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Unit 3 HDC > Bugs > Flashcards

Bugs Flashcards

1
Q

Actinomyces israelii - Characteristics, Epidemiology, Mode of Transmission

A

C: Anaerobic, gram (+) rods

E: Naturally live in mucosal tracts (UR, GI, VG)

MT: Endogenous infections - opportunistic - only when normal mucosal barriers are disrupted by trauma, surgery, infection

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2
Q

Actinomyces israelli Pathogenesis and VF

A

Path: breach in mucosal barrier –> development of chronic granulomatous lesions that become suppurative and form abscesses connected by sinus tracts –> Macroscopic colonies of organisms called sulfur granules are masses of filamentous organisms bound together by calcium phosphate

VF: Residing in normal mucosa

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3
Q

Actinomyces israelli clinical features and diseases

A

CF: Most infections cervicofascial - poor oral hygiene
Tissue swelling w/ fibrosis, scarring, abscesses

D: Actinomycosis

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4
Q

Actinomyces israelli diagnostics and treatment

A

D: Tissue/pus cultures collected - fastidious and grow slowly under anaerobic conditions - white, domed colonies

T: PCN is drug of choice (amoxicillin), non B-lactamase bug doesn’t need BL inhibitor

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5
Q

Streptococcus pyogenes characteristics, epidemiology, mode of transmission

A

C: Gram (+) cocci in chains
GAS
with M-protein cell wall

E: Children 5-15, pts w/ soft tissue infection, pts w/ prior strep

MT: Respiratory droplets or through breaks in skin after contact with infected person, transdermal, ingestion

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6
Q

Streptococcus pyogenes pathogenesis and VF

A

Path: Opportunistic

VF:
Hyaluronic acid capsule - antiphagocytic
Streptolysin O & S - lyses erythrocytes, leukocytes, platelets
M protein - binds to factor H –> disrupts C5 convertase –> no opsoninzation
Protein F - binds to fibronectin of epithelial cells –> adhesion
C5a peptidase - cleaves C5a –> prevents vasodilation and chemotaxis

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7
Q

Streptococcus pyogenes Clinical Features and Diseases

A

CF: diffuse inflammation, pharyngitis, sinusitis, rash

D: Rheumatic fever - M-protein molecular mimicry attacking cardiac myosin proteins
Scarlett fever - strawberry red tongue, sandpaper rash, fever, flushing
Impetigo - honey crusted lesions on erythematous base

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8
Q

Streptococcus pyogenes Diagnostics and Treatment

A

D: Gram (+)
Catalase (-)
B-hemolytic
Bacitracin (+)

T: Penicillin
1st & 2nd gen Cephalosporins
Macrolide (PCN allergy)

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9
Q

Rickettsia rickettsia characteristics, epidemiology, mode of transmission

A

C: Gram (-) rods w/ minimal peptidoglycan layer
Intracellular parasite - requires host ATP

E: maintained in reservoir hosts (rodents and arthropods), transmitted by arthropod vectors

MT: Hard ticks in North and South America
April - September most common

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10
Q

Rickettsia rickettsia pathogenesis and VF

A

Tick bite –> dormant rickettsiae activated by warm blood and are released from tick salivary glands –> enter cells by attaching to surface receptors and stimulating phagocytosis –> produces phospholipase to degrade phagosome –> released into cytoplasm to replicate

VF: OmpA - expressed on surface, responsible for adhesion to epithelial cells
Phospholipase - degrades phagosome

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11
Q

Rickettsia rickettsia Clinical Features and Diseases

A

Fever, headache, malaise, mayalgias, N/V/D

Rocky Mountain Spotted Fever
“Spotted” macular rash starting distally then working toward trunk
Neurologic, pulmonary, cardiac manifestations

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12
Q

Rickettsia rickettsia Diagnostics and Treatment

A

D: Giemsa stain, NAATs, Western blot
Does not gram stain well bc thin peptidoglycan layer

T: Tetracyclines first line - even in pregnant women and childre

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13
Q

E. coli characteristics, epidemiology, mode of transmission

A

C: Bacillus, gram (-)
E: females > males for UTI
Most common cause of bacterial diarrheal disease
MT: mostly endogenous - opportunistic - perforated intestines, translocated to other mucosal areas

