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Clinical Immunology > Infectious diseases > Flashcards

Infectious diseases Flashcards

1
Q

Characteristics of infectious diseases

A

-Influenced by both microorganism & host (health/age)
-Spread of organism (insects/travelers)

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2
Q

Development of infectious disease requires what in terms of the host?

A

-It has to pass the 1st line of defense and survive the 2nd & 3rd lines of defense (phagocy, complement, cell mediated)
-Effective mechanism of healthy person depends on Microorganism characteristics & port of entry.
-Routs of infection
-Oral (foodborne or waterborne)
Maternal-fetal transmission
Insect vectors
Sexual transmission
Parenteral routes (injection or transfusion of infected blood)
Respiratory transmissio

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3
Q

Traditional infectious lab testing

A
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4
Q

Streptococcal infections and syphilis are examples of what kind of infections

A

Bacterial infections

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5
Q

What substances are present in bacterial infections?

A

Lysosomes & phagocytosis is present— they are major immunologic defenses agains bacteria

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6
Q

Can microorganisms survive phagocytosis?

A

Yes, IF they have capsules~

capsules can release exotoxins, impede w/ attachement OR interfere w/ digestion.

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7
Q

What sets parasites infections apart from bacterial & viral infections?

A

Parasites
-Relatively large
-Resistant body walls
-Avoid phagocytosis by moving away from inflammation

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8
Q

what immune responses correspond to parasitic infections?

A

-immunoglobulins
-complement
-antibody dependent
-cell-mediated cytotoxicity
-cellular defenses (eosinophils & T cells)

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9
Q

Can cestodes be eradicated by the complement system?

A

Yes, but NOT all.
Some get opsonized by IgGs

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10
Q

What antibody is increased w/ helminth

A

IgEs

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11
Q

Are parasites affected by phagocytosis?

A

Yes, it may have SOME direct activity against parasites

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12
Q

Most effective protection against parasites are done by which immune response

A

Antibody dependent (Macrophages, Neutrophils, Eosinophils)
&
Cell mediated cytotoxicity

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13
Q

Cytotoxic cells are usually mediated by which immunoglobulin?

A

IgG

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14
Q

Eosinophil roles is what?

A

Complex lol
-may phagocytize immune complexes
-act as effector cells

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15
Q

Are T cells involved in parasitic infection

A

Yes, they;
-sequester microorganisms
-Helper T cells bring in B cells to specific organisms

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16
Q

Major protective mechanism against Giardia

A

-Nonspecific factors (non-stimulated monocytes)

-NK cells have direct activity to some parasites (& cancer)

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17
Q

True or False
Delayed hypersensitivity can prevent some parasitic infections

A

True, but can cause other diseases

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18
Q

Can parasitic infections can cause depositions of antigen-antibody complexes?

A

Yes, in cases of severe pathological lesions

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19
Q

True or False
Parasitic infections increase lvls of IgE and can lead to hypersensitivity

A

True, and can lead to anaphylaxis

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20
Q

True or False
Fungal diseases are only superficial

A

Flase

Normally superficially, but can enter via respiratory tract (spores) and cause systemic disease

Manifestation of disease depends on degree & type of immune response

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21
Q

True or False
Fungi can be harmless in mucuses membranes

A

True, it can also be found on the surface of the skin (candida albicans)

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22
Q

True or False
Fungi infections can be opportunistic agents

A

True, especially in immunocompromised ppl.

<—-Range from—->
unnoticed respiratory episodes to fatal hypersensitive reaction

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23
Q

What are the survival mechanisms of fungi

A

-Anti-phagocytic capsule
-Digestion resistance w/in macrophages
-Destroy phagocytes

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24
Q

Why are fungal infections increasing world wide?

