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Infectious Disease > Week 6 and 7 > Flashcards

Week 6 and 7 Flashcards

1
Q

Mycoplasma Pneumoniae:

Main features:

  • gram stain?
  • membrane contains ______
  • transmission?
A

No cell wall (does NOT gram stain)

Membrane contains cholesterol

Transmitted via inhalation of respiratory droplets (highly contagious)

Exclusively human pathogen

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2
Q

Mycoplasma Pneumoniae:

Pathogenesis

A

Inhaled → adheres to respiratory epithelium → inhibit ciliary motion and destroy mucosa → inflammation WITHOUT invasion into mucosa

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3
Q

Mycoplasma Pneumoniae:

Virulence factors (1)

A

P1 adhesin → allows cytotoxic effects on cilia

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4
Q

Mycoplasma Pneumoniae:

Diseases

A

1) Atypical pneumonia (walking pneumonia)
2) *Hemolytic anemia
3) Tracheobronchitis
4) Wheezing in infants
5) Pharyngitis
6) Rhinitis

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5
Q

Mycoplasma Pneumoniae: atypical pneumonia presentation

typically effects who?

A

Atypical pneumonia (walking pneumonia)

Symptoms: fever, headache, myalgia, tracheobronchitis, non-productive cough
Vague ill-defined or patchy opacities

Typically affects: young people - those in close quarters (prisons, military bases)

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6
Q

Mycoplasma Pneumoniae:

treatment (3)

A

Macrolide (erythromycin, azithromycin)

Tetracycline (doxycycline)

Fluoroquinolone

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7
Q

Mycoplasma Pneumoniae:

Diagnosis (3 ways)

A

Serology
Cold serum agglutination test
PCR

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8
Q

Cold serum agglutination test

A

non specific test for Mycoplasma Pneumoniae

autoimmune response involving cold hemagglutinins of IgM antibodies (molecular mimicry) and blood group antigen I of human RBCs → activates complement

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9
Q

Legionella Pneumophila:

Main features:

  • oxidase?
  • intra/extracellular?
  • gram stain? shape?
  • grows on what?
  • what special stain?
A

Facultative intracellular

Oxidase positive

Gram negative bacillus

Grows on charcoal yeast extract with iron and cysteine

Weak gram stain → SILVER STAIN

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10
Q

Legionella Pneumophila:

Transmission

A

Transmission via aerosols from environmental water sources (air conditioning systems, hot water tanks)

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11
Q

Legionella Pneumophila:

Disease

A

Legionnaire’s Disease

Pontiac Fever

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12
Q

Legionella Pneumophila:

Treatment

A

Macrolides (azithromycin)

Fluoroquinolones (levofloxacin)

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13
Q

Legionnaire’s Disease

A

severe, lobar pneumonia

Nonproductive cough
Confusion, diarrhea

Signs of kidney damage (proteinuria, microscopic hematuria)

Hyponatremia (due to SIADH and/or renal tubulointerstitial disease impairing sodium reabsorption)

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14
Q

Pontiac fever

A

mild flu-like illness (fever, chills, fatigue, malaise, headache) without respiratory symptoms

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15
Q

Legionella Pneumophila

Diagnosis

A

Presence of antigen in URINE

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16
Q

C. Diphtheriae:

Main features

-anaerobe, aerobe?
-spore forming?
-gram? shape?
-motility?
-appearance on microscopy?
Culture on what agar? appears what color?

A

Aerobic
Non-spore forming
Gram positive bacillus
Non-motile
“Chinese letter” appearance on microscopy
Culture on cystine-tellurite agar → BLACK colonies

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17
Q

C. Diphtheriae

colonizes where?
transmitted how?