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14
Q

E. coli pathogenesis and VF

A

Path: organism travels from colon –> urethra –> bladder

VF:
Flagella - motile
K antigen capsule protects from phagocytosis
P fimbriae - adhesion
Lipid A - endotoxin recognized by TLR4
HlyA - hemolysin

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15
Q

E. coli Clinical Features and Diseases

A

Variety of diseases and symptoms: UTI, gastroenteritis, meningitis, sepsis

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16
Q

E. Coli Diagnostics and Treatment

A

D: pink on MacConkey agar
Green sheen on Methylene blue agar
Cultures will grow on anything
Nitrate-reducing
Catalase (+)
Urinalysis + for leukocyte esterase

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17
Q

Borrelia burgdorferi characteristics, epidemiology, mode of transmission

A

C: Spirochete, gram (-), motile
E: Most commonly reported vector in US - Northeast and upper Midwest
MT: Bites from Idoxes tick, white-footed mouse in reservoir

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18
Q

Borrelia burgdorferi pathogenesis and VF

A

Path: microbe resides in tick using OspA –> tick bite –> microbe is transferred through saliva into blood stream –> binding of OspC to human plasminogen allows spirochete to spread from bite site –> symptoms show in 3 stages

VF: OspA - tick gut survival
OspC - survival in human
Endoflagella - motility
CRASP - binds to factor H –> dissociation of C3bBb

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19
Q

Borrelia burgdorferi Clinical Features and Diseases

A

Lyme Disease
Early stage: Erythema migrans, flu-like symptoms
Disseminated: Severe arthralgia, neuro symptoms - Bells Palsy, meningitis, carditis
Chronic: Chronic arthritis, late neurologic symptoms

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20
Q

Borrelia burgdorferi Diagnostics and Treatment

A

D: Clinical diagnosis of erythema migrans
Two-tiered serologic testing: ELISA and Western Blot

T: Doxycycline - 30S subunit binding
Disseminated stage - Ceftriaxone - 3rd gen Ceph - prevents cell wall synthesis

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21
Q

Moraxella catarrhalis characteristics, epidemiology, mode of transmission

A

C: gram (-) diplococcus, obligate aerobe
E: Most common in infant and small children, esp in daycare
More common in winter months
Naturally colonize in nasopharynx
MT: Respiratory droplets, opportunistic - normal upper respiratory tract flora

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22
Q

Moraxella catarrhalis pathogenesis and VF

A

Path: cofactor (ie viral infection) precipitates migration to middle ear via eustaschian tube

VF: UspA1 - adhesion to fibronection; also inhibition of host immune resposne - binds to CEACAM1 –> inhibits PI3K –> no inflammatory response
Produces B-lactamase

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23
Q

Moraxella catarrhalis Clinical Features and Diseases

A

Acute Otitis Media, Acute exacerbation of COPD, rhinosinusitis
Fever, ear pain, bulging TM, anorexia in infants

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24
Q

Moraxella catarrhalis Diagnostics and Treatment

A

D: Otoscopy - loss of TM landmarks, TM bulging/discoloration, hypomobility
Weber test, Rinne test
Blood or chocolate agar
Butyrate (+), Catalase (+), Nitrate reductase (+), Oxidase (+)

T: Augmentin - Amoxicillin + Clauvanic acid
Needs B-lactamase inhibitor
Macrolides (Azithromycin) for those with PCN allergy

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25
Q

Steptococcus pneumoniae characteristics, epidemiology, mode of transmission

A

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

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26
Q

Steptococcus pneumoniae pathogenesis and VF

A

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

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27
Q

Steptococcus pneumoniae Clinical Features and Diseases

A

Pneumonia, sinusitis, otitis media, meningitis, bacteriemia

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28
Q

Steptococcus pneumoniae Diagnostics and Treatment

A

D: Catalase (-), a-hemolytic, Optochin (S)
Quellung (+)
Bile solubility test - dissolves in bile

T: Inactive vaccines
PCN resistant - vancomycin + ceftriaxone

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29
Q

Haemophlius influenza characteristics, epidemiology, mode of transmission

A

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

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30
Q

Haemophlius influenza pathogenesis and VF

A

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

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31
Q

Haemophlius influenza Clinical Features and Diseases

A

Otitis Media, pneumonia, meningitis, conjunctivitis, sinusitis, cellutitis, bronchitis, arthritis

