Infectious diseases Flashcards
Characteristics of infectious diseases
-Influenced by both microorganism & host (health/age)
-Spread of organism (insects/travelers)
Development of infectious disease requires what in terms of the host?
-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
Traditional infectious lab testing
Streptococcal infections and syphilis are examples of what kind of infections
Bacterial infections
What substances are present in bacterial infections?
Lysosomes & phagocytosis is present— they are major immunologic defenses agains bacteria
Can microorganisms survive phagocytosis?
Yes, IF they have capsules~
capsules can release exotoxins, impede w/ attachement OR interfere w/ digestion.
What sets parasites infections apart from bacterial & viral infections?
Parasites
-Relatively large
-Resistant body walls
-Avoid phagocytosis by moving away from inflammation
what immune responses correspond to parasitic infections?
-immunoglobulins
-complement
-antibody dependent
-cell-mediated cytotoxicity
-cellular defenses (eosinophils & T cells)
Can cestodes be eradicated by the complement system?
Yes, but NOT all.
Some get opsonized by IgGs
What antibody is increased w/ helminth
IgEs
Are parasites affected by phagocytosis?
Yes, it may have SOME direct activity against parasites
Most effective protection against parasites are done by which immune response
Antibody dependent (Macrophages, Neutrophils, Eosinophils)
&
Cell mediated cytotoxicity
Cytotoxic cells are usually mediated by which immunoglobulin?
IgG
Eosinophil roles is what?
Complex lol
-may phagocytize immune complexes
-act as effector cells
Are T cells involved in parasitic infection
Yes, they;
-sequester microorganisms
-Helper T cells bring in B cells to specific organisms
Major protective mechanism against Giardia
-Nonspecific factors (non-stimulated monocytes)
-NK cells have direct activity to some parasites (& cancer)
True or False
Delayed hypersensitivity can prevent some parasitic infections
True, but can cause other diseases
Can parasitic infections can cause depositions of antigen-antibody complexes?
Yes, in cases of severe pathological lesions
True or False
Parasitic infections increase lvls of IgE and can lead to hypersensitivity
True, and can lead to anaphylaxis
True or False
Fungal diseases are only superficial
Flase
Normally superficially, but can enter via respiratory tract (spores) and cause systemic disease
Manifestation of disease depends on degree & type of immune response
True or False
Fungi can be harmless in mucuses membranes
True, it can also be found on the surface of the skin (candida albicans)
True or False
Fungi infections can be opportunistic agents
True, especially in immunocompromised ppl.
<—-Range from—->
unnoticed respiratory episodes to fatal hypersensitive reaction
What are the survival mechanisms of fungi
-Anti-phagocytic capsule
-Digestion resistance w/in macrophages
-Destroy phagocytes
Why are fungal infections increasing world wide?
-use of immunosuppressive drugs
-Diseases (AIDS) causing immunosuppressed hosts
True or False
Serologic tests play an important part in diagnosis of fungal infections
TRUE
True or False
Respiratory diseases are NOT associated with fungal infections
False- many fungal infections are associated w/ inhalation of spores.
reservoirs = dust, bird droppings, soil
Histoplasmosis
(Histoplasmosis capsulatum)
where is it found?
how is it transmitted?
symptoms?
diagnostic?
-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
Aspergillosis
What kind of reactions
Diagnostic
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)
Name the three forms of coccidiodomycosis
Pulmonary - primary
cutaneous - secondary
disseminated (spread thru out body)
Coccidiodmycosis
where is it found
how is it transmitted
diagnostic
-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)
North american blastomycosis
Symptoms
diagnostic
-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)
Sporotrichosis
(sporothrix schenckii)
symptoms
Progressive, subcutaneous lymphatic mycosis & chronic
-sporotrichotic chancre at side of innolculation ->nodules along lymphatics
-associated w/ injuries caused by thorns
Three forms of Sporotrichosis
Respiratory
lymphatic (MOST common)
-disseminated
Cryptococcus
(C. neogormans)
how is it transmitted?
symptoms?
-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
Viral
Richettsial
&
Mycoplasmal diseases
-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
Intermediate b/w virus & bacteria = obligatory intracellular organisms
Rickettsiae are closer to?
contain cell walls - closer to viruses
Intermediate b/w virus & bacteria = obligatory intracellular organisms
Mycoplasma are closer to?