A

Transmitted via respiratory droplets

Colonize nasopharynx

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18
Q

C. Diphtheriae

Virulence factors

A

AB exotoxin

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19
Q

C. Diphtheriae

AB exotoxin

A

catalyzes ADP ribosylation of EF-2 → inhibit EF2 and prevent tRNA translocation from ribosomal A-sites to P-sites

Encoded by bacteriophage

Causes cardiac (arrhythmia and myocarditis) and nervous (cranial/peripheral nerve palsy) effects

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20
Q

C. Diphtheriae

Disease

A

Grayish-white pseudomembranes in oropharynx (can cause suffocation)

Cervical lymphadenopathy (“Bulls neck”)

Myocarditis (if left untreated)

Progressive deterioration of myelin sheaths in CNS and PNS → blurry vision, pharyngeal/diaphragmatic paralysis

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21
Q

C. Diphtheriae

Diagnosis (2 ways)

A

1) visualization of gram (+) bacilli with metachromatic (blue and red) granules on specialized media (Loeffler’s)
2) Presence of toxin production via positive Elek test

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22
Q

C. Diphtheriae

Treatment

A

penicillin or erythromycin (for local colonization)

Antitoxin for toxin neutralization

DTaP booster to prevent recolonization

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23
Q

B. Pertussis:

Main features

  • gram? shape?
  • capsule?
  • oxidase?
  • aerobe/anaerobe?
  • culture on what two media?
A 
Gram negative, coccobacillus
Encapsulated
Oxidase positive
Strict aerobe
Cultured on Regan-Lowe or Bordet-Gengou (potato) agar
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24
Q

B. Pertussis

Transmission?

A

Humans are only reservoir of Bordetella pertussis

Transmitted via respiratory droplets

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25
Q

B. Pertussis

Virulence factors (3)

A

Pertussis toxin (AB toxin)

Adenylate cyclase toxin

Tracheal toxin

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26
Q

B. Pertussis

Pertussis toxin (AB toxin) - A component

A

ADP ribosylates Gi (remove ADP-ribosyl group from NAD and covalently attaches it to Gi) → Gi inactivation → increased cAMP

→ increased secretion of Na+, Cl-, H2O from cells → edema, neutrophil dysfunction

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27
Q

B. Pertussis

Pertussis toxin (AB toxin) - B component

A

Facilitates endocytosis

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28
Q

B. Pertussis

Adenylate cyclase toxin

A

increases intracellular cAMP → inhibit leukocyte chemotaxis and phagocytosis

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29
Q

B. Pertussis

Tracheal toxin

A

inhibits DNA synthesis in ciliated epithelial cells → cell death → loss of ciliated epithelial cells → debris accumulates in lungs → coughing fits

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30
Q

B. Pertussis

Disease

A

Whooping cough: “whoops” on inspiration, coughs on expiration

Incubation period = 2 weeks → 3 major phases

Cough lasting > 2 weeks

Highly contagious acute respiratory infection

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31
Q

B. Pertussis

major phases of whooping cough

A

Catarrhal phase: mild coughing and sneezing

  • Highly contagious
  • Mild clinical course

Paroxysmal phase: classic whooping cough, can induce post tussive vomiting

Convalescent phase: gradual reduction in severity and frequency of cough

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32
Q

B. Pertussis

Diagnosis (2 main things)

A

Absolute lymphocytosis (due to pertussis toxin)

Hypoglycemia (due to increased insulin secretion from increased cAMP)

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33
Q

B. Pertussis

Treatment
-when should it be given?

A

Macrolides (given during catarrhal stage)

  • Also used for prophylaxis in close contacts
  • Can decrease bacterial shedding, but does NOT alter disease course if given during paroxysmal stage

Supportive care

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34
Q

Sepsis

-what is the early predictor of bad outcome?

A

life threatening organ dysfunction due to dysregulated host immune response

Abnormalities of cognitive dysfunction are among most sensitive early predictors of bad outcome with sepsis

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35
Q

In a THIRD of patients with sepsis, an infectious organism is NEVER found…how is that possible?

