| Asymptomatic neurocgnitive impairment (ANI) |
What is defined as when the patient has impairments causing mild disturbance of ADL's? (difficulties in concentration, attention, memory) What does this progress from? |
HIV-associated mild neurocognitive disorder (MND) This progresses from ANI |
| What is the full progression of CNS disease via HIV? |
| HAD |
| What are the most common feature of HAD? |
| cognitive changes (forgetfulness, confusion, loss of memory) |
| Which two diagnostic tests detect HIV-specific antibodies? Problem with this test? |
| EIA; western blot. Must wait until immune response ("window of no positive serology") |
| Which viral antigen must be tested for all blood donors? What are they testing for? |
| p24 antigen; tests for HIV, especially when "window" period of no antibodies |
| What are the four strategies to prolong survival in those with HIV? |
-antiretroviral therapy -P. carinii prophylaxis -M. Avium prophylaxis -care by a physician with HIV-care experience |
| What happens if you stop reverse transcriptase? Which drug type does this? |
you stop any new virus from infecting person's cells; RTI's and NNRTI's do this (Reverse-transcriptase inhibitors and non-nucleoside reverse transcriptase inhibitors) ; Ex: neveripine; loviride |
| What do protease inhibitors do? Name three examples. |
Stop maturation of virus. Virus is made, but not infectious. ; saquinavir; indinavir; amprenavir |
| What does Selzentry do? |
| inhibits HIV-1 co-receptor CCR5 |
| What does Isentres (Raltegravir) do? |
| inhibits HIV-1 integrase |
| Is HIV monotherapy efficacious long term? Why or why not? (2 reasons) |
| It is NOT efficacious long term because you get resistance and because of the high mutation rate of the virus. |
| What is are the results of RTI's(NRTI's)? |
| -blocks production of viral DNA and inhibits further DNA synthesis via CHAIN TERMINATION |
| How does NNRTI work? |
| -it attaches to viral reverse transcriptase to block its function and it will block the further prodcution of viral DNA. |
| Does the latent virus DNA get killed by antiviral therapy? Why or why not? |
| No because it is already in the human genome. |
| What does HAART stand for? What does it consist of? |
| Highly active Antiretroviral Therapy: multiple drugs used for treatment of HIV; Old definition is 2 RTI's and something else; now it can be two NRTI's plus something else. |
| What are the three caveats of HAART? |
-does not prevent all new infections of susceptible cells -does not kill latent virus (NO CURE!!); latent infected T-cells are the major reservoir ; -patient is still infectious via sexual contact |
| What are two reasons why HAART must be adhered to faithfully? |
-drug resistance is a significant problem -latently infected T cells are the major reservoir. If HAART is stopped prematurely, latent cells will become active and progress to AIDS |
| What are two reasons why CD4 count increases rapidly with HAART? |
-initial redistribution of memory T cells -slow repopulation of naive cells |
| It must be noted that HIV therapy causes a lot of :__________. This is why it is important to know when to start therapy.; |
| toxicity |
| During primary infection, what 2 types of cells does EBV virus infect? After resolution of primary infection, EBV is a latent-persisent infection where? |
| epithelia cells and resting B cells; peripheral blood/memory B lymphocytes |
| During latency, where can Epstein-Barr virus occur due to a lytic infection after B cells spread to oropharynx? |
| saliva |
| If there are non-sense antibodies present in the body, what is the probably agent? |
| EBV |
| What type of antigen is EBV? |
| tyoe 1 T-INdependent antigen |
What are the two more unusual manifestations of EBV? ; |
splenomegaly heptaomegaly |
| Why is there a splenomegaly in EBV? |
| The spleen is the major organ for B cells in the body, and in Epstein-Barr disease, there is a huge proliferation of B cells. |
| What are three complications with EBV? |
lymphomas hairy leukoplakia multiple sclerosis |
| What drug do you never give if someone has infectious mono due to EBV? |
| Never give ampicillin! |
Treatment for EBV: What kind of treatment? Ampicillin? acetominophen? acyclovir? corticosteroids? |
supportive;; ; No ampicillin, acyclovir, corticosteroids. ; YES to acetominophen.; |
| Four ways of CMV transmission? |
-secretions -blood transfusion -vertical transmission -organ transplant recipients (if immunosuppressed, CMV = fatal) |
; Which agent is the most common cause of congenital infection? |
| CMV |
