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Infectious Disease 2 > Exam Review 2 > Flashcards

Exam Review 2 Flashcards

1
Q

What are the differences between viral and bacterial conjunctivitis?

A

Bacterial: 50-74% bilateral at onset, Mucopurulent discharge, No Preauricular adenopathy, Concurrent Otitis media in 20-73%; Viral: 35% bilateral at onset, watery discharge, Preauricular adenopathy, 10% Concurrent Otitis media

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2
Q

What are common causes of bacterial conjunctivitis?

A

Haemophilus influenza, Streptococcus pneumonia, Staphylococci, Gram negative bacilli, Neisseria meningitidis, Haemophilus aegyptius (cause of Brazilian purpuric fever)

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3
Q

What are common causes of viral conjunctivitis?

A

Adenovirus (fever, pharyngitis), Adenovirus keratoconjunctivitis, HSV, Enterovirus 70 and Coxsackie-virus A24, Rubella and rubeola

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4
Q

What is the epidemiology of otitis media?

A

Seasonal peak winter months (URIs); Highest incidence populations: children under 2, in daycare, cleft-palate, HIV, IgG and subclass deficiency; 70% bacterial but co-infection with viral infection is common; Pneumococcal vaccination has had significant impact colonization and development of OM; High rates of antibiotic resistance; occurs in 85% of children by age 3

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5
Q

Is otitis media usually bacterial or viral?

A

Often viral but may be complicated by bacterial

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6
Q

What are potential complications of otitis media?

A

hearing loss, mastoiditis and brain abscess

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7
Q

What is the pathogenesis of OM from the eustachian tube?

A

ET dysfunction, negative middle ear pressure; Host defenses and poor PMN response; bacterial invasion of middle ear

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8
Q

What are common causes of OM?

A

RSV, Parainfluenza, Influenza, Enterovirus, Strep pneumoniae, H. influenza, Moraxella catarallis, Grps A and B streptococcus

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9
Q

What are common causes of sinusitis?

A

S. pneumoniae, H. influenzae, M. catarralis, S. aureus, Anaerobic bacteria

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10
Q

What are the clinical presentations of sinusitis?

A

persistent (10 days) nasal discharge, cough; severe: high fever, nasal discharge for 3 days; worsening: recurrent fever, exacerbation cough, nasal discharge

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11
Q

How is sinusitis treated?

A

amoxacillin

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12
Q

What is tracheobronchitis?

A

Croup! Seal-like barking or brassy cough, dysphonia, inspiratory stridor, retractions; steeple sign of subglottic edema

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13
Q

What are common causes of croup?

A

parainfluenza 1,2,3; RSV, influenza A and B, adenovirus, human metapneumovirus, echoviruses, coxsackiviruses

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14
Q

What is the epidemiology of croup?

A

6 months- 2 years; seasonal peak in winter months

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15
Q

How is croup treated?

A

Steroids, Humidified air (the shower!)

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16
Q

What are common diseases that cause rashes in children?

A

Rubeola (the measles!), scarlet fever, rubella, erythema infectiosum, roseola infantum

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17
Q

What is another name for Measles?

A

Rubeola

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18
Q

What causes Scarlet Fever?

A

Group A Strep

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19
Q

What is another name for Rubella?

A

German Measles

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20
Q

What is another name for Erythema Infectiosum?

A

Fifth disease (caused by parvovirus B19)

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21
Q

What is another name for Roseola Infantum?

A

Sixth disease (caused by HHV 6 or 7)

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22
Q

What is the structure of measles?

A

Paramyxovirus, RNA virus- with a lipid envelop which comes from the host cell, H protein (hemagglutinin) mediates attachment, F protein (fusion) enhances cell-to-cell spread, M protein is critical for viral assembly

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23
Q

How is measles spread?

A

Transmission by respiratory secretions

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24
Q

What is the pathogenesis of measles?

A
  1. Inhaled or environmental exposure; 2. Replication in nasopharynx and regional lymph nodes; 3. Primary viremia
    (2-3 days after exposure); 4. Secondary viremia (5-7 days after exposure); 5. Rash (Day 14)
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25
Q

What occurs in the prodromal period of measles?

A

fever, cough, nonpurulent conjunctivitis

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26
Q

What occurs with the measles rash?

A

Rash begins on the face and spreads cephalocaudally, can cause confluence or desquamation; can also cause Koplick’s Spots

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27
Q

What complications can measles be associated with?