Pain in infected region, flu-like symptoms

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32
Q

Haemophlius influenza Diagnostics and Treatment

A

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

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33
Q

Epstein Barr Virus characteristics, epidemiology, mode of transmission

A

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”

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34
Q

Epstein Barr Virus pathogenesis and VF

A

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

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35
Q

Clinical Features and Diseases

A

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

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36
Q

Epstein Barr Virus Diagnostics and Treatment

A

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

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37
Q

Influenza A/B characteristics, epidemiology, mode of transmission

A

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

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38
Q

Influenza A/B pathogenesis and VF

A

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

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39
Q

Influenza A/B Clinical Features and Diseases

A

Flu, Viral pnuemonia,

Fever, chills, myalgias, headache, cervical lymphadenopathy, dry cough, malaise

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40
Q

Influenza A/B Diagnostics and Treatment

A

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

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41
Q

Small Pox characteristics, epidemiology, mode of transmission

A

Characteristics: largest virus, ovoid-brick shape
linear dsDNA

Epidemiology: exclusive human host range

MOT: Inhalation, aerosols, and direct contact with fomites

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42
Q

Small Pox pathogenesis and VF

A

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

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43
Q

Small Pox Clinical Features and Diseases

A

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%)

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44
Q

Small Pox Diagnostics and Treatment/Prevention

A

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

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45
Q

Polio characteristics, epidemiology, mode of transmission

A

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

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46
Q

Polio pathogenesis and VF

A

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

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47
Q

Polio Clinical Features and Diseases

A

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

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48
Q

Polio Diagnostics and Treatment/Prevention

A

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

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49
Q

Rabies characteristics, epidemiology, mode of transmission

A

C: -ssRNA, bullet-shaped, enveloped virus

E: Classic zoonotic infection

MOT: bite of infected animal, saliva

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50
Q

Rabies pathogenesis and VF

A

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

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51
Q

Rabies Clinical Features

A

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

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52
Q

Rabies Diagnostics and Treatment

A

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

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53
Q

Bacillus Anthracis characteristics, epidemiology, mode of transmission

A

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

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54
Q

Bacillus Anthracis pathogenesis and VF

A

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.

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55
Q

Bacillus Anthracis Clinical Features and Diseases

A

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

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56
Q

Bacillus Anthracis Diagnostics and Treatment/Prevention

A

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

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57
Q

Boredetella pertussis characteristics, epidemiology, mode of transmission

A

C: gram (-) coccobacillus bacteria
Obligate aerobe, non-fermentative

Epidemiology: incidence increasing since the 90s. More often in summer and fall

MOT: Droplets, inhalation

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58
Q

Bordatella Pertussis pathogenesis and VF

A

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

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59
Q

Bordatella Pertussis Clinical Features and Diseases

A

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.

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60
Q

Bordatella Pertussis Diagnostics and Treatment/Prevention

A

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

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61
Q

Coxsackievirus A 16 characteristics, epidemiology, mode of transmission

A

Naked, +ssRNA virus with icosahedral capsid

Newborns and neonates at highest risk

MOT: fecal-oral, respiratory droplets

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62
Q

Coxsackievirus A 16 pathogenesis and VF

A

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

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63
Q

Coxsackievirus A 16 Clinical Features and Diseases

A

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

64
Q

Coxsackievirus A 16 Diagnostics and Treatment/Prevention

A

D: clinical diagnosis

Treatment: supportive care

Prevention: Avoid exposure, good hygiene, no vaccine

65
Q

Rubeola characteristics, epidemiology, mode of transmission

A

-ssRNA, enveloped virus with helical nucleocapsid

Most at risk are unvaccinated, malnourished or immunocompromised people

MOT: Respiratory droplets

66
Q

Rubeola pathogenesis and VF

A

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

67
Q

Rubeola Clinical Features and Diseases

A

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)

68
Q

Rubeola Diagnostics and Treatment/Prevention

A

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.

69
Q

Mumps characteristics, epidemiology, mode of transmission

A

(-) ssRNA, enveloped virus with helical nucleocapsid

Unvaccinated and immunocompromised people most at risk

MOT: respiratory droplets and direct contact
Only through humans

70
Q

Mumps pathogenesis and VF

A

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

71
Q

Mumps Clinical Features and Diseases

A

Classic clinical finding: sudden onset of parotitis and fever

D: Mumps

72
Q

Mumps Diagnostics and Treatment/Prevention

A

D: Confirmed via RT-PCR or IgM assay

Treatment: supportive care

Prevention: Measles-mumps-rubella (MMR): live attenuated vaccine.

