Bugs Flashcards

Question

Steptococcus pneumoniae characteristics, epidemiology, mode of transmission

Answer 1

C: gram (+) diplococcus E: Common inhabitant of throat and nasopharynx MT: primarily host response to infection, can spread through airborne droplets

Answer 2

Path: disease occurs when organism spready to lungs, sinuses, ears or meninges, mediated by binding to epithelial cells by surface protein adhesins VF: Adhesin proteins Polysaccharide capsule - antiphagocytic Teichoic acid - activates alternate complement pathway Amidase - allows for cells wall release of components Phosphorylcholine - component of cell wall - binds to receptors necessary for platelet activation, allowing bacteria to enter cells --> bacteremia Pneumolysin - binds to hose cell membrane and creates pores --> activates classic complement pathway

Answer 3

Pneumonia, sinusitis, otitis media, meningitis, bacteriemia

Answer 4

D: Catalase (-), a-hemolytic, Optochin (S) Quellung (+) Bile solubility test - dissolves in bile T: Inactive vaccines PCN resistant - vancomycin + ceftriaxone

Answer 5

C: Coccobacillus, gram (-) E: present in almost all individuals, primarily respiratory tract MT: Opportunistic, respiratory droplets

Answer 6

Path: Colonizes respiratory tract in virtually people in first few months of life. Pili and adhesins mediate colonization of oropharynx --> cell wall components impair ciliary function --> damage of respiratory epithelial cells --> bacteria translocated across epithelial and endothelial cells --> enters blood VF: Lipid A --> meningeal inflammation Polysaccharide capsule --> antiphagocytic IgA protease --> prevention of neutralization

Answer 7

Otitis Media, pneumonia, meningitis, conjunctivitis, sinusitis, cellutitis, bronchitis, arthritis Pain in infected region, flu-like symptoms

Answer 8

D: chocolate agar - destroys inhibits of factor V (NAD) - required to colonize blood agar - satellite phenomenon - grows in presence of s. aureus Indole (+), Ornithine decarboxylase (+), Urease (+), Quellung (+) T: Vaccines - DTaP Broad spectrum antibiotics - Cephalosporins

Answer 9

C: enveloped, dsDNA virus, B herpes virus E: ~70% of population infected age 30 popular amongst adolescent/young adult age group MT: saliva, "kissing disease"

Answer 10

Path: EBV in saliva infects epithelial cells and naive resting B cells in tonsils --> growth of B cells stimulated by virus binding CD21 to C3d receptor --> expression of transformation and latency proteins --> cells proceed to follicles and germinal centers in LN --> infected cells differentiate into memroy cells --> EBV protein synthesis ceases --> Virus established latency 3 outcomes: 1. Replicate in B cells or epithelial cells permissive for EBV replication and produce virus 2. Cause latent infection of memory B cells in presence of competent T cells 3. Stimulate growth and immortalize B cells VF: Viral-encoded DNA genome - replicates viral genome EBV-encoded proteins - replace cellular proteins, not to kill but for continous growing Glycoprotein-containing envelope covering capsid - contains LMPs LMPs - membrane proteins with oncoprotein-like activity Several glycoproteins for attachment, fusion, escaping immune control

Answer 11

Infectious mononucleosis - battle between EBV infected B cells and protective T cells - classic lymphocytosis Malaise, headache, fever, spleenomegaly, pharyngitis, enlarged tonsils with exudate, lymphadenopathy Leukemia/Lymphoma - EBV infected cells hijack proteins needed for host cell cycle and cell signaling --> takes over cell --> unregulated growth --> mutations African Burkett Lymphoma - EBNA-T memory B cell + cofactors, CD8 T cells not effective, also often infected with malaria

Answer 12

D: PBS - Downy cells - atypical CD8 T cells Mono spot test - heterophile antibody test - non-specific PCR - confirmation T: no effective treatment, acute symptoms resolve in 1-2 weeks

Answer 13

C: segmented, -ssRNA virus, encapsidated by nucleoproteins, enveloped Influenza A - susceptible to drastic mutations that completely alter surface proteins - (antigenic shift) Influenza B - well conserved, only small gene mutations (antigenic drift) E: Influenza A - humans, pigs, horses, birds, marine mammals Influenza B - humans only MT: respiratory droplets, contaminated fomites

Answer 14

Path: virus enters body and comes in contact with cell --> hemagluttinin on virus surface attaches to cell membrane via sialic acid receptors --> intiates cell-mediated endocytosis --> virus enters cell --> virus uses M2 proton pumps to bring H+ ions into the cell --> H+ acidify and degrade the virus capid freeing viral RNA --> RNA translocates to nucleus --> endonuclease cap snatches 5` cap from host mRNA and transfers to viral RNA to use as primer --> replication of viral RNA via RdRp (RNA dependent RNA polymerase) --> translated by host ribosomes --> virion assembly by M1 protein --> virus leaves cell via cell budding --> virus releases neuraminidase to cleave hemaglutinnin and sialic acid receptors --> virus free to infect other cells VF: H - hemagluttinin NA - neuraminidase M2 proton pump M1 protein

Answer 15

Flu, Viral pnuemonia, Fever, chills, myalgias, headache, cervical lymphadenopathy, dry cough, malaise

Answer 16

D: Rapid antigen testing - high specificity, limited sensitivity Serologic testing - not relevant for acute T: olsemtimivir - Neuraminidase inhibitor Amantadine - Uncoating inhibitor Baloxavir - endonuclease inhibitor Vaccines - live attenuated, inactivated

Answer 17

Characteristics: largest virus, ovoid-brick shape linear dsDNA Epidemiology: exclusive human host range MOT: Inhalation, aerosols, and direct contact with fomites

Answer 18

Pathogen: Binds to cell-surface receptor--> envelope fuses with cellular membrane --> early gene transcription initiated on removal of outer membrane, (uncoating protein, uncotase) removes core membrane, liberating viral DNA into cytoplasm --> viral DNA replicates in electron-dense cytoplasmic inclusions (Guarnieri inclusion bodies), aka factories -->late viral mRNA is produced after DNA replication --> replicates in upper respiratory tract -> dissemination occurs via lymphatic and cell-associated viremic spread-> internal and dermal tissues are inoculated after a second more intense viremia, causing simultaneous eruption of the characteristic 'pocks' VF: 30% of genome is devoted to evading immune response * Factories (electron-dense cytoplasmic inclusions, Guarnieri inclusion bodies): viral RNA replicates here, it is in the cytosol. * Proteins that impede the interferon, complement, inflammatory, antibody, cell-mediated protective responses