A

endogenous antigens may also trigger sepsis

Noninfectious diseases can mimic sepsis:
-Acute MI, acute PE, acute pancreatitis, acute GI bleeding, adverse drug reactions, accidents (major trauma), severe burns

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36
Q

Common pathway of sepsis:

A

Sepsis → endothelial injury due to inflammation, oxidant stress and then increased coagulation/decreased fibrinolysis → organ failure → death

Maladaptive immune response is what causes disease

  • Young → hyperimmune
  • Old, malnourished, DM → deplete immune response, hypoimmune
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37
Q

Primary sepsis mediators (5)

A

IL-1, TNF-a, IL-10, ROS, lipids

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38
Q

Early cellular and molecular events during infection: (3)

A

1) Vasodilation and endothelial activation
2) Leukocyte recruitment and activation
3) Coagulation and NET formation → block microcirculation

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39
Q

Sepsis is a viscous cycle of…

A

hypoperfusion, vasodilation, capillary leak, endothelial damage, microvascular obstruction, myocardial depression, ischemia, microcirculatory shunts and acidosis

VASODILATION, ENDOTHELIAL DAMAGE→not enough circulating volume

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40
Q

In sepsis, alterations in microcirculatory blood flow → ?

A

abnormal microcirculation with inflammatory response

Decrease number of functional capillaries and blood is diverted → unable to extract O2 → anaerobic metabolism and production of lactate

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41
Q

Cytopathic mitochondrial dysoxia

A

Responsible for pathogenesis of septic organ failure

oxygen utilization by mitochondria is DYSFUNCTIONAL but oxygen delivery is PRESERVED

ATP not effectively generated

Due to cytokines

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42
Q

Resuscitation bundle used in sepsis

A

start immediately, complete within 3 hours

Blood and respiratory cultures

Broad spectrum abx - within 1 hr

  • Mortality increased by 7.5%/hr beyond first hr of shock
  • Must select CORRECT abx

IV N/S (30mL/kg in 1st 2 hr) + add albumin

Normalize serum lactate

Vasopressors

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43
Q

Yersinia Pestis

Transmission (3)

A

1) Flea bite (flea carries Y. pestis from infected animal to human host)
2) Respiratory droplets (from infected host)
3) Direct contact (with infected tissue or fluid from human or animal host)

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44
Q

Yersinia Pestis

Main features:

  • staining?
  • gram? shape?
  • motility?
  • intra or extracellular?
A
  • Bipolar “safety-pin” staining on Wayson stain
  • Wright-Giemsa staining
  • Gram negative bacillus
  • Pleomorphic
  • Nonmotile
  • Facultative intracellular
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45
Q

Yersinia Pestis

Virulence factors: (2)

A

Capsular F1 antigen

Type III secretion system

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46
Q

Yersinia Pestis

Capsular F1 antigen

A

prevent phagocytosis, generates antibody response

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47
Q

Yersinia Pestis

Type III secretion system

A

allows organism to inject Yops (yersinia outer proteins) → inhibit phagocytosis and cell signaling

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48
Q

Yersinia Pestis

3 types of plague?

A

1) Bubonic plague
2) Septicemic plague
3) Pneumonic plague

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49
Q

Bubonic plague

A

sudden onset fever, chills, weakness, headache → intense pain and swelling of lymph gland (BUBOES) resulting from bite of flea 2-5 days earlier → 60-90% mortality if untreated

Uncontrolled spread can cause organ abscess, cutaneous hemorrhage, and tissue necrosis

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50
Q

Septicemic plague

A

invasion of almost all organs, no significant evidence of prior disease

Nonspecific fever, GI illness and pain

Buboes are NOT present

Death occurs in 12-24 hours

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51
Q

Pneumonic Plague

A

primary or secondary lung infection which is infectious and 100% fatal if untreated - most infectious

Acquired by inhaling droplets or hematogenous spread

Sudden onset dyspnea, fever, pleuritic chest pain, cough, bloody sputum

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52
Q

Yersinia Pestis

Treatment (2)

