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Septicemia, Bacteremia, Toxemia | back 1 -
What?
-
Septicemia: any microbial blood infection producing
illness.
-
Lymphangitis: infection and inflammation of
lymphatic vessels is a sign of septicemia
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Bacteremia: septicemia caused by
bacteria
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Toxemia: bacteria remain at infection site; release
toxins into blood
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Signs/Symptoms?- fever, chills, nausea, vomiting,
diarrhea, malaise
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Septic shock: systemic inflammation = extremely
low blood pressure from dilation of vessels
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Osteomyelitis: inflammation of the bones (if
bacteria invade bones)
-
Toxemia symptoms:
Exotoxin= cytotoxins, neurotoxins;
Endotoxin: cause fever, disseminated
intravascular coagulation, damaged leaky blood vessels and
inflammation lead to low blood pressure = shock
-
Diagnosis?- signs/symptoms (only ~50% patients have
bacteria cultured from blood)
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| back 2 -
What?- fever, extreme fatigue, malaise, difficulty
breathing, and tachycardia (fast heart rate);
Inflammation of endocardium (lining inside
heart) and vegetations (bulky mass of
platelets/clotting to bury bacteria, hiding them from immune
system and drugs); embolus (pieces of
vegetation/clot) may break off and block vessels
-
Who?- many bacteria, opportunistic, microbiota;
“viridans streptococci” (green pigment in blood
culture)= 1/2 infections
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Diagnosis?- visualize vegetations via echocardiogram;
culture bacteria from blood
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| back 3 -
What?- fluctuating fever strikes every afternoon;
chills, sweating, headache, myalgia, and weight loss
-
Who?-
Brucella
: nonmotile, g(-), coccobacilli, no capsule;
endotoxin causes some signs/symptoms; intracellular in uterine,
placental, and phagocytic cells
-
How?- contaminated dairy products, animal blood,
urine, or placentas; invades through breaks in mucous membrane and
travels via phagocytes
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Diagnosis?- serological (Ab) test;
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Treatment?- usually no treatment needed; attenuated
vaccine for animals only
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| back 4 -
What?- skin lesions, swollen lymph nodes @ infection
site; then ascending lymphangitis; general
manifestations can last months/years
-
Who?-
Francisella
: small, nonmotile, obligate aerobe, g(-)
coccobacillus, capsule blocks phagocytosis, endotoxin causes many
symptoms; can survive phagocytosis by blocking fusion of lysosome
to phagosome; has beta-lactamase
-
How?- via tick bite or contact w/infected animals;
small, can enter
microabrasions; contact w/dead animals= highest
risk
-
Diagnosis?- difficult, general symptoms, serological
test needed which can take weeks to get results
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Treatment?- Abx; vaccine for high risk
people
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| back 5 -
Bubonic plague: enlarged lymph nodes called
buboes suddenly appear; then tissue death,
subsequent gangrene (Clostridium)
;
Pneumonic plague: bacterium inhaled or spreads to
lungs from blood; develops rapidly (hours)
-
Who?-
Yersinia pestis
: g(-) bacillus with capsule; virulence factors=
adhesins, capsule, T3SS (antiphagocytic proteins block adaptive
immune response)
-
How?-
bubonic: forms biofilm in flea esophagus,
starving flea rapidly spreads; endemic in rodents, other mammals =
amplifying hosts; contact w/flea feces and infected animals can
spread; untreated = 50% fatal <week.
Pneumonic: aerosols/ sputum spread, up to 100%
fatal
-
Diagnosis?- symptoms (can be nonspecific)
-
Treatment?- Abx, rodent/flea control, good
hygiene
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| back 6 -
What?- three phases in untreated: bulls-eye
rash, neurological symptoms (ie. meningitis), and severe
arthritis (caused by immune response) that can last years; rarely
fatal
-
Who?-
Borrelia
- g(-) large spirochete; uses manganese instead of
iron for metabolism, alters membrane proteins= evades defenses;
dies=endotoxin
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How?- via deer tick, needs to be
attached 36-48 hrs to infect w/enough bacteria; people moving to
woodland areas and protected deer populations = infection rates
going up
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Diagnosis?- signs/symptoms; bacterium rarely
detected, serological for Ab needed
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Treatment?- early phase = Abx; late phase = difficult
b/c immune system causing most symptoms
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Mononucleosis (Kissing disease; Mono) | back 7 -
What?- sever sore throat, fever; then swollen lymph
nodes, fatigue, appetite loss. Immune system against infected B
cells
-
Who?- Epstein-Barr Virus (EBV,
HHV-4): Nveloped dsDNA virus, icosahedral capsid;
established latent infection replicating in nucleus; suppresses
B-cell apoptosis; can lead to burkitt’s lymphoma
and other cancers in certain parts of the world
-
How?- via saliva; infects B cells which must be
killed by cyto-T cells; majority of adults have Ab against
EBV
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Diagnosis?- presence of large, lobed B-cells and
neutropenia (neutrophil deficiency)
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Treatment?- relieve symptoms; too widespread to