Answer 19

CF: **2 days of fever before rash** Consistent disease presentation with visible pustules After 5-17 day incubation period: high feve, fatigue, severe headache, backache, malaise, followed by vesicular rash in the mouth and soon after on the body. Vomiting, diarrhea, excessive bleeding would follow. * This diesease was eradicated in 1980. Diseases: 2 variants of small pox disease: variola major (15-40% mortality rate), and variola minor (mortaltiy rate 1%)

Answer 20

Diagnostic: presumptive diagnosis made clinically, confirmed with molecular testing (no specific test) Treatment: Supportive care and antiviral therapy (Tecovirimat) No carrier state - disease is shown fast and can quarantine them to avoid spreading Prevention: vaccine- Only one serotype = one type of antibody = immune against it all

Answer 21

C: small, naked, +ssRNA enterovirus Icosahedral virus - resistant to harsh environments Epidemiology: exclusively human pathogen Poor sanitation, crowded living conditions Nigeria, Pakistan, Afghanistan Young children, older adults most at risk MOT: fecal-oral

Answer 22

P: VP1 proteins at verticies of viron bind to cellular receptors. Binds to PVR/CD155. VP4 released, capsid is weakened --> genome injected into cell --> genome binds to ribosomes -->polyprotein (contains all viral protein sequences) synthesized in 10-15 min of infection --> viral proteins tether genome to ER membranes, machinery for replication, and is colected into a vesicle --> generates negative strand RNA for new mRNA to be synthesized --> forms capsid, then released on cell lysis VF: host CD155 - facilitates endocytosis RNA-dependent RNA polymerase Resistant to pH 3-9, detergents, heat

Answer 23

CF: 90% asymptomatic 5% confer minor illness - abortive poliomyelitis * Fever * Headache * Malaise * Sore throat * Vomiting 1-2% confer moderate illness - nonparalytic poliomyelitis/aseptic meningitis * Minor illness symptoms * Neck and back pain 0.1-2% confer major illness - paralytic polio - cytolytic infection of motor neurons of anterior horn and brain stem * Varying degrees of flaccid paralysis (w/ no sensory loss) 3-4 days after minor symptoms subside ○ Bulbar poliomyelitis - flaccid paralysis of pharyngeal muscles, vocal cords, and respiratory muscles § Historically treated with iron lung 75% mortality Diseases: Post-polio syndrome - 30-40 years after initial infection Decreased muscular function due to neuron loss

Answer 24

Diagnostics: Culture - isolated from pt's pharynx, feces Grows on monkey kidney tissue culture Serology and Virology for specific IgM/RT-PCR detection Treatment: Prevention: IPV (IM, inactive) or OPV (oral, live attenutated) vaccine 2m, 4m, 6-18m, 4-6y

Answer 25

C: -ssRNA, bullet-shaped, enveloped virus E: Classic zoonotic infection MOT: bite of infected animal, saliva

Answer 26

P: G protein attaches to host cell --> envelope fuses with membrane of endosome on acidification of the vesicle --> uncoats nucleocapsid --> released into cytoplasm where replication takes place --> replicates in muscle at site of bite, with minimal or no symptoms (incubation phase) --> virus infects peripheral nerves and travels up to CNS (prodrome phase) --> infection of brain causes classic symptoms VF: * Spikes are composed of trimer of glycoprotein (G) and cover the surface * G-protein: generates neutralizing antibodies. Attaches to host cell to be internalized by endocytosis. Binds to nicotinic acetylcholine receptor (AChR), neural cell adhesion molecule (NCAM), or other molecules. * Replication in cytoplasm * Helical nucelocapsid: within envelope, gives striated appearance * Nucleoprotein (N): major structural protein of virus, protects RNA from ribonuclease digestion and maintains RNA in configuration acceptable for transcription * Large protein (L) * Nonstructural proteins (NS) Long asymptomatic incubation period

Answer 27

CF: asymptomatic for weeks-months * Progressive encephalitis * Myoclonic jerks * Paresis * Dysphagia * Aerophagia * Hydrophobia * Various symptoms of dysautonomia *Ultimately ends in death

Answer 28

Diagnostic: Negri bodies within Purkinje cell (pathognomonic) Evidence of infection does not occur until it's too late for intervention Treatment: Inactivated vaccines are given as both pre-exposure prophylaxis (PEP) and post-exposure prophylaxis (PrEP) * Purified Chick Embryo Vaccine (PCECV) or Human Diploid Cell Vaccine (HDCV) Another part of PrEP is to administer human rabies immunoglobulin (HRIG) to provide passive immunity in the time it takes for the body to generate its own adaptive response

Answer 29

C: * Large bacillus, arranges in chains Forms thick polypeptide wall *Only medically important bacteria with PROTEIN capsule* Gram (+) Spore-forming (readily seen in culture, not clinical specimens) Non-motile Facultative anaerobe E: Primarily a disease of herbivores; humans infected through exposure to conaminated aniamls or animal products MOT: Inoculation, Ingestion, Inhalation

Answer 30

P: Protective antigen (PA): binds to host receptors, gets cleaved, releases small fragment and PA63 fragment left on cell surface --> PA63 self-associated on cell surface, makes a pore precursor --> pore binds up to 3 molecules of LF and/or EF (Competitive binding) --> Stimulates endocytosis and movement to acidic intracellular compartment, releaseing LF and EF into interior VF: * Protective antigen (PA) allows for edema factor (EF) and lethal factor (LF) into cell ○ EF --> increases intracellular cAMP --> edema ○ LF --> cleaves MAPK --> cell death * Endospore - resistant to external insults Capsule: protein capsule. Unique because most capsules are composed of polysaccharides. This one is proteins.