| Which agent are CMV manifestations very similar to? |
| EBV (but CMV is much more prevalent) |
| Are non-toxin mediated diseases contagious? What does that mean if a person is exposed? |
| All are contagious which means that a person exposed to infection will be colonized with the virulent strain, but not necessarily develop the disease. |
| Which four types of agents cause cellulitis? |
1. Gram-positive cocci (pyogenes, aureus, pneumoniae) 2. Gram-negative rods 3. Atypical mycobacteria (necrotizing skin lesions) 4. Fungal agents |
| Exposure to what predisposes a person to cellulitis and often involves bacteremia? (mycobacterium or vibrio) |
| exposure to fresh or seawater |
| Which epidemiologic factor predisposes a person to cellulitis and involves the agents Pasteurella and Capnocytophaga? |
| Animal (cat/dog) scratches or bites |
| Infections in areas adjacent to the oral cavity/in oral secretions predisposes people to cellulitis caused by which agent? |
| Eikenella corrodens |
| In cellulitis epidemiology, which etiology causes infections that occur within 72 hours of surgery? (2) |
1. gram positive cocci 2. C. perfringens |
| In cellulitis epidemiology, which etiology causes infections that occur between 10-->30 days? |
gram-negative rods (facultative anaerobes) gram-positive cocci |
| In cellulitis epidemiology, which etiology causes infections that occur between 2-3 months post-operative? |
diphtheroides coagulase negative staph |
| Describe the manifestation of the local infection of cellulitis. |
| -inflammation: erythema, pain, edema, warmth, NEVER sharply dermarcated |
| What treatment must be done for cellulitis? |
| I.V. antibiotics |
| As far as the epidemiology of anthrax, what type of disease is it? And what are the primary hosts? |
| Enzootic disease of *herbivores such as sheep, goats, cattle, etc. |
| What is formed by bacillus anthracis that can survive for years in the soil? |
| Anthrax spores |
| Which type of anthrax accounts for 95% of human cases? |
| cutaneous anthrax |
| In cutaneous anthrax, how does death occur? (2 reasons) |
| Death is due to both a Toxemia and a Bacteremia. |
| Which disease caused by P. aeruginosa must you make sure not to confuse with anthrax? |
| Ecthyma |
| What is the etiologic agent of erysipelas? What is another name for erysipelas? |
| Group A Strep; St. anthony's fire |
| What precedes erysipelas? |
| URT or skin infection caused by GAS |
| Erysipelas is similar to cellulitis except that: |
| -the illness begins with systemic signs and an erythema forms that is : bright red and indurated that IS SHARPLY DEMARCATED |
| Sole reservoir for smallpox? |
| humans |
| How is smallpox virus passed? (2) |
-respiratory secretions -contact with lesions |
| 4 complications of smallpox? |
-variola keratitis -encephalitis -cellulitis -secondary bacterial infection |
| DNA polymerase inhibitor that is used in the treatment of smallpox? |
| Cidofovir (Vistide) |
Which stage of smallpox is described as:
after exposure to the virus, this period is when people do not have any symptoms and feel fine. This period averages 12-14 days and people are not contagious.
|
| Incubation period |
Which stage of smallpox is described as:
first symptoms include fever, malaise, head/body aches. fever is usually very high and people are too sick to carry on ADL's. This stage my last 2-4 days. |
| prodrome phase |
| Which stage of smallpox is the most contagious? |
| early rash phase |
| Where does the early rash begin in smallpox? Within 24 hours, what happens to the rash? What happens to fever? |
| It begins on the tongue and in the mouth; In 24 hours, the rash spreads to all parts of the body; The fever falls down and the patient may feel better. |
| Which stage of smallpox is described as: the raised bumps become sharply raisd, usually round and firm to touch as if there is a small object under the skin. Like BB pellets under the skin. |
| Pustular rash |
| What happens after pustules develop in smallpox? What happens after scab phase in smallpox? When is the patient no longer contagious? |
| they form scabs; scars are formed. The patient is no longer contagious once all the scabs have fallen off. |
| Which areas of the body do most lesions of smallpox end up spreading to? |
| Extremities |
| What is the seasonal occurrence of chicken pox? |
| Winter-->spring |
| Where is the virus located in varicella and zoster? |
| The virus is located in the lesions; know that the lesions are contagious. |
| Where do lesions first develop in chickenpox? |
| They first develop on the head/scalp and spread to trunk |
