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Clinical Immunology > Strep/Mono/Vectors > Flashcards

Strep/Mono/Vectors Flashcards

1
Q

Streptococcus Pyogenes (Group A Strep): most common diseases

A

Pharyngitis
Scarlet Fever
Impetigo
Necrotizing Fascitis
Acute rheumatic fever*
Poststreptococcal glomerulonephritis*

*more important in terms of morbidity and mortality worldwide

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2
Q

S. pyogenes characteristics in Micro

A

Gram positive coccus

Beta-hemolytic

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3
Q

S. pyogenes: less common diseases

A

Otitis media in children
Sinusitis in adults
Osteomylitis
Septic arthritis
Neonatal septicemia
Pneumonia (rare)

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4
Q

Necrotizing Fasciitis

A

S. pyogenes

“flesh eating bacteria”

Rare, destroys skin and soft tissue, including fat and tissues surrounding muscles (fascia)

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5
Q

S. pyogenes morphological characteristics

A

Classified based on immunologic action of cell wall carbohydrates. Lancefield serogroups A-H, K & O.

Fimbriae
-structures near plasma membrane, project through cell wall and capsule, contain important
-EX: M Protein is a major virulence factor, found in association with hyaluronic capsule, it inhibit phagocytosis. Antibody against M protein provides type specific immunity

Lipoteichoic Acid
-important to adherence to human epithelium and initiation of infection

(Margin notes: S. pyogenes contains many antigenic structural components and produces several antigenic enzymes, which of which may elicit a specific antibody response from the infected host)

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6
Q

S. pyogenes Extracellular Products - Two Hemolysins

A

Streptolysin O (SLO): oxygen labile enzyme, binds to RBC membranes, allows submicroscopic holes in membranes and Hgb diffuses from cells. Antibody response to SLO is the most commonly used indicator of recent strep infection.

Streptolysin S: oxygen-stable, responsible for beta-hemolysis of blood agar, disrupts RBC membrane selective permeability (causing osmotic lysis), not antigenic

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7
Q

S. pyogenes extracellular products (non-hemolysins, facilitate rapid spread)

A

Hyaluronidase “spreading factor”: breaks down hyaluronic acid found in connective tissue

DNases A, B, C & D (immunologically distinct)

Streptokinase: enzyme that dissolves clots by coverting plasminogen to plasmin

Erythrogenic toxin: elaborated by scarlet fever associated strains (characteristic rash)

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8
Q

S. pyogenes Epidemiology

A

One of the most common human pathogens

Found in respiratory tract, spread by contact with large droplets, crowding increases spread (Upper resp. infections common in school age kids)

Some asymptomatic carriers

Rheumatic fever a major complication of infection (decreased in US due to early treatments)

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9
Q

S. pyogenes - Upper Respiratory Infection, Viral Pharyngitis symptoms

A

Both have age dependent manifestations

Infant/young child: rhinorrhea, coughing fever, vomit, anorexia

Kids >3 years: classic strep pharyngitis

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10
Q

S. pyogenes - Impetigo/Cellulitis signs and symptoms

A

Skin infection begins as papule

Lesion may itch, eventually crusting over and healing

Cellulitis - subq infection, warm, tender

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11
Q

S. pyogenes - Scarlet Fever signs & symptoms

A

Result of pharyngeal infection with a strain of group A that produces erythrogenic toxin

Rash along with regular signs and symptoms

After 1 week, face begins to peel

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12
Q

S. pyogenes infection complications

A

notallinfections

Upper respiratory infections may become acute rheumatic fever

Pharyngitis or skin infections may become poststreptococcal glomerulonephritis

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13
Q

S. pyogenes: Diagnostic Eval

A

Throat culture
Rapid antigen test on throat swab
Molecular test for GAS

Serological tests
-demonstrate Abs & extracellular products
-Antistreptolysin O (ASO) and anti-deoxyribonuclease B (anti-Dnase B) standard
-Specimen pairing: compare acute and convalescent sera collected 3 weeks apart

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14
Q

S. pyogenes - Antistreptolysin O (serological test)

A

Ability of patient serum to neutralize erythrocyte-lysing capability of SLO

Titer rises ~7 days after infection onset, maxes out ~4-6 weeks (can have elevated titer for up to a year)

The rise in the titer over 1-2 weeks more significant than one titer

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15
Q

S. pyogenes - Deoxyribonuclease B (serological test)

A

Dnase B produced by S. pyogenes, not other streps.