A

-use of immunosuppressive drugs
-Diseases (AIDS) causing immunosuppressed hosts

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25
Q

True or False
Serologic tests play an important part in diagnosis of fungal infections

A

TRUE

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26
Q

True or False
Respiratory diseases are NOT associated with fungal infections

A

False- many fungal infections are associated w/ inhalation of spores.

reservoirs = dust, bird droppings, soil

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27
Q

Histoplasmosis
(Histoplasmosis capsulatum)
where is it found?
how is it transmitted?
symptoms?
diagnostic?

A

-Found in soil with bird or bat pooooop
-spore inhalation
-Can be asymptomatic —> to chronic pulmonary disease
-Disseminated form of hepatosplenomegaly w/ lymphadenopathy
Fever, anemia, Leukopenia, weight loss, lassitude
-microscopic ID, isolation of culture & serological evidence

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28
Q

Aspergillosis
What kind of reactions

Diagnostic

A

Secondary to another diseases
Bronchopulmonary allergic reaction to toxins or endotoxins
Can also be invasive or disseminating

microsopic ID, serological, skin reactions & immunodiffusion (for negative culture)

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29
Q

Name the three forms of coccidiodomycosis

A

Pulmonary - primary
cutaneous - secondary
disseminated (spread thru out body)

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30
Q

Coccidiodmycosis
where is it found
how is it transmitted

diagnostic

A

-deserts like the San Juaquin fever Or valley fever
-inhalation of soil/dust containing athrospores coccidioides

-transdermal skin test (does not differentiate between recent & past exposures)

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31
Q

North american blastomycosis
Symptoms

diagnostic

A

-chronic fungal infection secondary to pulmonary involvement
-tumors in skin, lesions in - lungs, liver, spleen, kidneys, bone & subcutaneous tissues

-serologic test is problematic (high cross reactivity w/ components of organism)

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32
Q

Sporotrichosis
(sporothrix schenckii)
symptoms

A

Progressive, subcutaneous lymphatic mycosis & chronic
-sporotrichotic chancre at side of innolculation ->nodules along lymphatics
-associated w/ injuries caused by thorns

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33
Q

Three forms of Sporotrichosis

A

Respiratory
lymphatic (MOST common)
-disseminated

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34
Q

Cryptococcus
(C. neogormans)
how is it transmitted?

symptoms?

A

-Infection pigeons (vector) poop->fungus gets inhaled->grows culture as yeast

-asymptomatic initially-> typically develop pulmonary infection (Or brain)
-serious in immunocompromised/ debilitated patients
-w/ progression Ag appear and Abs decrease

after treatment
Ags decrease & Abs reappear = good prognosis

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35
Q

Viral
Richettsial
&
Mycoplasmal diseases

A

-associated w/ viral infections - cellular repliacation - may lead to cell death
-Zoonoses (rabies) most virulent viruses for humans
-Interferons & Abs (& macrophages) prevent entry and bloodborne/ spread of viruses
-can persists for years w/o symptoms then be reactivated

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36
Q

Intermediate b/w virus & bacteria = obligatory intracellular organisms
Rickettsiae are closer to?

A

contain cell walls - closer to viruses

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37
Q

Intermediate b/w virus & bacteria = obligatory intracellular organisms
Mycoplasma are closer to?

A

W/o cell walls - closer to bacteria

38
Q

Covid-19

A

-No widespread immunity
-high rate of transmission - can be asymptomatic - contagious several days before symptoms
-Higher risk if you deal with other disease like diabetes, asthma, cancer

39
Q

Covid-19 & ACE2 receptor

A

-ACE2 cells are in Alveolar cells lining the lungs, GI tract, heart & kidneys. Virus uses them to enter the epithelial cells.
-severe complication - cytokine storm

40
Q

What are the 4 main structures of the corona virus

A

N - Nucleocapsid
S - Spike
M - Membrane
E - Envelope

41
Q

Testing options for Covid-19

A

-Molecular based techniques & serological (Ab testing)
-Initial Emergency Use Authorization (EUAs)
-Real-time PCR (needs adequate viral load)
-Pooled testing

42
Q

Treatment & prevention for Covid-19

A

-convalescent plasma
-monoclonal Abs
-Interferons, steroids, stems cells - all try to reduce cytokine storm
-Vaccines