A

1) Streptomycin, Gentamicin
2) Doxycycline, Tetracycline

Prophylaxis: doxy or tetracycline

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53
Q

Francisella Tularensis

Main features

  • gram? shape?
  • where in the US it occurs?
  • intra or extracellular
  • immune evasion?
A

Gram negative coccobacilli
Occurs in Missouri and Arkansas
Pleomorphic
Facultative intracellular

Can undergo phase variation to avoid immune response

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54
Q

Francisella Tularensis

Transmission (3)

A

Bite by tick (Dermacentor variabilis) or deerfly

Handling infected animals (primarily rabbits)

Inhalation of aerosol

55
Q

Francisella Tularensis can/cannot be spread person to person?

Yersinia pestis can/cannot be spread person to person?

A

Francisella Tularensis CANNOT be spread from person to person

Yersinia pestis CAN be spread from person to person (pneumonic plague)

56
Q

Francisella Tularensis

Treatment (2)

A

1) streptomycin, gentamicin

2) levofloxacin and doxycycline

57
Q

Francisella Tularensis

Tularemia

A

site-specific infection and lymphadenopathy

Painful ulcer at site of infection + regional lymphadenopathy

Can cause granulomas with caseating necrosis in reticuloendothelial system (lymph nodes, spleen)

58
Q

Borrelia Burgdorferi

Transmission

A

Ixodes tick bite - mostly in summer in NE United States

Most infections in late spring and summer

Tick must feed for 48-72 hours to transmit sufficient bug

Ixodes tick also vector for Anaplasma and Babesia

59
Q

Borrelia Burgdorferi

Primary (natural) RESERVOIR are _________

________acts as intermediate HOST (food source for adult ticks)

A

Primary (natural) RESERVOIR are rodents (white-footed mouse)

White-tailed deer acts as intermediate HOST (food source for adult ticks)

60
Q

Borrelia Burgdorferi

Lyme disease - STAGE 1

A

Stage 1 = Early-Localized Lyme Disease: Erythema migrans +/- viral-like syndrome - occurs in 1-4 weeks after bite

Begins as homogenous erythema that may spread to develop central clearing = Bull’s-eye rash

61
Q

Borrelia Burgdorferi

Lyme disease - STAGE 2

A

Stage 2 = Early-Disseminated Lyme Disease: acute neural or cardiac involvement - weeks to months after tick bite

  • Lymphocytic meningitis
  • Facial nerve (Bell’s) Palsy
  • Peripheral neuropathy
  • AV heart block
  • Migratory arthralgias
62
Q

Borrelia Burgdorferi

Lyme disease - STAGE 3

A

Stage 3 = Late Lyme disease: chronic arthritis of large joints (knee) and encephalopathy

63
Q

Borrelia Burgdorferi

Lyme disease - Diagnosis

A

Empirical abx treatment without testing if pt has erythema migrans
Serologic testing + Western blot → abx treatment if positive
Do NOT treat if serologic treatment negative

64
Q

Borrelia Burgdorferi

Lyme disease - Treatment?

A

Doxycycline (early disease)

Ceftriaxone for neurologic disease

65
Q

Rickettsiae

main characteristics

  • motility? spores?
  • gram? shape?
  • intra/extracellular?
  • stain?
  • what carries disease?
A

Non-motile, non-spore forming

Weakly gram negative coccobaccili

Highly pleomorphic

Obligate intracellular bacteria

Stain with Giemsa stain

Have animal reservoirs - arthropod transmitted, humans are incidental hosts (except louse borne typhus fever

66
Q

Rickettsiae

Pathogenesis

A

Invade endothelial cells → disseminate through vascular system → anemia, hypovolemia, ischemia and rash
→ causes VASCULITIS and RASH

67
Q

Rickettsiae

Clinical presentation

A

Abrupt onset headache, fever, petechial rash

68
Q

Rickettsia Rickettsii

disease?