Answer 31

CF: * Cutaneous anthrax - inoculation of infected animal products ○ Painless papule with surrounding vesicles ○ Painful lymphadenopathy ○ Edema * Gastrointestinal anthrax - ingestion of undercooked meat ○ GI ulcers ○ Edema ○ Lymphadenopathy ○ Leads to sepsis with 100% mortality * Inhalation anthrax - inhalation of spores ○ Fever ○ Edema ○ Lymphadenopathy ○ Meningeal symptoms in 50% of patients Diseases: Anthrax poisoning, biological warfare

Answer 32

Diagnostics: * Culture ○ Non-hemolytic on blood agar ○ White colonies with ground-glass appearance, rough edges ○ Colonies remain upright when lifted (tenacity) * Labs Polypeptide capsule seen with India ink and Quellung Treatment: ○ resistant to penicillin, sulfonamides, extended-spectrum cephalosporins ○ Current empirical treatment is: ciprofloxacin or doxycycline with 1 or 2 additional antibiotics. Amoxicillin still recommended for cutaneous anthrax Prevention: * Vaccines - Given to animal herds, people in endemic areas, people who work with animal products from endemic areas, and military personnel ○ Contains portion of protective antigen Latex allergy cross-reactivity

Answer 33

C: gram (-) coccobacillus bacteria Obligate aerobe, non-fermentative Epidemiology: incidence increasing since the 90s. More often in summer and fall MOT: Droplets, inhalation

Answer 34

P: exposure to organism --> bacterial attachment to ciliated epithelial cells of respiratory tract--> proliferation of bacteria --> production of localized tissue damage and systemic toxicity, Pertussis toxin inactivates AC regulatory protein --> increase cAMP --> increase respiratory secretions Also increases tracheal colonization factor (TCF) and tracheal cytotoxin (TCT) --> inhibits ciliary movement VF: * Adhesion facilitated through pertactin, filamentous hemagglutinin (FHA) and fimbriae * Bordetella resistance to killing protein A (BrkA) ○ Allows for evasion of complement * Dermonecrotic toxin ○ Facilitates local tissue damage * Tracheal cytotoxin: inhibits cilia movement, disrupting normal clearance mechanisms in respiratory tree leading to characteristic pertussis cough Pertussis toxin: systemic toxicity. Inactivates protein that controls adenylate cyclase activity, leads to increase in cAMP levels -> increases respiratory secretions and mucus production

Answer 35

CF: * Incubation period: 7-10 days * Catarrhal period: 1-2 weeks ○ Rhinorrhea, malaise, fever * Paroxysmal period: 2-4 weeks * Whooping cough Diseases: * Whooping Cough ○ Period after cough development ○ Development of severe secondary complications ▪ Pneumonia, seizures, encephalopathy Pertussis: used to be pediatric disease, now includes adolescents and adults.

Answer 36

D: * Culture ○ Fastidious - will only grow on media supplemented with charcoal, starch, blood, or albumin Assays: nuclecic acid amplification assays targeted for B pertussis or for a variety of pathogens is diagnostic test of choice. Treatment: primarily supportive. Antibiotics can ameliorate clinical course and reduce infectivity. Macrolides are effective in eradicating the organisms. Prevention: * Vaccine ○ Acellular Inactivated Subunit Vaccine ▪ Pediatric: DTaP (Diphtheria, tetanus, acellular pertussis) Ø Scheduled at 1.5-2 months, 4 months, 6 months, 15-18 months, and before 4 years ▪ 10 years+: single dose Tdap (tetanus, diphtheria, acellular pertussis) - lower concentrations of diphtheria and pertussis Whole cell inactivated vaccine - not available in US

Answer 37

Naked, +ssRNA virus with icosahedral capsid Newborns and neonates at highest risk MOT: fecal-oral, respiratory droplets

Answer 38

Viral replication is initiated in the mucosa and lymphoid tissue of the tonsils and pharynx, virus later infects M cells and lymphocytes of the Peyer patches and enterocytes in the intestinal mucosa. Primary viremia spreads virus to receptor-bearing target tissues, including reticuloendothelial cells of lymph nodes, spleen, liver, to initaite second phase of viral replication, resulting in secondary viremia and symptoms VF: Impervious to stomach acid, proteases, ile. Capsid virus resistant to inactivation

Answer 39

CF: In children: vesicular, ulcerated lesions on hand, feet, mouth Herpangina: fever, sore throat, pain on swallowing, anorexia, vomiting. Classic finding is vesicular ulcerated lesions around soft palate and uvula. In adults: more severe findings - paralytic disease, encephalitis Diseases: HFM disease Can lead to aseptic meningitis

Answer 40

D: clinical diagnosis Treatment: supportive care Prevention: Avoid exposure, good hygiene, no vaccine

Answer 41

-ssRNA, enveloped virus with helical nucleocapsid Most at risk are unvaccinated, malnourished or immunocompromised people MOT: Respiratory droplets

Answer 42

Infects epithelial cells of respiratory tract-> viremia through lymphocytes -> replicates in cells of conjunctivae, respiratory tract, urinary tract, lymphatic system, blood vessels, CNS -> rash caused by T cell response to virus infected epithelial cells -> immunosuppression -> cell-mediated immunity essential to control infection (Virus can infect many cell types due to the presence of its receptors CD46, and PVRL4 (nectin 4 poliovirus receptor-like 4) on epithelial and other cells and CD150 on dendritic cells and lymphocytes) VF: N: nucleoprotein, major internal protein, protection of viral RNA P: phosphoprotein, C and V proteins. Part of transcription complex (C and V are antagonists of innate responses) M: matrix. Assembly of virions F: Fusion protein, promotes fusion of cells, hemolysis, viral entry H Glycoprotein: viral attachment protein L: polymerase

Answer 43

CF: **4 days of fever before rash starts** Cough, coryza, conjunctivitis Exanthem starting below ears and spreads over body Diseases: Measles Complications: 1. Acute encephalitis 2. Post infectious encephalitis (immune mediated, weeks-months after infection) 3. SSPE: subacute sclerosing panencephalitis (years to weeks later, measles variant that persists in the brain)

Answer 44

Diagnostics: Need labs to confirm - RT/PCR Cytopathology - multinucleated giant cells (syncitia) on Giemsa Stain Treatment: Vitamin A to increase T cell function, supportive care Antivirals (ribovirin) Prevention: Measles-mumps-rubella (MMR): live attenuated vaccine.

Answer 45

(-) ssRNA, enveloped virus with helical nucleocapsid Unvaccinated and immunocompromised people most at risk MOT: respiratory droplets and direct contact Only through humans

Answer 46

HN glycoprotein binds to sialic acid and initiates infection of epithelial cells of upper respiratory tract --> virus replicates in cytoplasm, penetrates cell by fusion with plasma membrane and exit by budding from plasma membrane without killing cell--> progresses to parotid gland (by stensen duct or by viremia) --> syncytia formation --> spread by virema throughout body to testes, ovvary, pancreas, thyroid, other organs VF: * HN binds to sialic acid and red blood cells (hemagglutinin and neuraminidase activity) * Neuraminidase facilitates release from cell; H N: nucleoprotein, major internal protein, protection of viral RNA P: phosphoprotein, C and V proteins. Part of transcription complex (C and V are antagonists of innate responses) M: matrix. Assembly of virions F: Fusion protein, promotes fusion of cells, hemolysis, viral entry HN (hemagglutinin-neuraminidase) glycoprotein: viral attachment protein L: polymerase

Answer 47

Classic clinical finding: sudden onset of parotitis and fever D: Mumps

Answer 48

D: Confirmed via RT-PCR or IgM assay Treatment: supportive care Prevention: Measles-mumps-rubella (MMR): live attenuated vaccine.