43
Q

Dengue Fever

Where is it found

Signs & Symptoms

A

-Urban adapted Aedes aegypti mosquito (vector)
-Expanding globally (50mil infections /100 countries)
-caused by positive-sense of RNA viruses (Flavivirus genus)

-Endemic to tropical/subtropical latitudes (India, Southeast Asia) & now Florida & coastal Texas

-Incubation of 3-5 days - mostly asymptomatic
w/ wide variety of clinical manifestations
Range from mild/server to fatal disease

44
Q

What are the three phases of Dengue Fever

A
  1. Initial febril phase
  2. Critcal phase at about time the fever subsides
  3. Final spontaneous recovery phase
45
Q

What are the factors of modern Dengue fever pandemic

A

-Global trade
-increases travel by viremic people
-urban crowding
-ineffective mosquito control

46
Q

Dengue Fever testing

&

Treatment

A

-Viral component testing
-detection of viral nucleic acid in serum by RT-PCR
-Serologic testing
-Detection of IgM seroconversion by ELISA

No current antiviral agents to treat
ONLY supportive treatment

47
Q

Function of the TORCHE(S) testing Panel

A

To detect infection that pregnant women may have that can affect the fetus

T - Toxoplasma gondii
O - Other (viruses: HIV, Hepatitis, Varicella, Parvovirus)
R - Rubella
C - Cytomegalovirus
H - Herpes simplex
(S) - Syphilis may be added for TORCHES

48
Q

Host of Toxoplasmosis
&
Three primary routs of transmission for Toxoplasmosis

A

Common house cat (oocytes present in their feces)

-Foodborne
-Animal to human (zoonotic)
-Mother to child (congenital)

49
Q

Sources of Toxoplasmosis

A

-Fecal contamination of food/water
-Inadequate hand-washing
-raw milk
-Inadequately cooked or infected meat
-lab workers thru accidental inoculation

50
Q

True or False
Oran transplants recipients can be infected from infected donor

A

True

51
Q

True or False
Transfusion transmitted is seen in leukocyte concentrates

A

TRUE

52
Q

True or False
Immunosuppressive agents are NOT associated with increased risk of contracting toxoplasmosis?

A

FALSE - you are at risk

53
Q

Transplacental Transmission of Toxoplasmosis

A

-all mammals can do this
-6/1000 pregnant women aquire primary infection during gestation
-45% untreated women = congenital infected babies
-All pregnant women should get tested for it

54
Q

Seroprevalence of toxoplasmosis

A

-96% of Wester Europe can
-10-40% in U.S.
AIDS patient who are seropositive
-25-50% will develop toxoplasmic encephalitis

55
Q

Signs & symptoms of Toxoplasmosis

A

-Adults/ children (NOT newborns) = Asymptomatic, but still has generalized infection
-Immunosuppressed = toxoplasmic encephalitis => death even w/ treatment

56
Q

Prevention of congenital transmission

A

-avoid touching MM while touching raw meat
-wash hands & wash kitchen surfaces
-cook meat to 18.8 (65.8F)
-wash fruits & veggie before consumption / protect from insects
-avoid cat poop from liter boxes/ gardening (wear gloves)

57
Q

Symptoms of acquired Toxoplasmosis

A

-Mild (infectious mononucleosis - chills, fever, headache, fatigue) BUT can become chronic (lymphadenopathy) in immunocompromised ppl.
-reactivation of cerebral toxoplasmosis not uncommon in AIDS Pts.