A

Otitis media (7%), Bronchopneumonia (6%), Diarrhea (8%), Encephalitis (1/1000 cases) with brain damage, Death (1-3/1000 cases) due to encephalitis or respiratory complications, Subacute sclerosing

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28
Q

What is subacute sclerosing panencephalitis?

A

Fatal, progressive degenerative disease of CNS (Personality changes, Myoclonus, Faccidity and autonomic dysfunction, Vegetative state), Occurs 7-10 years post natural measles, Pathogenesis not well understood

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29
Q

How is measles diagnosed?

A

Serology (Anti-measles IgM can be detected approximately 3 days after the exanthem); Viral culture (Difficult to do. Must talk to laboratory first); NOTE: ANY CASE OF MEASLES IS REPORTABLE TO THE DEPARTMENT OF HEALTH

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30
Q

How is measles treated?

A

ribavirin may have some benefit but prevention has been most effective

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31
Q

What is the epidemiology of rubella?

A

Pre-vaccine peaked in winter and spring months, School age children, Congenital infection

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32
Q

What is the structure of rubella?

A

Single stranded RNA virus, part of the Togavirus family

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33
Q

What are the symptoms of rubella?

A

Rash and conjunctivitis milder than measles

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34
Q

What is postnatal rubella?

A

Rash spreads head to toe in 24 hours; Rash lasts 3 days; Fever is mild

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35
Q

What is congenital rubella syndrome?

A

20% risk of infection if exposed in 1st or 2nd trimester; The earlier the infection, the more severe the defects; causes in-utero growth retardation, hearing loss, cataracts, cardiac defects, hepatosplenomegally, petechiae and purpura (“blueberry muffin”), adenopathy; SEVERE: Hemolytic anemia, low platelets, long bone abnormalities, meningoencephalitis, intellectual disability, pneumonia

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36
Q

What is the structure of mumps?

A

Paramyxovirus family; Enveloped RNA virus; Glycoproteins: Hemagglutinin and neuraminidase protein (HN), Cell fusion protein (F); 7 structural proteins

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37
Q

What is the pathogenesis of mumps?

A

Infection from respiratory viral secretions, Incubation period 16-18 days, Viral replication in nasopharyngeal mucosa and regional lymph nodes, Viremia and seeding of organs e.g. CNS, tests, salary glands

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38
Q

What are the symptoms of mumps?

A

1/3 subclinical or mild respiratory disease, Parotid swelling (unilateral but may be bilateral later), Morbilliform rash, Fever

39
Q

How do you diagnose mumps?

A

IgM antibody to Mumps by EIA, Rising IgG titer in acute and convalescent titers, Culture (pharynx near duct of Stensen, CSF, urine), PCR

40
Q

What are complications of mumps?

A

CNS (with/without parotidis)– common; neurotropic virus; Orchitis (14-35%); Arthralgia and arthritis (large joints); Myocarditis; Gestational mumps has lead to endocardial fibroelastosis in children

41
Q

What is roseola?

A

DNA virus transmitted by respiratory secretions; Primary infection occurs between 6 months to 3 years; Reactivation of latent virus (Especially in CNS and in immunocompromised patients)

42
Q

What are the symptoms of roseola?

A

3-5 days of high fever followed by resolution of fever and rash; Bulging fontanelle; CNS symptoms e.g. febrile seizures; Other: hepatitis, mono-like illness, hemophagocytic syndrome

43
Q

What is parvovirus 19?

A

(Erythema infectiousum, Fifth Disease) - DNA virus, Replicates only in human erythrocyte precursors due to receptor on erythroid cell lines, the blood group P antigen, Genome: 1 nonstructural protein and 2 capsid proteins

44
Q

What is the epidemiology of parvovirus 19?

A

Common in childhood, Transmission by respiratory droplets and by blood products

45
Q

What is the clinical presentation of parvovirus?

A

Asymptomatic; febrile illness with rash; Polyarthropathy syndrome (uncommon in children); Chronic bone marrow failure (HIV/AIDS; immune deficiencies); Miscarriage; Hydrops fetalis (cardiac decompensation due to sever anemia and myocarditis in fetus)

46
Q

What are the 3 categories of herpesviruses?

A
  1. Alpha - short reproductive cycle,variable host range, latent in sensory neurons (HSV 1, 2, VZV); 2. Beta: long reproductive cycle, narrow host range, latent in lymphoid cells & others (salivary glands, kidney) (CMV, HHV 6, 7); 3. Gamma: narrow host range; latent in lymphoid cells, associated with tumors (EBV, KSH, HHV8)
47
Q

What does the VZV rash look like?