Answer 49

P: Replication of rubella prevents (process called heterologous interference) the replication of superinfecting picornaviruses. Infects upper respiratory tract and then spreads to local lymph nodes, with a period of lymphadenopathy. Follows by establishment of viremia (spreads virous throughout body). Infection of other tissues and characteristic mild rash occurs. Prodromal period lasts 2 weeks. Infected person can shed virus in respiratory droplets during prodromal period and for 2 weeks after onset of rash VF: heterologous interference 14-21 day incubation period

Answer 50

C: **1 day of fever before rash** Maculopapular rash starts on head and spreads to trunk and extremities Lymphadenopathy Diseases: German measles Congenital rubella syndrome - fetus at major risk until 20th week

Answer 51

D: Need labs to confirm - detection of antirubella-specific IgM Treatment: Supportive care Prevention: Measles-mumps-rubella (MMR): live attenuated vaccine.

Answer 52

Smallest DNA virus Nonenveloped, ssDNA virus (+ or -) with icosahedral capsid Epidemiology: approx 65% of population infected by age 40 Common in ages 4-15 MOT: Respiratory and oral secretions

Answer 53

Infects mitotically active erythroid precursor cells in bone marrow and establishes lytic infection --> binds to erythrocyte blood group P antigen (globoside), and its internalization, virion uncoats, and the single-stranded DNA delivered to nucleus --> ssDNA converted to dsDNA (for transcription and replication), they fold back and hybridize w the genome to create a primer for cells DNA polymerase. Complementary strand replicates the genome. VP1 and VP2 (major nonstructural proteins) capsid proteins are synthesized in cytoplasm, and structural proteins go to nucleus, to assemble the virion --> VP2 cleaved to produce VP3. nuclear and cytoplasmic membrane degenerates, virus released on cell lysis VF: * Capsid virus: resistant to inactivation * Contagious period: precedes symptoms Virus crosses placenta and infects fetus

Answer 54

CF: **5 days of fever before rash "Slapped cheeks" facial rash, exanthem forms "lacy pattern", not contagious once rash appears** Initial phase is related to viremia: flulike symptoms and viral shedding Later phase is related to immune response: circulating immune complexes of antibody and virions that do not fix complement. Erythematous maculopapular rash, arthralgia, and arthritis Diseases: Fifth Disease/Erythema Infectiousum - mild febrile exanthematous disease in children. Responsible for Aplastic crisis in pts with chronic hemolytic anemia, and is associated with acute polyparthritis in adults. B19 infection of seronegative mother increases risk for fetal death: can kill erythrocyte precursors causing anemia, edema, hypoxia, and congestive heart failure (hydrops fetalis) Seropositive pregnant women have no adverse effect on fetus.

Answer 55

Diagnosis: clinical presentation Definitive: specific IgM or IgG detected through PCR Treatment: supportive care

Answer 56

HHV-6 Large, enveloped icosadeltahedral capsid containing dsDNA genomes At least 45% of the population is seropsotivie for HHV-6B and HHV-7 by age 2 years, almost 100% by adulthood. MOT: saliva

Answer 57

Viral glycoproteins binds with cell-surface receptors of T cells, epithelial cells and neuronal cells --> fuse with envelope with the plasma membrane, releasing nucleocapsid into cytoplasm --> enzymes and transcription factors carried into the cell in the tegument of the virion --> nucleocapsid docks with nuclear membrane and delivers the genome into the nucleus, genome is transcribed and replicated --> immediate early proteins (alpha): regulation of gene transcription and takeover the cell, early proteins (beta): transcription factors and enzymes (including DNA polymerase), and late proteins (gamma) consisting of structural proteins, generated after virial genome replication has begun --> Empty procapsids assemble in nucleus, filled with DNA --> bud into and out of the ER, and into the golgi membrane --> exit cell by exocytosis or by lysis of the cell --> lies latent in HPC and T cells VF: Immediate early proteins, early proteins, late proteins all important for replication of viral genome. Viral encoded DNA polymerase: replicates viral genome. Viral encoded scavenging enzymes: provide deoxyribonucleotide substrates for the polymerase.

Answer 58

CF: characterized by rapid onset of high fever of a few days duration, followed by a rash on the trunk and face, and then it spreads and lasts only 24-48 hours. Not contagious once rash appears D: Roseola Most common cause of febrile seizures in childhood

Answer 59

D: clinical diagnosis Treatment: supportive

Answer 60

Smallest genome of HHVs enveloped icosadeltahedral capsids containing dsDNA genomes Epidemiology: children < 5, in daycare, crowded households, etc Experienced by 30% of US population MOT: respiratory droplets, inhalation, direct contact with lesions

Answer 61

Varicella-zoster virus (VZV) infects the nasopharyngeal lymphoid tissue through airborne droplets --> viremia consisting of VZV-infected T cells that traffic through these tissues and subsequently throughout the body --> VZV enhances infection by inhibiting multiple host defenses, such as downregulation of major histocompatibility complex (MHC) class I expression and inhibition of interferon response genes --> virus partially evades the immune response --> VZV overcomes local immune-mediated defenses, such as alpha interferon (IFN-a) production by epidermal cells during prodromal period --> Rash develops --> cell-free virus, only in skin vesicles, is postulated to infect nerve endings in skin and move retrograde along sensory axons to establish life-long latency in neurons within the regional ganglia VF: Encodes a thymidine kinase and is susceptible to same antiviral drugs. Virus overcomes inhibition by IFN-alpha, and vesicles are produced in the skin.