58
Q

Symptoms of congenital infection

A

-Harmful to fetus w/ infected mothers
-Can result in CNS malformation/ prenatal mortality
-75% of infected newborns not diagnosed at birth will be discovered when symptoms become apparent
(Blindness, encephalomyelitis, mental retardation, convulsions & death)

59
Q

Diagnostic evaluation of toxoplasmosis

A

-serologic, IgG determines if person is infected
-IgM along w/ avidity tests
-Direct observation of parasite in stained tissues/ biopsys
-molecular techniques for DNA in amniotic fluid

60
Q

Issues with serological tests and toxoplasmosis

A

-Relatively high proportions of people have Abs to T. Gondii => makes interpretation difficult
-IGM => frequent FALSE positives & negatives (in adults)
-IgG => appear 1-2wks after initial infection, Peak at 6-8wks, decline gradually, can persist for life

61
Q

Difference in Toxoplasmosis Avidity test for IgG
low avidity vs HIGH avidity

A

Low = infection w/in past 8months
high= infection 5 or more months before assay performed

62
Q

Toxoplasmosis Sabin-Feldman Dye test (DT)

A

-Sensitive & specific neutralization - was gold standard
-live organisms are lysed in presence of complement & Pts serum
-Negative = rules out infection (unless Pts is Hypogammaglobinemic)

63
Q

Toxoplasmosis Indirect fluorescent Ab test (IFA)

A

Uses killed organisms as substrate w/ Pts serum agains them
-measures same Abs as DT
-False positives can occur with sera w/ antinuclear Abs
-False negative with Pts w/ low titers

64
Q

Toxoplasmosis and Polymerase chain reaction (PCR)

A

-Performed mainly on amniotic fluid
-Used to detect DNA in body fluids & tissues
-Negative doesn’t rule out PCR inhibitors in serum

65
Q

Toxoplasmosis and histological diagnosis

A

-Wright-Giemsa stain can be used
-Demonstration of tachyzoites in tissue or body fluid smears - diagnosis of acute infection

66
Q

Toxoplasmosis and cell culture tests

A

-Cell culture method using monocytes
-Uses immunofluorescence

67
Q

Rubella Etiology

A

-Acquired rubella = AKA german/3-day measles
-Enveloped RNA virus (Togaviridae family)
-Endemic to humans - highly contagious thru respiratory secretions
-occurred in childhood but also adults (before vaccine)

68
Q

Rubella epidemiology

A

-Epidemic proportions would occur at 6-9 year intervals
-High incidence of infection w/ epidemics in places w/o vaccines
-1964- >20,000 congenital rubella syndrome & unknown # of still births
-Live, attenuated vaccine in 1969

69
Q

Rubella epidemiology (w/ Immunizations)

A

-Need high rate immunizations to suppress epidemics
-U.S. average for vaccination is 92%
-unvaccinated kids = outbreaks w/ eroding head immunity
-Infection & vaccination = only way to develop immunity
-low titters still have immunity
-critical for women of childbearing age
-If women is not immune - should be vaccinated ASAP & NOT be pregnant for 3 months

70
Q

Rubella signs & symptoms

A

-Vary widely from person to person. Not recognized in some or may have a light rash
-May resemble other disorders like mono & drug induced rashes

71
Q

Aquired rubella infection

A

-Incubation 10-21 days (typically 12-14 days)
-Contagious for 12-15 days (5-7 days prior to rash)
-Acute infection last for 3-5 days (generally requires little treatment)
-Starts like cold->moves to lymph nodes-> maculopapular face rash (&neck + trunk)
-Mild in kids (self limiting)

72
Q

Congenital Rubella infection

A

-infected pregnancy = effects on fetus
-10-20% infected in utero => dies w/in 18 months
-point of gestation greatly affects severity (earlier is worse)
-Fatal abnomalitites: encephalitis, hepatomegaly, bone defects, metnal retardation, cataracts, thrombocytopenic purpura, cardio defects, splenoMegaly, microcephaly, low birth weight & failure to thrive
-Most have immunity BUT 1/3 loose Ab & become susceptible - Need vaccine.