A

Vesicular - Vesicular fluid is highly infectious. Well-formed virions are suspended in it. Rash not always present, especially in zoster. Scratching the rash liberates the virus into the air

48
Q

How is VZV spread?

A

Virus is aerosolized from skin lesions and reaches the respiratory mucosa of a susceptible

49
Q

What is the structure of VZV?

A

phospholipid envelope, tegument, icosahedral capsid, DNA core; The smallest of the herpesviruses; Receptors: heparan sulfate, mannose-6 phosphate receptor (MPR), insulin degrading enzyme (IDE)

50
Q

How does VZV stay latent?

A

VZV latency is established by free virions that infect sensory nerve endings; latency is established during primary infection, dormant in dorsal root ganglion; Viremia associated w/ infected T cells - can bring to neurons and infect them that way (cranial nerve ganglia); Proteins of regulatory genes are expressed in cell cytoplasm, not nucleus; Suggests regulatory proteins are blocked from normal action, leading to inhibition of cascade of gene expression preventing lytic infection from occurring (latency) (infection proceeds in cascade of gene expression leading to lytic infection)

51
Q

How does VZV spread within the body?

A

In varicella, VZV is transported from the respiratory mucosa to the blood (viremia) in T cells, where virus is not accessible to antibodies; Cell-to-cell spread is slow, so the incubation period of varicella is long (2 weeks); Slow spread prevents host from being overwhelmed before the adaptive immune response develops (decreases viral load); T helper, cytotoxic T cells, and natural killer (NK) cells (innate immunity) are important for control of virus by the host.

52
Q

What is the natural history of VZV?

A

primary infection: varicella, Secondary infection: zoster

53
Q

What causes zoster?

A

Zoster is due to reactivation of latent VZV; Rare asymptomatic shedding of VZV compared to HSV; Zoster (reactivation) can occur in absence of rash

54
Q

What are the symptoms of varicella?

A

rash (characteristic centripetal distribution and pruritic), fever, malaise; Complications: bacterial superinfection, encephalitis, pneumonia, congenital syndrome, severe/fatal in immunocompromised (e.g. leukemia)

55
Q

Where does varicella remain latent?

A

Latency from skin rash or viremia established in neurons (dorsal root ganglia (DRG), cranial nerve ganglia (CNG), enteric nervous system (ENS)

56
Q

How is zoster localized?

A

Limited to 1-3 dermatomes; May disseminate in immunocompromised hosts.

57
Q

What happens when VZV occurs in the immunocompromised?

A

Varicella is likely to be severe (Prevent or modify with pre-formed antibodies just after exposure (passive immunization); Virus spreads from cell-cell in body; Treat most immunocompromised patients immediately with acyclovir or similar drug); The frequency of zoster is increased, Likely to suffer post-herpetic neuralgia

58
Q

What are potential zoster complications?

A

Retinitis (blindness), Meningitis, Vasculopathy (Stroke), Giant cell arteritis, Paralysis (cranial and other nerves), Post herpetic neuralgia (PHN)

59
Q

What herpesvirus has a vaccine?

A

varicella - Live, attenuated, infectious virus (Oka strain); given in 2 doses; current herd immunity is leading to decrease in varicella; Contraindications: pregnancy, immunocompromised, allergy to vaccine components; Subsequent zoster is rare/unusual

60
Q

How is VZV diagnosed?

A

PCR on skin rash (rapid); study saliva or CSF if no skin rash; culture (difficult), DFA; Antibody titers, IgG (ELISA); slow; Antibody titers, IgM

61
Q

How should VZV and HSV be treated?

A

Acyclovir - Antiviral activity (inhibits DNA synthesis) only in infected cells (TK); Newer drugs: famciclovir, valacyclovir; overall pretty well tolerated

62
Q

What is mono?

A

Caused by Epstein Barr Virus (EBV); Usually occurs in young adults; symptoms, signs: fever, adenopathy, exudative pharyngitis, rash (ampicillin), hepatosplenomegaly, fatigue

63
Q

How is mono diagnosed?

A

Positive heterophile antibody (monospot), non-specific; EBV specific antibodies (Anti VCA (develops early, persists), Anti EBNA (develops late, persists), Positive aby VCA, neg aby EBNA = acute mononucleosis)

64
Q

What can EBV cause?

A

Infectious mononucleosis, nasopharyngeal carcinoma, lymphomas (including Burkitt’s), oral hairy leukoplakia (lytic infection), post-transplant lympho-proliferative disease (PTLD) (B cells)

65
Q

What does EBV have to do with latency?