Reliable Ab test for skin & throat infections.

50% patients with S. pyogenes acute glomerulonephris will have elevated Dnase B with normal ASO titer

LESS SUSCEPTIBLE TO FALSE POSITIVES THAN ASO due to bacterial growth in specimen, liver disease and oxidation of the antigen

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16
Q

S. pyogenes Toxic Shock Syndrome (STSS) - Etiology

A

Portal of entry unknown in 50% of cases

Has been associated with use of super tampons

Appears after cocci have invaded areas of injured skin

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17
Q

S. pyogenes Toxic Shock Syndrome (STSS) - Immunological Mechanisms

A

Pyrogenic exotoxins cause fever and help induce shock by lowering the threshold to exogenous endotoxin

Induction of cytokines in vivo is likely the cause of shock

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18
Q

S. pyogenes Toxic Shock Syndrome (STSS) - Epidemiology

A

Highest rates in young children and older adults

50+ % have underlying chronic illness

up to 70% mortality

rare infection, ~300 cases per year

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19
Q

S. pyogenes Toxic Shock Syndrome (STSS) - Signs & Symptoms

A

Fever, blotchy rash, red/swollen/pain on infected skin

Average incubation time 2-3 days

80% cases have clinical signs of soft tissue infection

20% have influenze like symptoms

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20
Q

S. pyogenes Toxic Shock Syndrome (STSS) - Laboratory Findings

A

Serological confirmation shows 4x rise against SLO(ASO) & Dnase B

Milk leukocytosis, immature neutrophils 40-50%

Positive blood cultures in 60% of cases

Hemoglobinuria & serum creatinine 2.5x normal (renal involvment)

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21
Q

S. pyogenes Toxic Shock Syndrome (STSS) - Treatment

A

IV fluids, blood pressure maintenance medication

Can be deadly, requires immediate treatment

Skin may peel as rash heals, may need to debride with surgery

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22
Q

Streptococcus agalactiae (Group B Strep) Disease - Epidemiology

A

Fatality rates 26-70% for men & non-pregnant women

30+% women asymptomatic carriers in genitourinary tract. Leading cause of early-onset neonatal sepsis in US

Universal screening at 35-37 weeks pregnancy, intrapartum antibiotics reduce GBS disease in newborns.

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23
Q

Streptococcus agalactiae (Group B Strep) Disease - Etiology

A

Gram positive

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24
Q

Streptococcus agalactiae (Group B Strep) Disease - Laboratory Data

A

Mostly isolated from blood

Latex test not as effective as culture or molecular
PCR assay from culture broth (commonly used)

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25
Q

Streptococcus agalactiae (Group B Strep) Disease - Signs & Symptoms

A

Skin & soft tissue infections

Neonatal infection during birth

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26
Q

Epstein-Barr Virus (EBV) - Etioilogy

A

Human herpes virus that infects B lymps

Causes infectious mononucleosis, burkitt lymphoma, neoplasms of thymus/parotid gland/supraglottic larynx

Can compicate cardio, ocular, respiratory, hematologic, digestive, renal & neurologic symtoms (so everything)

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27
Q

Epstein-Barr Virus (EBV) - Epidemiology

A

~95% world population has been exposed

Herpes DNA virus that infects B lymphs

Variant lymphs produced have T cell characteristics (mononucleosis from large effector CD8 Tc cell reponse against EBV infection of circulating B cells)

Transmitted by oral-pharyngeal secretions touching smooch. Can also be trasmitted by blood transfusion or transplacental route (not common).

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28
Q

Epstein-Barr Virus (EBV) & Immunocompromised folks

A

Major concern!