A

Rocky Mountain Spotted Fever (RMSF)

69
Q

Rocky Mountain Spotted Fever (RMSF)

  • infection where?
  • transmission?
A

Infection of endothelial cells
Transmitted to humans from bite of Dermacentor tick

Typically in North Carolina

Humans are an incidental host

70
Q

Rocky Mountain Spotted Fever (RMSF)

Symptoms?

A

acute onset fever, headache, myalgias → petechial rash that starts on ankles and wrists and spreads to trunk

RASH: appears on PALMS and SOLES then spreads
**STARTS on extremities and moves to trunk (CENTRIPETAL)

Can get thrombocytopenia and hyponatremia

71
Q

Treatment of Rocky Mountain Spotted fever?

A

Doxycycline

72
Q

Rickettsia Typhi

Disease?

A

Endemic (murine) Typhus

73
Q

Endemic (murine) Typhus

Transmission?

A

Carried by rats and transmitted to humans from feces of fleas

74
Q

Endemic (murine) Typhus

Symptoms?

A

hills, high fever, headache, myalgias

Maculopapular RASH: starts on trunk and moves to extremities (CENTRIFUGAL) sparing face, palms, and soles

8-16 day incubation

75
Q

Rickettsia Prowazekii

Disease? (2)

A

Epidemic Typhus

Brill’s Disease

76
Q

Epidemic Typhus

Transmission?

A

Transmitted from feces of lice

Tick bites, and defecates → spread to blood by itching

77
Q

Epidemic Typhus

Symptoms

A

encephalitis, confusion, myalgias, arthralgias, pneumonia, RASH that spreads from trunk out to extremities

78
Q

Ehrlichia and Anaplasma

Main features?

gram? shape?
intra/extracellular?
-infects what kind of cells?
-trasmission?

A

Gram-negative bacilli

Obligate intracellular - enter cell, prevent fusion of lysosomes, inhibits host cell apoptosis

Infect phagocytic cells and multiple inside vacuoles

Transmitted by ticks, reservoir is deer

79
Q

Ehrlichia and Anaplasma

Clinical presentation?

A

fever, headache, malaise WITHOUT rash
→ Leukopenia and thrombocytopenia
Elevated AST and ALT

80
Q

Erhlichiosis

  • transmitted by what?
  • found where?
  • infection of what cell type?
A

Morulae (intracytoplasmic inclusions) within monocytes

Transmitted by Lone Star Tick → infection of monocytes and macrophages

Found in Mid-Atlantic, Southeastern, and South Central states

81
Q

Anaplasmosis

  • transmitted by what?
  • found where?
  • infection of what cell type?
A

Morulae within granulocytes
Transmitted by Ixodes Tick → infection of neutrophils
Found in NE and upper Midwest

82
Q

Oxygen and Anaerobes:

A

Oxygen is TOXIC for anaerobes - why?

  • Direct oxidation of cellular components
  • Production of H2O2 and O2- → Strict anaerobes lack catalase and SOD

Anaerobes that cause disease are usually AEROTOLERANT → may produce catalase and/or SOD

83
Q

Anaerobic Normal Flora:

A

Anaerobes are THE predominant component of human microbial flora → oral cavity, colon, female genital tract, skin

ANY of these can cause infections in adjacent tissue

84
Q

Abscess formation of anaerobes - acute vs. chronic stage?