| What is the most common agent of secondary infection that causes the hospitalization of children with varicella? |
| Secondary infection by GAS or staph aureus |
| What does a zoster-infected pt. manifest with? |
| VARICELLA! (chickenpox) not ZOSTER (shingles) |
| What age group does herpes zoster occur in? what types of children does this occur in? |
| adults above 60 years old; immunocompromised children |
| Why does shingles occur? |
| Recrudescence of VZV due to waning cellular immunity |
| Manifestations of herpes zoster: |
| ASYMMETRICAL maculopapular crusting rash FOLLOWS DERMATOME or cranial nerve distribution; SEVERE PAIN |
| What are three complications of herpes zoster? |
-opthalmic/otic zoster -postherpetic neuralgia (severe burning pain from non-noxious stimuli; very debilitating) -acute peripheral facial palsy: paralysis |
| What must you NOT give for treatment of varicella in children? Why? |
| NEVER give aspirin because of Reye's syndrome. |
| What antiviral therapy for varicella is recommended only for people at high risk for severe disease? |
| oral acyclovir |
| Which antiviral therapies are used for zoster within 72 hours of onset of rash? |
| Acyclovir, famciclovir, valacyclovir |
| What type of vaccine is Varivax and what is it used for? |
| Varivax ia a live attenuated vaccine for the prevention of varicella |
| After administration of Varivax, can children manifest with varicella? what is the difference? |
| Children can manifest with with EXTREMELY MILD varicella and no significant sequelae occur. |
| Name two contraindications for Varivax vaccine: |
-pregnant women -immunocompromised children |
| What is the agent for erythema infectiosum? |
| Human Parvovirus B19 |
| Name two other diseases caused by Parvovirus B19? |
| Arthropathy and Aplastic Crisis |
| Treatment of diseases caused by Parvovirus B19? |
-supportive only -antipyretics, analgesics, and NSAIDS -transfusion for those with aplastic crisis |
| Name a risk factor for aplastic crisis: |
| immunosuppressed pt. at risk for anemia, chronic bone failure |
| What is HHV-6 and HHV-7 closely related to? |
| CMV |
| What are the agents for exanthem subitum? |
| HHV-6 and HHV-7 |
| primary mode of transmission for HHV-6 and HHV-7? |
| saliva secretions |
| Agent frequently responsible for first febrile illness in 6-12 months of age? |
| HHV-6 |
| HHV-8 is associated with all forms of what complication (particularly in underdeveloped countries)? |
| Karposi sarcoma |
| Agent for which 100% of infected persons are seropositive for? What will cause reactivation of this virus? |
| HHV-6; immunosuppression will reactivate virus |
| What is the agent of pityriasis rosa? |
| HHV-7 |
| What is the usual progression of exanthem subitum? |
| High fever then defervescence, then rash |
| Main reason for spinal taps of little children? Why? |
| High fever with no rash; spinal tap done to check for aspetic meningitis |
| What class of virus does mumps, measles, and rubella fall under? |
| paramyxoviruses |
| Age group most infected for measles? Seasonality for measles? portal of entry? primary attack rate for measles (% of infected that manifest Dx)? |
-children <5 -winter-spring -upper respiratory tract ->90% attack rate |
| Leading causes of death in children 1-5 in developing countries as complications of measles? |
| Diarrhea and pneumonia |
| What occurs 10-12 days after infection of measles and 3-4 days before exanthem/enanthem? |
PRODROME: coryza unproductive cough conjunctivitis with photophobia
|
| Is the rash for measles symmetrical or asymmetrical? opposite as which disease? |
| Measles rash are symmetrical whereas herpes zoster is asymmetrical |
| Can measles cross the placenta? |
| yes |
| Treatment for measles? |
supportive: vitamin A; gamma globulin for immunocompromised (6 days after exposure) |
| Prevention of measles: who do you not administer vaccine to? |
| live, attenuated MMR. Don't administer to pregnant women! |
| Two other names for rubella? |
| german/soft measles |
| Primary age groups for rubella?; seasonality?; Is rubella just as infectious or less infectious than chickenpox and measles?; What populations are at risk? |
| adolescents, young adults; winter and spring; rubella is less infectious, meaning there are asymptomatic infections that occur; immigrants from developing countries and continental Europe |
| Prodromal symptoms present in rubella? |
| Prodromal symptoms are minimal/absent; fever is low-grade in rubella vs. high grade in rubeola; arthralgia appears like when caused by human parvovirus B19 |