Answer 62

CF: **3 days of fever before rash** maculopapular, pruritic rash - thin walled vesicle on erythematous base "dew drops on rose petal" then pustular and crusted All stages of lesions observed Diseases: Chicken pox Interstitial pneumonia Shingles - dermatomal

Answer 63

D: clinical diagnosis Tzanck smear -> looks for giant multinucleated cells (From syncytia formation) (board relevant, not clinically relevant) Treatment: children <12 - supportive care >12 - antivirals (acyclovir, valacyclovir) Prevention - live attenuated VZV vaccine

Answer 64

+ssRNA, enveloped, nonsegmented virus Worldwide pandemic - 44% of world population infected 1/3 total cases from South Asia/India MOT: Direct person-to-person, respiratory droplets, airborne

Answer 65

Sars-CoV-2 is inhaled or makes direct contact --> virus spreads in body via mucus membrane and/or entering blood --> virus binds to host receptor ACE2 (angiotensin-converting enzyme) on cells, mimics ACE2 --> enters cell via endocytosis, or with activation from host cell TMPSSR2 virus enters via membrane fusion --> virus disassembles and releases viral RNA --> uses host ribosomes to make viral proteins --> viral RNA polymerase synthesizes new viral RNA --> new viral RNA packaged and released from cell --> cell death and spread of infection VF: Spike protein - facilitates entry by attaching to ACE2 receptor of host cell - ACE-2 mimicry E2 glycoprotein: responsible for mediating viral attachment and membrane fusion, target of neutralizing antibodies. E1 glycoprotein: transmembrane matrix protein.

Answer 66

Incubation period - 4-14 days after exposure, asymptomatic Initial presentation - if symptomatic - Cough, myalgia, headache, rhinitis, Shortness of breath, sore throat, smell or taste abnormalities Asymptomatic COVID19 - positive virologic test w/ no symptoms Mild COVID19 - symptoms of covid w/o dyspnea, hypoxemia, pneumonia Moderate COVID19 - Viral pneumonia, No hypoxemia (>94% on RA) Severe COVID19 - pneumonia w/ dyspnea, hypoxemia < 94% and/or lung infiltrates >50% Critical COVID19 - Respiratory failure, septic shock, MODS Diseases: COVID-19

Answer 67

Lab findings Lymphopenia Elevated aminotransaminase levels Elevated LDH Elevated inflammatory markers Image findings Chest X ray may be normal or show infiltrates Abnormal will show consolidation and ground-glass opacities Diagnostic confirmation PCR testing - high sensitivity and specificity for SARS-CoV-2, 1-3 days for results Antigen testing - less sensitive but high specificity, results available in 15-30 mins, cheaper, widely available Treatment: Pharmacotherapy Antivirals - Remdesivir - adenosine nucleotide analogue --> inhibition of RNA replicase --> decreased RNA synthesis --> decreased viral replication Corticosteroids - Dexamethasone - Reduces inflammatory response IL6 pathway inhibitors - Tocilizumab - Monoclonal antibody against IL6 receptor --> decreased IL6 levels --> decreased immune response JAK inhibitors - Baricitinib - Selective JAK1 and JAK2 inhibitor that reduces inflammation Antithrombotic therapy - LMWH Prevention: Vaccines - mRNA or adjuvanted recombinant protein vaccine PPE, hand hygiene, social distancing

Answer 68

Gram (+), club-shaped bacillus Nonsporulating Immobile Aerobic Contains metachromatic granules Pleomorphism Epi: Normally colonize skin, upper respiratory tract, GI tract and urogenital tract Disease found world-wide, particularly poor urban areas w/ low vaccine rates. MOT: Maintained in population by asymptomatic carriage in oropharynx/skin of immune people. Transferred via respiratory droplet or skin contact. Humans only known reservoir.

Answer 69

C. diphtheria colonizes mucous membrane of respiratory tract --> bacteriophage facilitates transfer of tox gene from toxic diphtheria to nontoxic, residential diphtheria --> pathogen made of AB fragments; Receptor-binding region of B subunit binds to Heparin-binding Epidermal Growth Factor receptor on cell --> Translocation region of B subunit assists A subunit in endocytosis --> Catalytic region of A subunit catalyzes transfer of ADP-ribosylation of EF-2 --> inhibition of EF-2 --> arrested protein translation and synthesis --> cell death and necrosis --> destruction of respiratory epithelium VF: Exotoxin - tox protein coded by tox gene released from bacterial cell as host cell metabolizes bacteria Two polypeptide subunits A - active enzyme activity B - binding of toxin to cell receptor (HBEGF) Three functional regions A - Catalytic Region B - Receptor binding region B - Translocation region

Answer 70

CF: malaise, exudative pharyngitis, low grade fever Deposition of necrotic epithelium --> pseudomembrane over pharynx, tonsils (pathognomoneic) Pseusomembrane cannot be removed/peeled off - will cause tissue bleeding as it's embedded Cutaneous Diphtheria Scaly, erythematous rash Impetigo or deep, punched out ulcers No systemic effects Diseases: Diphtheria Myocarditis Neurotoxicity

Answer 71

Tinsdale medium: reduced by C. diphtheriae, appears gray/black. Brown halo around colonies. Requires addition of horse serum. Media of choice Loffler medium - shows the metachromatic granules Elek test- detects presence of diphtheria toxin. Agar culture that is embedded with an antitoxin-impregnated paper Diphtheria toxin production results in bands of precipitation Catalase (+) Treatment: early administration of diphtheria antitoxin to neutralize exotoxin before it is bound by host cell. One cell internalizes toxin, cell death inevitable. Can treat with penicillin or erythromycin. Therapy should be started immediately upon suspicion, even before diagnosis is confirmed

Answer 72

Thin Bacillus, non-motile, obligate aerobic bacteria Humans are only natural reservoir. Populations at risk are homeless persons, drug and alcohol abusers, prisoners, HIV patients. About 1/4th of the worlds population is infected. MOT: * Direct contact * Aerosols * Droplets * Ingestion ○ Unpasteurized milk from infected cow ○ Direct contact ○ Aerosols ○ Droplets ○ Ingestion Unpasteurized milk from infected cow

Answer 73

Enters respiratory airways -> infectious particles penetrate alveoli -> phagocytized by alveolar macrophages-> M. tuberlocis prevents fusion of phagosome with lysosomes (blocks early endosomal autoantigen (EEA1) -> phagosome is able to fuse w other interacelular vesicles giving access to nutrients and intracellular replication --> Cord factor and release of host cytokines --> caseating necrosis and granuloma formation --> formation of fibrin capsule surrounding necrotic macrophages and M. tuberculosis bacteria --> latent tuberculosis infection VF: Lipid-rich cell wall - resistance to detergents, some antibiotics, and the host immune response Inhibit phagosome and lysosome fusion ○ Sulfatides - Blocks endosomal autoantigen 1 (EEA1) --> inhibits phagolysosome formation ○ Catalase and peroxidase activity - Resistance of host oxidation ○ Cord factor - helps with linear growth and increases macrophage activation; inhibit leukocyte migration and mitochondrial respiration and oxidative phosphorylation ○ TNF-a - assists with granuloma formation-> leads to weight loss (consumption); intracellular killing by macrophages causes cells to form around bacteria and close off their oxygen supply-> bacteria become dormant-> necrosis in lungs; production of NO * LAM - Inactivates macrophages; scavengers free radicals; inhibits MHC II presentation * ESAT 6 & CFP10 (intracellular) - Form complex that inhibits TLR2 --> prevents TNF-α and IL-12 release --> decreased macrophage response