A

Mixed (polymicrobial) infection with anaerobes plus facultative or aerobic organisms

Acute stage: aerobes and facultative organisms predominate → hypotensive

Chronic stage: formation of fibrin-encased abscess
Anaerobes predominate - polymicrobial

85
Q

Bacteroides fragilis

A

Frequent isolate from anaerobic abscesses (BELOW the diaphragm) - Minor component of gut flora, BUT isolated from 80% of abdominal abscesses

86
Q

Bacteroides fragilis

Virulence factors? (3)

A

Aerotolerant (catalase and SOD production)

Extracellular enzymes (phospholipase, collagenase)

Capsule - abscess formation

87
Q

C. Tetani

A

In feces and soil

Spores introduced into wounds → germinate and devitalized tissue → locally produce tetanospasmin → transported to CNS via retrograde axonal transport along peripheral motor neurons

→ block release of inhibitory neurotransmitters (GABA, glycine)

Disease: Tetanus

88
Q

C. Botulinum - spores

A

Spores in soil and water, commonly contaminate food and wounds

Pressure sterilization required to kill SPORES

TOXIN is heat-labile and destroyed by cooking

89
Q

Botulism

A

Botulinum toxin blocks ACh transmission at neuromuscular junctions → “DESCENDING flaccid paralysis”

Babies ingest honey with SPORES → form TOXIN in gut

Adults ingest PREFORMED TOXIN

90
Q

Pathogenesis of Foodborne Botulism:

A

Spores from soil/water contaminate food → spores germinate, grow, and produce toxin (WITHOUT signs of spoilage)

Food (toxin) consumed (uncooked) and enters bloodstream → synapses at NMJ

91
Q

Zoonotic Viruses

A

viruses that normally exist within animal reservoirs and cause disease when transmitted to humans

92
Q

Rabies Virus

Main features:

  • genome?
  • symmetry, capsid?
  • enveloped or non-enveloped?
  • virus family?
A

Linear, nonsegmented negative ssRNA

  • Bullet shaped helical capsid symmetry
  • Enveloped
  • Rhabdovirus
93
Q

Rabies Virus

Transmission

A
  • ONLY ANIMAL –> HUMAN
  • Transmitted from animals to humans, but do NOT exhibit human to human transmission under natural conditions

Bite from a rabid animal

Highest risk with canine rabies virus (eliminated in USA), so mostly due to bats (overall), skunks (west, and racoons/foxes (east)

Virus shed into saliva and secretions of other organs (virus travels down peripheral nerves) → spread via aerosols or bites

94
Q

Pathogenesis of Rabies Infection

A

Rabies virus glycoprotein binds nicotinic ACh receptors in postsynaptic muscle membrane of NMJ and enters → infection and replication within striated muscle cell at site of wound

Eventually virions cross synaptic cleft → bind neural cell adhesion molecules (NCAMs) and enter motor and sensory neurons → retrograde axonal transport to CNS

95
Q

Negri Bodies

  • where are they?
  • what do they look like?
  • what is going on here?
A

eosinophilic cytoplasmic inclusions, where replication and transcription of rabies virus occurs

Located in neuron cell bodies in spinal cord and CNS (especially Purkinje cells in cerebellum and pyramidal cells of hippocampus)

96
Q

Rabies virus Incubation period

A

weeks to months (PROLONGED)

Longer incubation when bite on lower extremities (longer distance for virus to travel before it can get to CNS and replicate)

→ allows for POSTEXPOSURE PROPHYLAXIS

97
Q

Disease caused by Rabies virus?

A

Flu-like prodrome (fever, malaise, anorexia, headache, nausea, vomiting)

→ Acute neurologic syndrome: hydrophobia, aerophobia, photophobia, autonomic instability, hallucinations

Dysphagia due to pharyngeal muscle spasms

Generalized flaccid paralysis and coma after acute neurologic phase

Rapidly fatal encephalitis (travels to brain)

Without treatment, is uniformly fatal

98
Q

Treatment: Rabies post-exposure prophylaxis (3)

A

1) Wash wound
2) Give rabies vaccine (killed virus) (4 doses - given at different site than immune globulin)
3) Human rabies immune globulin (passive immunity)

99
Q

Hantavirus (Sin Nombre) Virus

Main features:

  • enveloped or non enveloped?
  • shape, capsid?
  • genome?
  • virus family?
A

Enveloped, helical capsid virus

Negative sense segmented sdsRNA

Bunyavirus

100
Q

Hantavirus (Sin Nombre) Virus

Transmission

A

Rodent borne virus (primary reservoir is deer mouse)

-Transmitted from animals to humans, but do NOT exhibit human to human transmission under natural conditions (similar to rabies)

Inhalation of aerosol of virus shed by rodent hosts in feces and urine

101
Q

Two diseases caused by Hantavirus?