| Complication of Rubella?; most critical timing for this complication?; consequences? |
| CRS: congenital rubella syndrome; first trimester of maternal pregnancy; teratogenicity and birth defects |
| Lab diagnoses for newborn uses what test? what does each letter stand for? What is measured? |
STRCH test: syphilis toxoplasmosis rubella CMV herpes IgM in cord blood is measured |
| Treatment for rubella? |
| DO NOT TREAT WITH IMMUNOGLOBULIN. Based on risks physicians may actually suggest therapeutic abortion. |
| What test do you use before or during pregnancy to determine maternal immune status for rubella? |
| LCAT |
| Name three diseases that are superficial mycoses: |
| Pityriasis Versicolor; Black or white piedra; Tinea Nigrans |
| Agent for pityriasis versicolor? Who is most affected?; clinical manifestations? (3) |
Malassezia furfur; young adults; -brown colored patches/lesions on chest abdomen or back -Pityrosporum folliculitis (acne like pustules on upper trunk/arms) -Dandruff; seborrhic dermatitis |
| Treatment of pityriasis versicolor? |
Antifungal (ketoconazole or ciclopirox) 1% selenium sulfide ointment or shampoo (selsun blue) |
| Agent of black piedra? white piedra? |
Black: piedra hortai White: trichosporon beigelii |
| What is formed on external hairshaft? |
| Ectothrix is formed, which is a sheath of arthrospores |
| Although there are no symptoms for black or white piedra, what does white piedra resemble?; Therapy? |
| Nits/lice; cut off or shave infected hair |
| Agent for Tinea Nigrans?; 95% of this happens in what age group? Which gender does it predominate in? |
| Hortaea Werneckii; persons under 18 years old; 75% female |
| Where does the black/brown mottled macules form in tinea nigrans? Treatment? |
| It forms on the palm or plamer surface of fingers; keratinolytic agents |
| Most common fungal agent for dermatophytoses? (ringworm); what does it infect? Other two agents for dermatophytoses? |
| trichophyton; hair, skin and nails; epidermophyton and microsporum |
| Pt. risk factors for pityriasis versicolor and dematophytoses? |
| malnutrition, antibiotics, low epithelial cell turnover rate, hyperridosis |
| Hair, skin, and nails share what common quality? |
| They are Keratinized. |
| "Tinea" indicates what disease? |
| Ringworm |
| Agent for dermatophytic onychomycosis? |
| Tinea unguium; nails crumble |
| Any fungal infection of skin, nails, or hair caused by a fungi other than a dermatophyte is caused by?; three forms? name of diseases? |
| candida alblicans; yeast, pseudohyphae; hyphae; dermatomycoses |
| How to treat cutaneous candidosis? |
| 1% crystal violet; nystatin, amphotericin B, ketoconazole (systemic) |
| Which agent infects gardners and lumberjacks?; clinical manifestations?; how to treat? |
| Sporothrix schenckii; painless chronic infections with nodular lesions along lymphatics; itraconazole/amphotericin B; apply heat 4x a day |
| What must be done to determine etiology of hepatitis before any treatment is initiated? |
| blood tests must be done before any treatment! |
| Three forms of chronic hepatitis (cirrhosis/liver cancer)? |
| B, C, and D only |
| Two characteristics about the incubation period of viral hepatitis? Why can hepatitis transmission be hard to control? |
can be prolonged is highly variable
-patient is infectious before Signs and Symptoms occur |
| what follows the prodrome phase of hepatitis? do prodromal symptoms continue? High levels of what produce dark urine and clay stool? |
| after prodrome phase, there is icteric phase. Yes, prodromal symptoms continue; bilirubin |
| What happens during convalescent phase of hepatitis? |
| disappearnce of jaundice; fatigue may still persist |
| Which two hepatitis viruses do vaccines exist for A person immune to HBV is also immune to? |
| Hep. B virus and Hep. A virus; HDV |
| What is HBV also known as? Production of which antigen anitbody results in complete recovery from HBV infection and immunity from future infection? What is this called? |
| serum hepatitis; production of SURFACE antigen antibody causes "neutralizing immunity" |
| Which antigen of HBV cannot be detected by clinical kits and does not result in neutralizing immunity? |
| Core antigen HBcAg (vs. HbsAg) |
| Three types of antigen of HBV? |
HBsAg (surface) HBcAg (core) HBeAg (soluble) |
| Which antigen of HBV has the ability to infect others? |
| HBeAg |
| Transmission of HBV? Most important route of transmission? Two other routes of transmission? |
| SSS: serum, saliva, and semen; sexual contact esp. homosexuals. percutaneous (needle stick/IVDU) and perinatally |