W/o cell walls - closer to bacteria
Covid-19
-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
Covid-19 & ACE2 receptor
-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
What are the 4 main structures of the corona virus
N - Nucleocapsid
S - Spike
M - Membrane
E - Envelope
Testing options for Covid-19
-Molecular based techniques & serological (Ab testing)
-Initial Emergency Use Authorization (EUAs)
-Real-time PCR (needs adequate viral load)
-Pooled testing
Treatment & prevention for Covid-19
-convalescent plasma
-monoclonal Abs
-Interferons, steroids, stems cells - all try to reduce cytokine storm
-Vaccines
Dengue Fever
Where is it found
Signs & Symptoms
-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
What are the three phases of Dengue Fever
- Initial febril phase
- Critcal phase at about time the fever subsides
- Final spontaneous recovery phase
What are the factors of modern Dengue fever pandemic
-Global trade
-increases travel by viremic people
-urban crowding
-ineffective mosquito control
Dengue Fever testing
&
Treatment
-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
Function of the TORCHE(S) testing Panel
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
Host of Toxoplasmosis
&
Three primary routs of transmission for Toxoplasmosis
Common house cat (oocytes present in their feces)
-Foodborne
-Animal to human (zoonotic)
-Mother to child (congenital)
Sources of Toxoplasmosis
-Fecal contamination of food/water
-Inadequate hand-washing
-raw milk
-Inadequately cooked or infected meat
-lab workers thru accidental inoculation
True or False
Oran transplants recipients can be infected from infected donor
True
True or False
Transfusion transmitted is seen in leukocyte concentrates
TRUE
True or False
Immunosuppressive agents are NOT associated with increased risk of contracting toxoplasmosis?
FALSE - you are at risk
Transplacental Transmission of Toxoplasmosis
-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
Seroprevalence of toxoplasmosis
-96% of Wester Europe can
-10-40% in U.S.
AIDS patient who are seropositive
-25-50% will develop toxoplasmic encephalitis
Signs & symptoms of Toxoplasmosis
-Adults/ children (NOT newborns) = Asymptomatic, but still has generalized infection
-Immunosuppressed = toxoplasmic encephalitis => death even w/ treatment
Prevention of congenital transmission
-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)
Symptoms of acquired Toxoplasmosis
-Mild (infectious mononucleosis - chills, fever, headache, fatigue) BUT can become chronic (lymphadenopathy) in immunocompromised ppl.
-reactivation of cerebral toxoplasmosis not uncommon in AIDS Pts.
Symptoms of congenital infection
-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)
Diagnostic evaluation of toxoplasmosis
-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
Issues with serological tests and toxoplasmosis
-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
Difference in Toxoplasmosis Avidity test for IgG
low avidity vs HIGH avidity
Low = infection w/in past 8months
high= infection 5 or more months before assay performed
Toxoplasmosis Sabin-Feldman Dye test (DT)
-Sensitive & specific neutralization - was gold standard
-live organisms are lysed in presence of complement & Pts serum
-Negative = rules out infection (unless Pts is Hypogammaglobinemic)
Toxoplasmosis Indirect fluorescent Ab test (IFA)
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
Toxoplasmosis and Polymerase chain reaction (PCR)
-Performed mainly on amniotic fluid
-Used to detect DNA in body fluids & tissues
-Negative doesn’t rule out PCR inhibitors in serum
Toxoplasmosis and histological diagnosis
-Wright-Giemsa stain can be used
-Demonstration of tachyzoites in tissue or body fluid smears - diagnosis of acute infection
Toxoplasmosis and cell culture tests
-Cell culture method using monocytes
-Uses immunofluorescence
Rubella Etiology
-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)
Rubella epidemiology
-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
Rubella epidemiology (w/ Immunizations)
-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
Rubella signs & symptoms
-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
Aquired rubella infection
-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)
Congenital Rubella infection
-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.
Immunological manifestation of congenital Rubella syndrome
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
Immunological manifestations of acquired rubella infections
-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
Diagnostic evaluation for Rubella
-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
Rubeola (Measles)
NOT the same as Rubella
-Humans only reservoirs
-Rubeola (virus) = Measles
-HIGHLY infectious (90% in non-immunized) via respiratory droplets
-Single-strand RNA virus = genus Morbillivirus (paramyxoviridae)
Epidemiology of Rubeola (measles)
-No endemic since 1990’s
-High rate of vaccination
-small outbreaks only in unvaccinated ppl
How to prevent Rubeola (measles)
-MMR vaccine (live attenuated virus )
-Pregnant / immunosuppressed should avoid vaccine
-given @ 12-15months (AGAIN @ 4-12yrs)
Laboratory testing for Rubeola (measles)
-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
Cytomegalovirus (CMV) - is a Herpes virus
-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
How is Cytomegalovirus transmitted
-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
True or False
Once Cytomegalovirus in human body it stays for life
True
True or False
Most CMV infections are silent
True
Latent Cytomegalovirus infections
- 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)
Congenital infection of Cytomegalovirus
-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
Signs & symptoms of Cytomegalovirus
-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
Three types of transfusion in acquired Cytomegalovirus infections
-Primary infection
-Reactivated infection
-Reinfection
True or False
Newborns w/ CMV are more prone to cytomegalic inclusion disease (CID)
TRUE
True or False
Severe for of CMV doe not cause permanent neurologic issues
False
-Can be permanent
-Hearing lsoss in 20-50%
-Visual impairment in 20%