Infectious mononucleosis postperfusion syndrome
-blood transfusion from immune donor to nonimmune recipient
-may be from CMV rather than EBV

Maintain EBV as chronic, latent infection

Low % of patients experience symptomatic reactivation

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29
Q

Epstein-Barr Virus (EBV) - Signs & Symptoms

A

Asymptomatic for most infants (they ain’t got no B cells lieutenant dan)

Typical illness in teens

Incubation 10-50 days

Extreme fatigue, malaise, sore throat, fever, cervical lymphadenopathy.

Splenomegaly in 50% of cases. Rare jaundice.

Lasts 1-4 weeks.

Significant # of patients do not manifest cassic signs (cool cool cool)

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30
Q

Epstein-Barr Virus (EBV) - Laboratory Diagnostic Eval

A

High leukocytes in most cases (10-20 x 10^9). 10% of patients leukopenic.

Relative lymph counts 60-90% (with 5-30% of those being mono/varient lymphs)

Increase in virus specific CD8+ T cells (important for life-long control of EBV disease)

Serologic antibody testing for non-classic symptoms. Abs present are heterophile & EBV.

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31
Q

Epstein-Barr Virus (EBV) - Heterophile Antibodies

A

Broad class, may be present in low concentrations in healthy person.

Titer of > 1:56 clinically significant for suspected mono.

IgM appears in acute phase

(IgM reacts with horse/ox/sheep RBCs, absorbed by beef RBCs, not absorbed by guinea pig kidney cells, does not react with EBV specific antigens)

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32
Q

Epstein-Barr Virus (EBV) - Serology

A

10-20% of adults don’t produce heterophile antibodies

50%+ of kids younger than 4 with mono are heterophile negative

EBV serology recommended for people without classic symptoms, heterophile negative, immunosuppressed

EBV infected B cells express new antigens encorded by virus

Viral capsid antigen, early antigen & nuclear antigen all corresponding antibody responses
-assays for IgM & IgG antibodies to these EBV antigens are available

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33
Q

Epstein-Barr Virus (EBV) - Viral Capsid Antigen

A

produced by infected B cells & found in cytoplasm

Anti-VCA IgM detectable, but low concentration, in early infection. Desappears ~2-4 months.

Anti-VCA IgG detectable within 4-7 days and persis for a long time, possibly forever

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34
Q

Epstein-Barr Virus (EBV) - Early Antigen

A

Early antigen-diffuse (EA-D)
-found in nucleus & cytoplasm of B cells
-IgG type (indicative of acute infection)

Early antigen-restriced (EA-R)
-Found as a mass only in cytoplasm
-IgG usually only seen in young children

Neither consistent indicators of disease stage

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35
Q

Epstein-Barr Nuclear Antigen (EBNA, NA)

A

Found in nucleus of all EBV infected cells

Anti-EBNA IgG doesn’t appear until patient has entered convalescence

Titers gradually increase and reach plateau 3-12 months after infection

Most healthy individuals with previous exposures have titers ranging from 1:10 - 1:160

Should be taked in combination with patient symptoms, history & Ab response patterns

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36
Q

VCA IgG Antibody Formation (blue chart)

A

No previous exposure: negative

Recent acute infection: positive

Past infection (convalescent): positive

Reactivation of latent infecgtion: positive

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37
Q

EBNA IgG Antibody Formation (blue chart)

A

No previous exposure: negative

Recent acute infection: negative

Past infection (convalescent): positive

Reactivation of latent infecgtion: positive

38
Q

Epstein-Barr Virus (EBV) - Immunofluorescence

A

Common method for EBV serology

Antigen substrate slide containing EBV infected cells incubate with serum

Fluorescein-conjugated antihuman IgG or IgM

Cons: time consuming, difficult to interpret, prone to interference from other serum components

39
Q

Vector-Borne Diseases (overview)

A

Bacterial/viral diseases transmitted by mosquitoes, ticks & fleas

Travelers & military at highest risk

Discovery and surveillance often done with serologic testing

40
Q

Lyme Disease - Etiology

A

Spirochete Borrelia burgdorferi

Transmitted by Ixodes ticks. Can be carried into household on dogs & cats.

White footed mouse for larval and nymphal stages. White tailed deer for adult stages.

41
Q

Lyme Disease - Epidemiology

A

Most common vector-borne illness in US (95%!). But found worldwide.