73
Q

Rubella pathogenesis and VF

A

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

74
Q

Clinical Features and Diseases

A

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

75
Q

Rubella Diagnostics and Treatment/Prevention

A

D: Need labs to confirm - detection of antirubella-specific IgM

Treatment: Supportive care

Prevention: Measles-mumps-rubella (MMR): live attenuated vaccine.

76
Q

Parvo B19 characteristics, epidemiology, mode of transmission

A

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

77
Q

Parvo B19 pathogenesis and VF

A

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

78
Q

Parvo B19 Clinical Features and Diseases

A

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.

79
Q

Parvo B19 Diagnostics and Treatment

A

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

Treatment: supportive care

80
Q

Roseola characteristics, epidemiology, mode of transmission

A

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

81
Q

Roseola pathogenesis and VF

A

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.

82
Q

Roseola Clinical Features and Diseases

A

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

83
Q

Roseola Diagnostics and Treatment

A

D: clinical diagnosis

Treatment: supportive

84
Q

Varicella-zoster characteristics, epidemiology, mode of transmission

A

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

85
Q

Varicella-zoster pathogenesis and VF

A

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.

86
Q

Varicella Zoster Clinical Features and Diseases

A

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

87
Q

Varicella zoster Diagnostics and Treatment/Prevention

A

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

88
Q

SARS-CoV-2 characteristics, epidemiology, mode of transmission

A

+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

89
Q

SARS-Cov-2 pathogenesis and VF

A

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.

90
Q

SARS-CoV-2 Clinical Features and Diseases

A

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

91
Q

SARS-CoV-2 Diagnostics and Treatment/Prevention

A

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

92
Q

Corynebacterium diphtheriae characteristics, epidemiology, mode of transmission

A

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.

93
Q

Corynebacterium diphtheriae pathogenesis and VF

A

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

94
Q

Corynebacterium diphtheriae Clinical Features and Diseases

A

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

95
Q

Corynebacterium diphtheriae Diagnostics and Treatment

A

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

96
Q

Mycobacterium tuberculosis characteristics, epidemiology, mode of transmission

A

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

97
Q

Mycobacterium tuberculosis pathogenesis and VF

A

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

98
Q

Mycobacterium tuberculosis Clinical Features and Diseases

A

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

99
Q

Mycobacterium tuberculosis Diagnostics and Treatment

A

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

100
Q

Aspergillus Fumigatus characteristics, epidemiology, mode of transmission

A

Mold; Septate hyphae that branch at acute angles

Common throughout the world; Ubiquitous in air, soil, decaying matter

Inhalation of spores

101
Q

Aspergillus Fumigatus pathogenesis and VF

A

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

102
Q

Aspergillus Fumigatus Clinical Features and Diseases

A

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%

103
Q

Aspergillus Fumigatus Diagnostics and Treatment

A
  • 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

104
Q

Pneumocystis Jjrovecii characteristics, epidemiology, mode of transmission

A

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

105
Q

Pneumocystis jjrovecii pathogenesis and VF

A

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

106
Q

Pneumocystis jjrovecii Clinical Features and Diseases

A

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

107
Q

Pneumocystis jjrovecii Diagnostics and Treatment

A

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).

108
Q

Histoplasma capsulatum characteristics, epidemiology, mode of transmission

A

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

109
Q

Histoplasma capsulatum pathogenesis and VF

A

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

110
Q

Histoplasma capsalatum Clinical Features and Diseases

A

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

111
Q

Histoplasma capsalatum Diagnostics and Treatment

A
  • 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

112
Q

Coccidioides immitis characteristics, epidemiology, mode of transmission

A

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

113
Q

Coccidioides immitis pathogenesis and VF

A

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

114
Q

Coccidioides immitis Clinical Features and Diseases

A

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

115
Q

Coccidioides immitis Diagnostics and Treatment

A
  • 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

116
Q

Blastomyces dermatitidis characteristics, epidemiology, mode of transmission

A

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

117
Q

Blastomyces dermatitidis pathogenesis and VF

A

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)

118
Q

Blastomyces dermatitidis Clinical Features and Diseases

A

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

119
Q

Blastomyces dermatitidis Diagnostics and Treatment

A
  • 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

120
Q

Candida albicans characteristics, epidemiology, mode of transmission

A

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

121
Q

Candida albicans pathogenesis and VF

A

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.