Answer 74

CF: Insideous onset, nonspecific complaints of malaise, weight loss, cough, night sweats, fever, Blood-streaked sputum production (hemoptysis) associated w tissue destruction (cavitary disease) Diseases: Tuberculosis, Primary Active or Secondary Reactivation

Answer 75

Diagnostics: Culture * Extremely slow-growing on agar-based or egg-based media, faster on broth-based * Colonies nonpigmented, light tan (compared to other species that may have more color) Catalase (+), oxidase (+) Histology shows caseating granulomas Langhans giant cells - epithelioid cells with central core of necrotic mass surrounded by T cells and NK cells Acid-fast stain- vivid red or pink against blue background (mycolic acids in cell wall- can't take up other stains) Diagnosis relies on radiographic evidence of pulmonary disease, positive skin test reactivity, and laboratory detection of mycobacteria * Tuberculin skin test: reactivity to intradermal injection of mycobacterial antigens (**PPD**) can differentiate b/w infected and noninfected pts ○ BCG Vaccine can cause false positive --> IFGR (IFN-γ release assay) testing to confirm/rule out false positive * CXR/CT - Cavities in lower lobes, active TB will present with consolidation in upper lobes and medastinal lymphadenopathy (**Ghon complex**) * Sputum Samples ○ Culture 3x at least 8 hrs apart AFB Smear + Culture - Gold Standard for active TB Treatment: resistant to most antibiotics. Pts must take multiple antibiotics for an extended period or antibiotic-resistant strains develop. Pyrazinamide and either ethambutol r levofloxacin 6-12 months Prevention: only for those in endemic contries - BCG vaccine

Answer 76

Mold; Septate hyphae that branch at **acute angles** Common throughout the world; Ubiquitous in air, soil, decaying matter Inhalation of spores

Answer 77

Inhaled conidia are met by the innate defenses provided by resident phagocytes, specifically airway epithelial cells and alveolar macrophages --> These cells secrete inflammatory mediators after recognition of key cell wall components (eg, beta-D-glucan) --> neutrophil recruitment and the activation of cellular immunity VF: * Conidia binding to fibrinogen and laminin within alveoli - adhesion * Elastases and Proteases - Hyphal invasion - Degrade surrounding host environment --> spread to other tissues through blood stream * Conidia resistant to neutrophilic-killing, germinating/sexual spores are not * Melanin - Confers resistance to caspofungin and amphotericin B; protection against oxidative damage and harsh temperatures * Gliotoxin - Inhibits macrophage phagocytosis and T-cell activation/proliferation

Answer 78

CF and Diseases Bronchopulmonary form: asthma, pulmonary infiltrates, peripheral eosinophilia, elevated serum IgE, hypersensitivity to antigens. Allergic sinusitis: shows lab evidence of hypersensitivity Aspergillus bronchitis usually occurs in setting of underlying pulmonary disease (like cystic fibrosis, chronic bronchitis, bronchiectasis) <- formation of bronchial casts/plugs made of hyphal elements and mucinous material Blood tinged sputum seen if aspergillus invades beyond cavity into healthy tissue Apsergilloma: can form in paransal sinuses or preformed pulmonary cavity secondary to old tuerculosis or other chronic cavitary lung disease (seein on X-ray) Invasive aspergillosis: setting of mild immunosuppression to destructive, locally invasive pulmonary or disseminated aspergillosis May cause wheezing, dyspnea, hemoptysis Invasive pulmonary aspergillosis and disseminated aspergillosis are devastaing in neutropenic and immunodeficient pts. Presents w fever and pulmonary infiltrates, with pleuritic chest pain, hemoptysis. Mortality 70%

Answer 79

* Cultures ○ Grown on media that does not contain cycloheximide ○ Stains poorly w H&E, well visualized by PAS, GMS, Gridley fungal stains. * Labs ○ Catalase (+) Rapid diagnosis of invasive aspergillosis: immunoassays for aspergillus antigen in serum, **bronchoalveolar lavage (BAL) fluid**, and CSF Treatment: * Aspergillus infections: **voriconazole** for less serious infections * Aspergillomas must be surgically removed * Angio invasive disease: use **amphotericin B** Can also use echinocandins as salvage therapies

Answer 80

Fungus but closely resembles protozoan - disc-shaped cyst Clustered within foamy, eosinophilic exudate within alveolar spaces, with interstitial filtration of plasma cells Symptoms only seen in immunocompromised pts (AIDS-defining illness) MOT: Opportunistic - respiratory droplets and airborne

Answer 81

Pathogen: not completely understood VF: * Adherence facilitated through mannose * β-1,3-glucan may play a role in eliciting a host response that damages alveolar pneumocytes Damaged AP are unable to facilitate gas exchange --> hypoxia and death

Answer 82

CF and Disease Pneuomocystis Pneumonia (PCP) * Insidious onset of Dyspnea, Cyanosis, Tachypnea, Non-productive cough, Fever

Answer 83

Diagnostics: PAS and Silver stain Toluidine blue stain BAL analysis CXR - in immunosuppressed pts Lungs will have ground glass appearance and crushed ping pong ball appearance Treatment: Bactrim (trimethoprim and sulfamethoxazole) Sulfa allergies: can use pentamidine Cell membrane lacks ergosterol and hence antifungal agents such as azoles and amphotericin B products are not active against Pneumocystis. The fungus must synthesize its own folic acid and hence this is a typical target for treatment (e.g TMP/SMX).