73
Q

Immunological manifestation of congenital Rubella syndrome

A

IgG can cross placental barrier BUT can tell difference b/w maternal & neonatal origin
-IgM is BEST for testing neonates. Can’t cross placental barrier. Therefore a Positive IgM is diagnostic in congenital rubella syndrome

74
Q

Immunological manifestations of acquired rubella infections

A

-IgM are detectable a few days after signs & symptoms
-Peak at 7-10 days
-Persists but diminish over 4-5wks until gone
-IgG Abs increase rapidly 7-21 days then lvl off/ decrease in strength
-Remain present & protective indefinitely
-Useful indicator in paried specimen testing

75
Q

Diagnostic evaluation for Rubella

A

-Cross reactivity seen w/ parovirus IgM
-Ppl w/ mono can sometimes have rubella-specific IgM in low concentrations
-Pregnant women can demonstrate IgM Abs also to CMV, varicella, & measles virus

76
Q

Rubeola (Measles)

NOT the same as Rubella

A

-Humans only reservoirs
-Rubeola (virus) = Measles
-HIGHLY infectious (90% in non-immunized) via respiratory droplets
-Single-strand RNA virus = genus Morbillivirus (paramyxoviridae)

77
Q

Epidemiology of Rubeola (measles)

A

-No endemic since 1990’s
-High rate of vaccination
-small outbreaks only in unvaccinated ppl

78
Q

How to prevent Rubeola (measles)

A

-MMR vaccine (live attenuated virus )
-Pregnant / immunosuppressed should avoid vaccine
-given @ 12-15months (AGAIN @ 4-12yrs)

79
Q

Laboratory testing for Rubeola (measles)

A

-Measles-specific IgM Abs in serum
-Isolation of measles virus
-Detection of RNA by nucleic acid amplification
-Acute infection confirmation using IgM & IgG serial testing
-Seroconversion after immunization

80
Q

Cytomegalovirus (CMV) - is a Herpes virus

A

-Large enveloped DNA virus (replicative cycle w/ DNA expression & nucleocapsid assembly w/ nucleus)
-All share characteristic of being cell associated
-World wide infection (U.S. 50-80% demonstrate infection)
-Pregnant/ immunocompromised ppl are at major risk

81
Q

How is Cytomegalovirus transmitted

A

-Oral, respiratory, veneral (all body secretions)
-Blood transfusion (need to screen donors)
-Pregnant women can transmit to fetus
-Postnatal (breast milk) can lead to morbidity/mortality of VLBW infants

82
Q

True or False
Once Cytomegalovirus in human body it stays for life

A

True

83
Q

True or False
Most CMV infections are silent

A

True

84
Q

Latent Cytomegalovirus infections

A
  • CMV can be persistent in latent state - infections characterized by periods of reactivation
    -Active CMV can occur in pregnancy, immunosuppressed, after bone/organ/stemcell transplants
    -High risk mortality are allograft transplants (negative patient w/ seropositive donor)
85
Q

Congenital infection of Cytomegalovirus

A

-MOST common virus transmitted to fetus (Mom transmission in utero)
-Mom w/ Ab to CMV prior to conception provides protection to newborns
-1 in 150 children born w/ congenital CMV infections
-1 in 5 born w/ be ill or will have long term health problems

86
Q

Signs & symptoms of Cytomegalovirus

A

-Incubation period 3-12wks
-Asymptomatic (usually) & can develop mono like symptoms (sore throat, fever, swollen glands, chills, malaise & myalgia + Lymphadenopathy & splenoMEGALY)
-uncommon complications (intersitial pneumonitis, hepatitis, G-Barre syndrome, meningoencephalitis, myocarditis, thrombocytopenis, hemolytic anemia)
-life threatening to immunosuppressed Pts

87
Q

Three types of transfusion in acquired Cytomegalovirus infections

A

-Primary infection
-Reactivated infection
-Reinfection

88
Q

True or False
Newborns w/ CMV are more prone to cytomegalic inclusion disease (CID)

A

TRUE

89
Q

True or False
Severe for of CMV doe not cause permanent neurologic issues

A

False
-Can be permanent
-Hearing lsoss in 20-50%
-Visual impairment in 20%

90
Q
A

Clinical Immunology (14 decks)

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