122
Q

Candida albicans Clinical Features and Diseases

A

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

123
Q

Candida albicans Diagnostics and Treatment

A

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)

124
Q

Cryptococcus neoforms characteristics, epidemiology, mode of transmission

A

Encapsulated yeast
Obligate aerobe

Epidemiology - immunocompromised pts (AIDS-defining illness)

MOT: * Inhalation
Usually through dust containing contents of bird droppings

125
Q

Cryptococcus neoforms pathogenesis and VF

A
  • 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
126
Q

Cryptococcus neoforms Clinical Features and Diseases

A

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

Disease:
Cryptococcal meningitis

127
Q

Cryptococcus neoforms Diagnostics and Treatment

A
  • 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

128
Q

Human immunodeficiency virus characteristics, epidemiology, mode of transmission

A

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

129
Q

Human immunodeficiency virus pathogenesis and VF

A

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

130
Q

Human immunodeficiency virus Clinical Features and Diseases

A

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

131
Q

Human immunodeficiency virus Diagnostics and Treatment

A

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

132
Q

HHV- 8 characteristics, epidemiology, mode of transmission

A

Member of Herpes family

More prevalent in certain geographic areas - Italy, Greece, Africa
Pts with AIDS

MOT: Sexually transmitted (most likely)

133
Q

HHV-8 pathogenesis and VF

A

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

134
Q

HHV-8 Clinical Features and Diseases

A

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

135
Q

HHV-8 Diagnostics and Treatment

A

Treatment: Regression with HIV/AIDS management

136
Q

A 4 day history of fever before the onset of rash is indicative of

A

Measles

137
Q

A 3 day history of fever before the onset of rash is indicative of

A

Chickenpox

138
Q

A 1 day history of fever before the onset of rash is indicative of

A

Rubella

139
Q

What are the incubation periods for Measles, Small pox, Chickenpox, and Rubella?

A

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

140
Q

What are the major steps in viral replication?

A
  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
141
Q

A rash outbreak after the fever has already broken is indicative of

A

Roseola

142
Q

Which common childhood virus would you need to order labs for to confirm?

A

Measles, Rubella

143
Q

Which common childhood virus would you treat with anti-viral therapy

A

Chickenpox in adults or immunosuppressed

144
Q

Which common childhood virus would you isolate while presenting with a rash?

Which wouldn’t you isolate?

A

Measles, Rubella, Varicella

Parvo and Roseola not contagious once rash appears

145
Q

Which common childhood illnesses would you report to the state department?

A

Measles, Rubella, Varicella

146
Q

What childhood disease is associated with the following complications:
Shingles
Pneumonia in adults

A

Varicella

147
Q

What childhood disease is associated with the following complications:
Pneumonia
Encephalitis - acute or SPPE

A

Measles

148
Q

What childhood disease is associated with the following complications:
Congenital complications

A

Rubella

149
Q

What childhood disease is associated with the following complications:
Aplastic anemia - cytotoxic to erythrocyte precursors
Hydrops fatalis

A

Parvovirus B19 (Fifth Disease)

150
Q

What childhood disease is associated with the following complications:
Febrile seizures
Transplant failure

A

HHV-6 Roseola

151
Q

What childhood disease is associated with the following complications:
Dehydration
Asepctic meningitis

A

Cocksackievirus (HFM)

152
Q

What common childhood disease is associated with the following complications:
Orhcitis
Thyroiditis
Pancreatitis

A

Mumps

153
Q

Tsetse fly is a vector for

A

T brucei

154
Q

Kissing bug is vector for

A

T cruzi

155
Q

Sandfly is a vector for

A

Leishmaniasis

156
Q

Because they both use the same vector [ ], these two diseases are often coinfections

A

Ixodes tick

Lyme Disease and Babesia

157
Q

What is the life cycle for Malaria?

A

Ring –> Trophozoite –> Schizont –> Gametocyte

Unit 3 HDC (8 decks)

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