NE and upper midwest.

42
Q

Lyme Disease - Signs & Symptoms

A

After tick bite, spirochetes migrate outwardly into skin (skin lesions, erthema chronicum migrans (ECM))

60-80% begin with flu like symptoms, evolves through stages.

Bullseye rash. Most patients have ECM (50% of these patients develop secondary lesions), .25% have arthritis. Rarely, neurologic & cardiac issues.

43
Q

Lyme Disease - Stage 1

A

~4 weeks afater infection

ECM or other skin eruptions, flulike symptoms, neurologic symptoms

44
Q

Lyme Disease - Stage 2

A

Variable latent period

Nervous system, heart, eyes, skin can all manifest abnormalities

45
Q

Lyme Disease - Stage 3

A

Weeks to years later

Arthritis, late neurologic complications, acrodermatitis chronica atrophicans

46
Q

Lyme Disease - Arthritis

A

Common sign of early Lyme

May be associated with long-standing infiltration of the joints by spirochetes along with local inflammatory response

47
Q

Lyme Disease - Cardiac Manifestations

A

Lyme carditis in ~8% of untreated patients within 1-2 months

Lightheadedness, syncope, dyspnea, palpitations, chest pain

Usually self-limited and mild course

48
Q

Lyme Disease - Neurologic Manifestations

A

~15% of untreated patients

2-8 weeks after onset

Aseptic meningitis, cranial nerve palsies, peripheral radiculoneuitis, peripheral neuropathy

Severe headache, mild neck stiffness

Maybe chronic encephalopathy

49
Q

Lyme Disease - Pregnancy

A

Transplancental transmission possible

Infant dies shortly after birth, mother acquired infection early in pregnancy with no treatment

50
Q

Lyme Disease - Immunologic Manifestations

A

Cellular immune responses begin concurrent with early clinical illness

Increase in spontaneous suppressor cell activity and reduction in NK cell activity

Mononuclear cell, Ag specific responsese develop during spirochete dissemination and humoral respones soon follow

Serodiagnostic tests insensitive during first several weeks

After 1 month, most patients have IgG antibodies - both IgM & IgG can persist for years

Ab formed: cryoglobulins, immune complexes, antibodies to B. burgdorferi, anticardiolipin antibodies

51
Q

Lyme Disease - Diagnostic Eval

A

Culter is definitive diagnosis, but rare. Usually from biopsy samples, less often from plasma or CSF.

Usually based on clinical findings, history of exposure, antibody response to B. burgdorferi

Might find spirochetes in a blood smear! But very transient, will be there one day, gone the next

52
Q

Lyme Disease - Antibody detection

A

CDC recommends two step process

EIA or IFA, then Western blot

Only positive if BOTH tests are positive

53
Q

Lyme Disease - Western Blot Analysis

A

Verifies reactivity of antibody to surface/flagellar protein of B. burgdorferi

Helpful in borderline results

More definitive test later in disease

54
Q

Lyme Disease - ELISA

A

Standard test method

Low sensitivity, lengthy processing time

55
Q

Lyme Disease - PCR

A

Detects spirochetes in synovial fluid from joints, other samples

Directly IDs pathogen, useful when patient is seronegative

56
Q

Lyme Disease - CSF for Ab Detection

A

Not recommended unless patied has pronouced neurological manifestations

57
Q

Lyme Disease - Treatment

A

How long tick was attached, probability of tick being a carrier, risk of antibiotic reactions all influence treatment decisions

Antibiotics
-tetracyclines (bacteriostatic unless in high doses)
-amoxicillin (more effective than penicillin)
-unclear if antimicrobial treatment will prevent Lyme disease

58
Q

Lyme Disease - Prevention

A

None really! No vaccine.

Check for ticks, wear light-colored clothes, tuck socks into pants

59
Q

Human Ehrlichiosis - Etiology

A

First described in US in 1986

Can be fatal, needs prompt treatment!

Tick-borne rickettsiae, genus Ehrlichia

Ehrlichia chaffeensis - agent of human monocytic ehrlichiosis in us

60
Q

Human Ehrlichiosis - Epidemiology

A

Prevelance in low, primarily southern Mid-Atlantic & south central states during spring and summer

Lone Star Tick main vector for E. chaffeensis. White tailed deer principle reservoir. In easern US, maybe white-footed mouse.