Answer 84

Dimorphic fungi Spherule size: smaller than RBC Found intracellularly in macrophages Mold at 25°C - Hyphae with tuberculate macroconidia Yeast at 37°C - Budding yeast cells, narrow base **Epidemiology: Within Ohio and Mississippi River Valleys, some part of Eastern US - "in caves/nature"** MOT: Inhalation of spores from bird/bat droppings

Answer 85

Mold conidia are inhaled --> convert to yeast form within host --> infect host phagocytes ->can become systemic. Granulomous formations and calcium deposits. To survive in macrophages it alters pH of phagosome with urease and siderophores, and has calcium binding proteins. VF: * Phosphoinositol-containing sphingolipids prevent phagocytosis and oxidation * Calcium-binding protein (CBP) and siderophores - crucial for growth and modulating pH of phagolysosome * Melanin ○ Confers resistance to caspofungin and amphotericin B Protects against oxidative damage and harsh temperatures

Answer 86

CF: asymptomatic in most cases * Immunocompromised and pediatric patients ○ Bronchial obstruction ○ Oral ulcers ○ Hepatosplenomegaly ○ Pericarditis ○ Arthritis ○ Pancytopenia (if bone marrow involvement) ○ Erythema nodosum (painful red nodules on shins) ○ Might see oral ulcers on tongue and palate 'fevers, cough, diffuse pulmonary infiltrates' Disease: Histoplasmosis

Answer 87

* Cultures ○ Slow growth on mycologic media * KOH stain. * Rapid serum/urine antigen testing preferred Chest xray: diffuse pulmonary infiltrates Microscopy using BAL Treatment: * Local and mild infection: azole drugs (fluconazole and ketoconazole) Systemic infections and immunocompromised: amphotericin B

Answer 88

Dimorphic fungi Mold at 25°C - Barrel-shaped arthroconidia with alternating disjunctor cells Yeast at 37°C - Circular yeast cells (spherule of spores in lungs, releases endospores) Spherule size is larger than Red blood cell. Also known as Valley Fever Epidemiology: **Southwestern US ** seen in immunocompromised pts MOT: inhalation of spres from contaminated soil/dust

Answer 89

Mold conidia are inhaled and convert to yeast form inside host --> grows into spherules filled with endospores, eventually released * Can have infection at extrapulmonary sites as well. Can still affect tissue, bone, joints, meninges. Can cuase meningitis. In immunocompromised: forms granulomas VF: * Urease - Allows for neutralization of low pH lysosomal enzymes --> allows for intramacrophage growth Can contribute to ability to invade CNS

Answer 90

CF: Asymptomatic pulmonary infection in most cases Can present as pneumonia - fever, sweat, arthralgia "Desert bumps" Immunocompromised - skin and lung lesions, sand dissemination of bone Disease: Coccidioimycosis * Immunocompromised pts develop symptoms and possible disseminated infection ○ Skin ○ Bones ○ Joints ○ CNS

Answer 91

* Culture ○ Rapid growth on mycologic media ○ Colonies change color from white to brown with age KOH stain as well Treatment: Local infections: azole drugs suffice Systemic infections: amphotericin B

Answer 92

Dimorphic fungi Mold at 25°C - Lollipop-like unbranched structures that extend the length of hyphae - **branched at 90 degree angle** Yeast at 37°C - Budding yeast cells, **large broad base**, double-contoured thick walls **Epidemiology: Ohio and Mississippi River Valleys, the Carolinas, Great Lakes** Seen in immunocompromised pts MOT: inhalation of spores in decaying matter in soil

Answer 93

Mold conidia are inhaled --> convert to yeast form within host --> cause local lung infection --> May form granulomas within lungs or disseminated tissue Can also spread and become systemic infection -> lesions within bone and skin VF: WI-1 surface protein allows for macrophage evasion, masked by 1,3-α-glucan Being dimorphic Modulates immune response by generating more TH2 response (anti-inflammatory response)

Answer 94

Most are asymptomatic - Pneumonia is acute or chronic, considered a local lung infection but can spread to other organs especially in immunocompromised. Immunocompromised person: most likely to occur in skin and bone (osteomyelitis) Clinical features CNS: hemiparesis, aphasia, carotid bruits CT of head: 'multiple ring-enhancing lesions in R cerebrum with surrounding vasogenic edema and midline shift; significant encephalomalacia and generalized atrophy in L cerebral" Disease: Pulmonary disease May migrate to extrapulmonary sites in immunocompromised patients - skin, bone, genitourinary, CNS

Answer 95

* Cultures ○ Will grow on most mycologic media ○ Grows very slowly (up to 1 month) ○ Appearance is variable depending on temperature and media * Labs ○ KOH Stain as well (see a round yeast w single bud) ○ PAS stain ○ GMS stain Treatment: Local infections: azoles Disseminated infections: amphotericin B

Answer 96

Dimorphic fungi 37C- cell and germ tube formation; 20C yeast form w pseudo hyphae formation Epidemiology - Colonizers of humans and warm-blooded animals. GI tract from mouth to rectum. And in vagina and urethra, on skin, under fingernails and toenails. Hospitalized pts at risk for mortality MOT: Endogenous infection - opportunistic Exogenous infection - direct contact

Answer 97

Pathogen: There are three major routes by which Candida gain access to the bloodstream: ●Through the gastrointestinal tract mucosal barrier ●Via an intravascular catheter ●From a localized focus of infection, such as pyelonephritis VF: Phenotype switching - can survive in many different environmental microniches within human host.

Answer 98

Ranges from superficial mucosal and cutaneous candidiasis to widespread hematogenous dissemination including target organs: liver, spleen, kidney, heart, brain. * Mucosal infections (thrush): may be limited to oropharynx or extends to esophagus and entire GI tract ○ Vaginal mucosa is also common site of infection - 'white cottage cheese' like patches on mucosal surface. ○ May cause localized skin pruritic rash w erythematous vesiculopustular lesions * Urinary tract involvment ranges from asymptomattic to renal abscesses secondary to hematogenous seeding * Intraabdominal candidiasis Hematogenous candidiasis (may be acute or chronic), results in seeding of deep tissues, including abdominal viscera, heart, eyes, bones, joints, brain) Diseases: Diaper rash Oral candidiasis (Non-AIDS-defining illness) Candida esophagitis (AIDS-defining illness) Vaginal candadiasis Endocarditis

Answer 99

Diagnostics: Culture: Forms smooth, white, creamy domed colonies Chromogenic medium like CHROMagar candida -> green colonies Labs: Scrapings of mucosal/cutaneous lesions, with KOH containing calcofluor white Treatment: Azoles for minor infections, amphotericin B for severe infections Oral/esophageal candiditis: nystatin (liquid, taken swish and spit or swallow depending on where infection is)

Answer 100

Encapsulated yeast Obligate aerobe Epidemiology - immunocompromised pts (AIDS-defining illness) MOT: * Inhalation Usually through dust containing contents of bird droppings