| Nearly all of which groups will develop chronic infection if they have Hep B? What will 15-25% of patients die from? |
| infants and young children; cirrhosis/carcinoma |
| The "natural history" for chronic HBV infection can be divided into which four phases? |
immune tolerance immune clearance inactive surface Ag carrier state reactivation |
| immune tolerance phase of chronic HBV occurs in patients infected when? persistently normal levels of what? |
| patients infected at birth or early childhood; ALT |
| Treatment of HBV? |
| PEG-interferon-@2a; antiviral drugs such as lamivudine, adefovir dipivoxil, entecavir |
| Passive immunization for HBV occurs via which vaccine? Active immunization is recommended for who? where do you inject active vaccine in adults? |
| HBVIG; all children in the US (engerix; tiwnrix) deltoid muscle in adults |
| What do you administer to infants born to infected mothers with HBV? |
administer BOTH: HBIG and HBV vaccine |
| What does HDV need to replicate?; HDV causes greatest morbidity by how? |
| HBV!; increasing severity and accelerating pace of chronic HBV infection (cirrhosis/liver cancer) |
| What is the most efficient mode of transmission for HDV? |
| percutaneous exposures |
| If HDV is present, what MUST be present? |
| HBV! coinfection |
| Presence of which antibodies to delta antigen helps diagnose HDV?; how to prevent HDV? |
| IgG; treat HBV via pre/post-exposure prophylaxis |
| Whereas HCV and HDV are RNA viruses, what kind of genome does HBV have? |
| DNA genome |
| What is the single most common reason for liver transplants? |
| HCV; |
| What accounts for the most of cases of chronic hepatits (70%) and many cases of ESLD in the US? |
| HCV |
| Which ages are affected in HCV? Where is peak incidence? |
| ALL ages are affected; peak incidence is 20-39 |
| In HCV, the rapid accumulation of ______ in the _______ region of the envelope allows the virus to escape ______ ________ by the host. This leads to chronic infection |
| MUTATIONS; HYPERVARIABLE; IMMUNE SURVEILLANCE |
| Three biggest risk factors of HCV? |
IVDU repeated transfusions tattoos/piercings |
| Chronic liver disease occurs at a high rate (70% of asymptomatic; 85-100% of symptomatic) for which type of hepatitis? |
| HCV |
| Appearance of what after 5-12 weeks after onset of hepatitis C will diagnose HCV? Presence of what and for how long differentiates acute vs. chronic HCV? |
-appearance of anti-HCV Ab's -presence of liver enzymes >6 months |
| Treatment of HCV: (problematic) |
PEG-interferon-@ and ribavirin. Very expensive, exteremly difficult to tolerate |
| What type of virus is HAV (RNA/DNA)? Which populations are at risk for HAV? Main transmission for HAV? |
| RNA virus; day-care center workers, closed populations, oyster-eaters; fecal/oral transmission with food and water as major vehicle (person-to-person may occur) |
| Does HAV become chronic? |
| NO. only B, C, and D do |
| HIV binds to human cells via which two glycoproteins? |
| gp41 and gp120 |
What is the agent for infectious mononucleosis? What is the manifestation of IM in early childhood? Who primarily manifests with IM in the industrialized world? |
1. EBV aka HHV-4 2. SUBCLINICAL manifestation in early childhood 3. primary infection occurs in adolsecsents and adults |
| If "Downey Cells" are found in blood, what is the likely virus? |
| EBV |
| Which agent is responsible for causing a seropositive marking in nearly 100% of all adults? |
| CMV |
| What do CID and SNHL stand for, and what disease are they associated with? |
CID: cytomegalic inclusion disease SNHL: bilaterla sensorineural hearing loss
CMV! |
| What does a child with CMV at birth manifest with? |
jaundice blood clotting petechial rash pneumonia(resp. distress) chorioretinitis of the eye seizures (microencephaly) lethargy motor disability |
| Outcome of CID? |
| Death is common in days to weeks later; survivors have significant sequelae |
| Number one infection of infancy in the first 3 months? |
| CMV! |
| Four manifestations of CMV in AIDS pt.? |
pnemonia retinitis encephalitis gastroenteritis |
| If you have a "negative" on which test, should you expect CMV-IM? What shape of cells would you expect to find? |
| Negative heterophile-agglutination test; "owl-eye" cells |
| Treatment of CMV? Treatment of CMV retinitis in AIDS patients? |
Ganciclovir Foscarnet Cidofovir **acyclovir resistant
-Formivirsen |
| How to prevent CMV? |
CMVIG (esp. for transplant pt.) Vaccine: orphan drug = phosphoprotein 65; glycoprotein B |