61
Q

Human Ehrlichiosis - Signs & Symptoms

A

‘Ehrlichiosis’ is the general term for human granulocytic ehrlichiosis (now called anaplasmosis) and human monocytic ehrlichiosis (HME)

Most patients not suspected of having rickettsial infection. Symptoms nonspecific: fever, chills, headache

62
Q

Human Ehrlichiosis - Three Developmental Stages

A

Elementary bodies enter leukocyte by phagocytosis, multiply rapidly

3-5 days later, tightly packed elementary bodies visible

Over 7-12 days, initial bodies developp into morular (mulberry) forms

63
Q

Human Ehrlichiosis - Diagnostic Eval

A

Direct observation on Wright-Giemsa stain (rapid, inexpensive)

PCR test of skin biopsy of rash or EDTA whole blood

Specific immunohistochemical detection

In anaplasmosis: diagnosis by seroconversion or by single titer higher than 1:80 w/ supporting systems

64
Q

Human Ehrlichiosis - Treatment & Prevention

A

Doxycycline (no guideline for long term therapy)

Prevention/reducing tick exposures

65
Q

Rocky Mountain Spotted Fever - Etiology

A

RMSF - tick-borne disease caused by bacterium Rickettsia rickettsii

found in N & S America

Transmitted by American dog tick , Rocky Mountain wood tick, brown dog tick

66
Q

Rocky Mountain Spotted Fever - Epidemiology

A

Reported since 1920 in every state except Vermont & Maine

Geographic distribution tied to location of various tick species

Most illness reported in June and July

67
Q

Rocky Mountain Spotted Fever - Signs & Symptoms

A

First symptoms 2-14 days after bite, often go unnoticed

Sudden onset of fever and headache, 90% have rash, some nausea & vomiting

68
Q

Rocky Mountain Spotted Fever - Diagnostic Eval

A

If rash present: PCR on biopsy or immunohistochemical staining

Ab detected within 7-10 days (85% negative during first week)

IFA with 2 paired specimens with four-fold increase in titers the gold standard. First sample asap, second 2-4 weeks later

both IgM & IgG remain elevated for months

69
Q

Rocky Mountain Spotted Fever - Treatment & Prevention

A

Earlier treatment corresponds to quicker recovery. Doxycycline first line of treatment, most effective if started before 5th day of symptoms. Durations of treatment 7-14 days.

IV antibiotics, prolonged hospitilization, intensive care for more sever course

70
Q

Babesiosis - Etiology

A

Rare, severe, sometimes fatal

Tick-borne, caused by Babesia (microscopic parasite that infects RBCs)

71
Q

Babesiosis - Epidemiology

A

Reportable in 37 states

Transmitted by I. scapularis tick. Larvae feed on white-footed mouse, nymphs and adults feed on white-tailed deer

Most common in older individuals, splenectomized patients, immunocompromised

72
Q

Babesiosis - Signs & Symptoms

A

Incubation period 7-21 days—may take 1-8 weeks for symptoms to appear

Clinical presentation is variable: ranges from asymptomatic to rapidly progressive and sometime fatal

Disease can cause fever, fatigue, and hemolytic anemia lasting several days to months

73
Q

Babesiosis - Diagnostic Eval

A

Observation of parasites in blood (symptomatic people)

Difficult to distinguish from malaria, can used PCR

No test is approved for blood donors :)

74
Q

Babesiosis - Treatment & Prevention

A

No standardized treatments have been developed

Some drugs used for malarial treatment have shown effectiveness

Antibiotic therapy recommended for splenectomized or immunodeficient patients

Combo of azithromycin and oral quinine

Exchange transfusion for patients with high level of parasites (>10%), severe disease, or massive hemolysis

Prevention requires diligence in tick infested areas

75
Q

Chikungunya Disease - Etiology & Epidemiology

A

Chikungunya virus is transmitted through mosquito bites

Outbreaks in Africa, Asia, Europe, and the Indian and Pacific Oceans
U.S. cases from returning travelers

76
Q

Chikungunya Disease - Signs & Symptoms

A

Symptoms begin 3-7 days after bitten by infected mosquito

Fever, joint pain, headache, rash, joint swelling

77
Q

Chikungunya Disease - Diagnostic Eval

A

IgM and IgG antibody testing by ELISA method

IgM suggests new, active infection

IgG suggests current or past infection

Parallel testing of acute and convalescent together suggested

78
Q

Chikungunya Disease - Treatment & Prevention

A

No vaccine!