Answer 101

* Antiphagocytic polysaccharide capsule ○ Main virulence factor, repeating polysaccharide antigen * App1 inhibits CR2 and CR3 --> interferes with C3b-mediated phagocytosis * Melanin ○ Confers resistance to caspofungin and amphotericin B Protects against oxidative damage and harsh temperatures

Answer 102

CF: * Fever * Headache * Visual Disturbances * Photosensitivity * Impaired mental status * Seizures *Only severely immunocompromised pts succumb to symptoms* Disease: Cryptococcal meningitis

Answer 103

* Culture: ○ Rapid growth on most mycologic media ○ Colonies vary in appearance in pigmentation (spectrum from tan to red) ○ Converts caffeic acid to melanin on glucose-free media --> indicates presence of phenoloxidase * Labs: ○ PAS or silver stains ○ India ink stain - shows halo-like budding yeast ○ Fontana-Masson stain * Urease (+) Latex agglutination test: detects polysaccharide capsular antigent, causes aggulutination Treatment: joint therapy with amphotericin b, and flucytosine. Followed by fluconazole for maintenance therapy

Answer 104

Enveloped, +ssRNA virus with cone-shaped capsid made of p24 Pseudodiploid - 2 RNA molecules Epidemiology: HIV-1: most prevalent world wide HIV-2 restricted almost completely to West Africa Impact on US is disproportionately high in southern states MOT: Blood, semen, vaginal fluid, mother's milk

Answer 105

Virus infects any cell with CD4 receptor (myeloid lineage) --> Gp120: CD4 binds to CCR5 receptor and, later, CXCR4 receptor --> Gp41 facilitates fusion and release of RNA --> Integrase integrates the viral DNA pro-virus into the host genome ○ Facilitated by Vpr protein --> Host RNA polymerases transcribe viral mRNA and new genomes, promoted by the transcription factor NF-κB --> Tat protein binds to a sequence in the transcriptional activation region (TAR) of the long terminal repeat sequence (LTR) and prevents transcription from shutting off --> Rev protein – controls RNA export and splicing; in the early stages of infection, only gag, env, and pol are expressed, but in later stages, the entire viral genome is expressed --> Host ribosomes translate viral proteins --> Host protease (furin) cleaves Gp160  Gp120 (Env) and Gp41 (Env) --> Viral protease (HIV-1 PR) cleaves Gag-Pol polyprotein --> Vpu protein mediates virion assembly --> virions bud from infected cells VF: *pol* gene - protease, RT, integrase *env* gene - gp41, gp120 *gag* gene - p24 and p17 *rev* - regulation of RNA splicing *nef* - decreases cell surface CD4 - facilitates T cell activation - **essential for progression to AIDS** *vif* - Virus infectivity, promotion of assembly, blocks antiviral protein *vpu* - facilitates virion assembly/release, induces degradation of CD4 *vpr/vpx* - transport of complementary DNA to nuclear, arrest of cell growth, facilitates macrophage replication *tat* - transactivation of viral and cellular genes

Answer 106

CF: Initial flu-like symptoms * Fever * Malaise * Fatigue * Lymphadenopathy * Rashes * Oral ulcers Hepatomegaly and/or splenomegaly *Including list of non-AIDS-defining illnesses* Diseases: Acquired Immunodeficiency Syndrome (AIDS) caused by diminished CD4 T cells

Answer 107

Diagnostics: Serology testing p24 antigen ELISAs 3rd generation and below - HIV antibody assays – IgM and IgG 4th generation and above – Combination HIV antibody with HIV antigen – IgM, IgG, p24 Only 5th generation can detect between HIV-1 and HIV-2 Western Blot – only IgG Virologic Testing – detects viral load of HIV CD4+ count (< 200 = AIDS) Treatment: ART (2) NRTIS + INI/PI/EI

Answer 108

Member of Herpes family More prevalent in certain geographic areas - Italy, Greece, Africa Pts with AIDS MOT: Sexually transmitted (most likely)

Answer 109

B cell is primary target cell (like EBV) - Produces cyclin D and several inhibitors of p53. not enough alone to make KS, but needs a cofactor (like AIDS) Latent infection - virus resides in B cell Lytic infection - virus goes on to infect other cells --> infected B cells promote infection of endothelial cells --> HHV infection of endothelial cells necessary for development of kaposi sarcoma --> the spindle cells produce proinflammatory and angiogenic factors, which recruit inflammatory and neovascular components of the lesion, and latter components supply signals that aid in spindle cell survival and growth VF: Proteins resemble human proteins and promote growth and prevent apoptosis of infected and surrounding cells. * Includes IL-6 homolog (Growth and apoptosis) * Bcl-2 analog (antiapoptosis) * Chemokines * Chemokine receptor These proteins promote growth and development of polyclonal kaposi sarcoma cells in AIDS patients and others

Answer 110

Clinical Features: -Classic (sporadic) type - lesions on distal lower extremities - rarely aggressive -Endemic (African) type - lesions more locally aggressive, lower extremity lymphadema, visceral involvement common in children -Iatrogenic (Immunosuppression related) - Lesions on distal lower extremities, may be disseminated, visceral involvement common - may regress with modification of immunosuppression - AIDS associated - Localized or disseminated, visceral involvement common with poor HIV control - very aggressive - may regress with HIV treatment Disease: Kaposi Sarcoma

Answer 111

Treatment: Regression with HIV/AIDS management

Answer 112

Chickenpox

Answer 113

Measles: 9-12 days Small pox: 12-14 days Chickenpox: 13-17 days Rubella: 17-20 days | Farther a pathogen has to travel, the longer the incubation period

Answer 114

1. Recognition 2. Attachment 3. Penetration 4. Uncoating 5. Transcroption 6. Protein synthesis 7. replication 8a/9a. Envelopment/ Budding and release 8b/9b. Assembly/ Lysis and release

Answer 115

Measles, Rubella

Answer 116

Chickenpox in adults or immunosuppressed

Answer 117

Measles, Rubella, Varicella Parvo and Roseola not contagious once rash appears

Answer 118

Measles, Rubella, Varicella

Answer 119

Parvovirus B19 (Fifth Disease)

Answer 120

HHV-6 Roseola

Answer 121

Cocksackievirus (HFM)

Answer 122

Leishmaniasis

Answer 123

Ixodes tick Lyme Disease and Babesia

Answer 124

Ring --> Trophozoite --> Schizont --> Gametocyte