A

Hemorrhagic fever with renal syndrome (HFRS)

Hantavirus cardiopulmonary syndrome (HCPS)

102
Q

Hemorrhagic fever with renal syndrome (HFRS):

A

Fever, hemorrhage, hypotension, renal failure

103
Q

Hantavirus cardiopulmonary syndrome (HCPS)

A

Rapid onset (12-24 hours)

Capillary leak into pulmonary bed after flu-like prodrome

Fever + bilateral diffuse interstitial edema (resembles ARDS)

104
Q

How do you diagnose hantavirus?

A

serology

105
Q

Disease caused by west nile virus? (2)

A

1) WNV neuroinvasive disease

2) WNV fever

106
Q

WNV fever

A

rapid onset of low grade fever, headache, malaise, back pain and myalgias

107
Q

WNV neuroinvasive disease

A

Risk for severe disease with OLDER age

→ fever + meningitis, encephalitis, and flaccid paralysis

108
Q

West Nile virus transmission

vector?
host?
-non-vector transmission?

A

Birds act as major host (also horses)

Mosquitos = VECTOR for transmission

Transmitted from animals to humans, but do NOT exhibit human to human transmission under natural conditions

Can also get NON-VECTOR transmission of WNV (organ transplant, blood transfusion - check with RT-PCR)

109
Q

Ebola Virus

Main features:

  • virus family?
  • envelope?
  • genome?
  • capsid, shape?
A

Filovirus

Enveloped

Nonsegmented negative sense ssRNA

Helical capsid

Thread-like filamentous structure

110
Q

Ebola:

Pathogenesis of infection:

A

Ebola enters body → infects and lyses endothelial cells, hepatocytes, macrophages, and dendritic cells → spread to regional lymph nodes → dissemination to lymphoid tissue

Causes consumptive coagulopathy triggered by aberrant production of TISSUE FACTOR by virally infected macrophages

111
Q

Ebola:

Disease?

A

acute hemorrhagic fever with high mortality rate

Incubation period of 5-7 days and up to two weeks

112
Q

Ebola

Transmission?

A

Transmit from animals to humans and can cause limited cycles of human to human transmission - requires close contact with bodily fluids for transmission

113
Q

Lassa Fever Virus:

Main features:

  • virus family?
  • envelope?
  • genome?
  • shape?
A

Arenavirus
Enveloped
Helical
Segmented (ambisense) ssRNA

114
Q

Lassa Fever Virus:

Disease

A

causes acute hemorrhagic fever

Restricted to West Africa

115
Q

Lassa Fever Virus:

Transmission

A

Transmit from animals to humans and can cause limited cycles of human to human transmission

Transmission to humans via rodent urine and feces or through close contact with infected individuals

ANIMALS –> HUMANS and LIMITED HUMAN –> HUMAN

116
Q

3 Main families of arboviruses

A

Bunyaviruses
Flaviviruses
Togaviruses

117
Q

Bunyaviruses

Main features of genome?

A

Segmented, enveloped, helical negative sense ssRNA

118
Q

Flaviviruses

Main features of genome, envelope, capsid?

Includes what 5 viruses?

A

Main features:
-Non-segmented, enveloped, icosahedral, positive sense ssRNA

Arthropod borne:

1) Dengue fever - most common
2) Yellow fever
3) Japanese encephalitis
4) St. Louis encephalitis
5) West Nile Virus

119
Q

Togaviruses

Main features of genome, envelope, capsid?

Includes what 1 virus?