Prevent mosquito bites

Treatment to relieve fever/pain only option…

79
Q

Dengue Virus - Etiology

A

Dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS)

Caused by 4 related viruses (1-4 serotypes)

Transmitted by mosquitos

80
Q

Dengue Virus - Epidemiology

A

Endemic in at least 100 countries

Most cases in U.S. acquired by travelers

81
Q

Dengue Virus - Signs & Symptoms (without warning signs)

A

Fever and

Two of the following: nausea, vomiting, rash, aches and pains, leukopenia, positive tourniquet test

82
Q

Dengue Virus - Signs & Symptoms (with warning signs)

A

Can include any of the following: abdominal pain and tenderness, persistent vomiting, clinical fluid accumulation, mucosal bleeding, lethargy, restlessness, liver enlargement >2 cm, lab finding of increases hct, red cell mass concurrent with rapid decrease in platelet count

83
Q

Dengue Virus - Signs & Symptoms (severe dengue)

A

Must include dengue symptoms with at least one of:
Severe plasma leakage leading to shock (DSS) or fluid accumulations with respiratory distress; severe bleeding; severe organ involvement: Liver- AST or ALT >1000, CNS-impaired consciousness, failure of heart and other organs

84
Q

Dengue Virus - Diagnostic Eval

A

CDC: Testing is divided into confirmatory testing and testing for probably or suspected dengue infection

Probable testing (Detection on IgM anti-DENV)

Suspected testing (Absence of IgM anti-DENV)

Dengue infection results in long-lasting immunity with a specific serotype—crossreactive protection is shortlived (1-3 years)

85
Q

Dengue Virus - Treatment & Prevention

A

No vaccines available—prevent mosquito bites

Treatment is consistent with classification of disease

86
Q

West Nile Virus - Etiology & Epidemiology

A

WNV-member of Japanese encephalitis virus group of flaviviruses
Mosquito-borne pathogen

Has been in the U.S. since at least summer of 1999

87
Q

West Nile Virus - Signs & Symptoms

A

Fever, headache, fatigue, aches, sometimes a rash

Can last a few days to several weeks

88
Q

West Nile Virus - Diagnostic Eval

A

Serologic tests or virus isolation

IgM antibody—7-8 days after symptom onset

IgG antibody 3-4 weeks

Some FDA approved ELISA kits available—need confirmation by CDC or state health lab

89
Q

West Nile Virus - Treatment & Prevention

A

No specific treatment—mild cases resolve over time

More severe cases with hospitalization—supportive treatment including IVs

Prevent mosquito bites

90
Q

Zika Virus - signs & symptoms

A

Infection during pregnancy—can cause microencephaly—incomplete brain development and other severe fatal brain defects; also have eye defects, hearing defects, impaired growth

Many people won’t have symptoms or only mild: fever, rash, joint pain, conjunctivitis—can last for several days to a week

90
Q

Zika Virus - Etiology & Epidemiology

A

Spread primarily by the bite of an infected Aedes spp. Mosquito
Pregnant women can transmit to fetus
Sexual contact

Typically tropical areas; Puerto Rico and Florida
High point in 2016—5168 symptomatic cases in U.S.
2018– 74 Zika cases

91
Q

Zika Virus - Diagnostic Eval

A

Based on person’s recent travel history, symptoms, and test results

Molecular Assay
-rRT-PCR for RNA performed on paired serum and urine samples

Serologic Test
-IgM typically develop at end of first week of illness

Zika MAC-ELISA
-Used for qualitative detection of IgM antibodies in serum or CSF
-Has some nonspecific cross-reactivity

Clinical Immunology (14 decks)

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