A

B cells are latently infected in mononucleosis; T cells (atypical lymphocytes) are the host response, Latency develops in memory B cells after mononucleosis; Rarely, severe chronic illness follows mononucleosis

66
Q

How is mono treated?

A

give steroids if airway obstruction, hemolytic anemia, severe cardiac, neurologic disease (no specific antiviral therapy)

67
Q

What does herpesvirus 6, 7 cause?

A

Roseola in infants (rash, fever, seizures), Fevers in immunosuppressed, Rare mononucleosis syndrome in adults, Suggestive evidence for other diseases

68
Q

What does KHSV cause? (aka herpesvirus 8)

A

Closely related to EBV; Infections are rare in children; Causes Kaposi’s Sarcoma (Elderly, HIV-infected), primary-effusion lymphoma

69
Q

What is meningitis?

A

inflammation of meninges

70
Q

What is encephalitis?

A

inflammation of brain parenchyma

71
Q

What is meningoencephalitis?

A

inflammation of meninges and of brain parenchyma

72
Q

What is aseptic meningitis?

A

signs/symptoms of meningitis without evidence of bacterial/fungal/parasitic infection; most is viral

73
Q

What are clinical features of encephalitis?

A

headache, fever, altered consciousness, confusion/cognitive impairment, seizures, weakness

74
Q

What is the difference between encephalopathy and encephalitis?

A

Encephalopathy can occur with or without inflammation; encephalitis implies inflammation that goes along with systemic symptoms like fever

75
Q

What is neurotropism?

A

ability of a virus to infect cells of CNS

76
Q

What is neuroinvasiveness?

A

ability of a virus to enter CNS

77
Q

What is neurovirulence?

A

ability of a virus to cause disease in CNS

78
Q

What is the neuroinvasiveness and neurovirulence of rabies? HSV-1? Mumps?

A

Rabies: high/high; HSV-1: low neuroinvasiveness/high neurovirulence; Mumps: high neuroinvasiveness/low neurovirulence

79
Q

How can a virus cause encephalitis?

A
  1. Direct infection of vascular endothelium; 2. Disruption of tight junction by vasoactive cytokines; 3. Trojan horse
80
Q

How does virus move retrograde/anteretrograde?

A

pulled by dynein/kinesin

81
Q

What makes a virus neurovirulent?

A

Latency, neuronal death

82
Q

What is seen in CSF with encephalitis?

A

Mild elevation in WBC, lymph/monocyte predominance, normal glucose, mildly elevated or normal protein

83
Q

What is the typical outcome of viral encephalitis?

A

HSV vital in about 70% without therapy and 20% with, neurological sequelae common in eastern equine, West Nile

84
Q

What should be given to treat HSV encephalitis?

A

acyclovir

85
Q

What is enteroviral meningitis?

A

Caused by enteroviruses; most common in very young infants, sometimes young children, in summer months; febrile prodrome; most cases uncomplicated and recover in 1 week; adults may have more prolonged course; diagnosis by PCR

86
Q

What is the vector of West Nile? The dead-end hosts? The amplifier host?

A

vector - mosquito, amplifier host - bird, dead-end host - horse, human

87
Q

How does West Nile present?

A

Most WNV cases are asymptomatic; fever w/ abrupt onset occurs in 25% (accompanied by headache, weakness, rash, myalgia), fatigue after for weeks-months; neuroinvasive disease in 1/200 - meningitis, encephalitis, acute flaccid paralysis; long-term neurocognitive defects

88
Q

How is West Nile treated?

A

No good treatment, prevention and mosquito control key

89
Q

What is the structure of rabies?

A

Lyssavirus, - ssRNA

90
Q

What is the pathogenesis of rabies?

A

Animal bite, viral replication in muscle, binds to nicotinic acetylcholine receptors, travels within axon in peripheral nerves via retrograde fast axonal transport, replicates in DRG, goes to brain

91
Q

What is the clinical presentation of rabies?

A

Incubation period can be 1 week - 1 year; prodromal phase of fever, chills, malaise, myalgias, nausea/vomiting; acute neurologic phase; pure ascending paralysis

92
Q

How is rabies diagnosed?

A

clinical suspicion, multiple tests (saliva, skin biopsy, serum CSF); often post-mortem testing

93
Q

What is rabies PEP?

A

wound cleansing, rabies vaccine (5 doses), rabies immune globulin

Infectious Disease 2 (6 decks)

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