A

Main features:
-Non-segmented, enveloped, icosahedral, positive sense ssRNA

Chikungunya

120
Q

Outcome of Arbovirus Infection in Humans: (6)

A

**All cause encephalitis and fever

1) Asymptomatic
Dengue virus, WNV, and Zika → Majority asymptomatic
Chikungunya virus → Majority symptomatic

2) Febrile illness: abrupt onset fever, chills, muscle pain

3) Neurologic disease: *encephalitis, meningitis, AFP
Mortality or long term neurological sequelae in survivors

4) Arthritis/MSK: *fever, intense pain in peripheral joints, inflammation in joints, muscle, tendons → can develop chronic disease
5) Hemorrhagic fever
6) Congenital disease (e.g. Zika)

121
Q

Transmission cycle of arboviruses:

VECTOR?

A

Arthropod VECTORS

Primarily mosquitoes, but also ticks, biting flies

Infected vectors transmit virus to vertebrate hosts during feeding

122
Q

Mosquito and virus cycle of infection? (5 steps)

A

1) Female mosquito ingests blood from viremic vertebrate
2) Virus replicates in mosquito midgut
3) Systemic spread in mosquito
4) Virus replicates and accumulates in salivary glands
5) Mosquito injects saliva/virus into skin during next blood meal

123
Q

Transmission cycle of arboviruses:

HOSTS? 2 kinds of hosts

A

1) Those that do not serve as reservoirs, but have overt disease
2) Those that serve as main source for infections of vectors = RESERVOIRS

124
Q

Arbovirus reservoirs?

A

Those that serve as main source for infections of vectors = RESERVOIRS

May or may not develop disease

Presence of high titer serum viremia of long duration required to infect adequate number of vectors

125
Q

Humans are often DEAD END HOSTS (not high enough titer serum viremia)

Humans are NOT dead end hosts for…(4)

A

Dengue
Yellow Fever
Zika
Chikungunya

126
Q

Dengue Virus:

A

Most common arbovirus worldwide

Four serotypes of virus

127
Q

Dengue Virus:

Disease? 3 possible outcomes

A

Majority of infections are asymptomatic (75%)

Dengue Fever

Dengue hemorrhagic fever

128
Q

Dengue hemorrhagic fever

A

mainly in SE Asia and S. America

Circulatory failure and shock

Increased vascular permeability, marked thrombocytopenia, fever for 2-7 days, hemorrhagic tendency

129
Q

Dengue Fever

A

Headache, retro-orbital pain
Marked muscle and joint pain (“break bone fever”)
Bleeding of skin and nose

130
Q

Pathogenesis of multiple infections with Dengue Fever:

what happens after the 1st infection?

what does this mean for the 2nd infection?

A

1st infection → ab response to 1st infection

  • Protects from second infection with SAME serotype
  • Provides some initial protection for cross-reactive serotypes that decline and becomes sub neutralizing over time

2nd infection → cross-reactive sub-neutralizing antibodies generated during first infection mediates enhanced infection of specific cells → increased viral replication and immune activation (increased cytokines)

**Preexisting, subclinical protection → MORE severe disease

131
Q

Chikungunya Virus

Part of what virus family?
genome?

A

Togavirus (alphavirus)

Non-segmented, enveloped, icosahedral, positive sense ssRNA

132
Q

Chikungunya Virus

Causes what disease?

A

Re-emerged recently

Endemic to West Africa, but has spread to Caribbean

High grade fever

Bilateral polyarthralgia

Macular or maculopapular rash

Can have chronic phase with chronic inflammatory rheumatism and MSK disorders

133
Q

Zika Virus

Part of what virus family?
Genome?

A

Flavivirus

Non-segmented, enveloped, icosahedral, positive sense ssRNA

134
Q

Zika virus

Disease?

A

Majority asymptomatic

Recent re-emergence

Fever, muscle/joint pain, conjunctivitis

Linked to severe fetal disease and Guillain-Barre Syndrome in adults

Infectious Disease (9 decks)

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