prevent
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| back 8 -
What?- most asymptomatic; in fetus, newborn,
immunocompromised causes hepatomegaly, splenomegaly, jaundice,
anemia; may be teratogen
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Who?- Cytomegalovirus (CMV): a
herpesvirus, infects early in life and remains latent until
immunocompromised
-
How?- via bodily secretions: STD, in utero,
transfusions; 50-100% adults
-
Diagnosis?- signs (enlarged cells, etc)
-
Treatment?- Fomivirsen (RNAi drug) stops spread;
doesn’t cure
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| back 9 -
What?- 3 stages: fever, headache, muscle aches; then
remission period; then delirium, seizures, coma,
hemorrhaging
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Who?- yellow fever virus (a
flavivirus
): enveloped ssRNA(+), icosahedral capsid;
Aedes
mosquito vector; monkey reservoir
-
How?- via
Aedes
bite; travels to liver to replicate; today in South
America and Africa; hasn’t returned to US; 20% mortality
rate
-
Diagnosis?- detect viral Ag in blood
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Treatment?- supportive care, vaccine available,
mosquito control
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| back 10 - What?- DF two stages: fever, edema, head and
muscle pain; then fever returns and red rash. Dengue
hemorrhagic fever (DHF): internal bleeding, shock,
possibly death= severe hyperimmune response to second viral
infection
- Who?- Dengue viruses
1, 2, 3, and 4 (flavivirus): enveloped ssRNA(+),
icosahedral capsid
- How?- Aedes
bite, infects monocytes, 1st infection mild, 2nd
severe
- Diagnosis?- signs/symptoms of people who travel to
endemic area; coming back in Florida and Texas
- Treatment?-
control mosquitoes; vaccine would be bad if it
can’t stop hemorrhagic fever once Ab recognize it
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African Viral Hemorrhagic Fever | back 11 -
What?- fever, fatigue, dizziness, muscle pain,
exhaustion; then minor capillary hemorrhaging
(petechiae); finally severe internal
hemorrhaging, bleeding from orifices; death from shock,
seizures, or kidney failure
-
Who?-
Ebolavirus
and
Marburgvirus
: ssRNA(-), filamentous capsid; infected macrophages
induce localized blood clotting, depletes clotting
proteins = susceptible to massive bleeding
-
How?- contact of bodily fluids of infected person;
possible bat vector; no carrier state; mostly
found in Africa
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Diagnosis?- symptoms and finding virus in
blood
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Treatment?- fluid/electrolyte replacement; possible
vaccines being studied
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| back 12 -
What?- fevers, chills on 2-3 day cycle correlating to
cell lysis; anemia, fatigue, weakness
-
Who?-
Plasmodium
, 4 species,
P. falciparum
most severe,
P. vivax
also common; vector is
Anopheles mosquito; Lifecycle;
Virulence factors on guide if time
available
-
How?-
P. falciparum
most severe because adhesins making RBCs stick to
capillary walls block blood flow = hemorrhaging and tissue death;
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Diagnosis?- Identify
Plasmodium
in blood
-
Treatment?- species dependent, many resist
chloroquine; heterogenous sickle cell trait = resistance; Duffy
resists
P. vivax
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| back 13 -
What?- most asymptomatic; poor immunity = fever,
malaise, inflammation of lungs, liver, and heart;
Contraction during pregnancy bad
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Who?-
Toxoplasma gondii
: cats definitive hosts; apicomplexan
-
How?- ingest oocysts from contaminated food, cat
fecal matter on hands; pseudocysts ingested from undercooked meat;
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Diagnosis?- detect in tissues
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Treatment?- only with immunocompromised and pregnant;
sulfonamides
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| back 14 -
What?- swelling, nonspecific symptoms; chronic
manifestations many years after infection leading
to heart failure
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Who?-
Trypanosoma cruzi
: endemic in south and central America;
Triatoma
is vector; circulates in bloods with intracellular
stage in macrophages and heart muscle cells
-
How?-
Triatoma
feces rubbed into bite; a leading cause of death in
Latin America
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Diagnosis?- identify trypanosomes microscopically;
xenodiagnosis (sterile bug takes blood meal, dissect bug a
month later)
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Treatment?- can only treat early stage (only 1%
develop early symptoms)
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| back 15 -
What?- parasitic blood fluke (very common); transient
dermatitis due to larval burrowing; eggs in other parts of body
can calcify and cause renal failure, heart failure, bladder
obstruction, death
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Who?-
Schistosoma
(blood fluke, 3 species): larvae from
freshwater snails penetrate human skin, mature
and breed in humans, eggs passed into environment via urine or
feces, eggs hatch into a different larvae type that infects
snails.
-
How?- swim in ponds with infected snails; not in
US
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Diagnosis?- identify spiny eggs in stool or urine
sample;
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Treatment?- praziquantel
drugs
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Normal Microbiota of the respiratory system | back 16
Upper respiratory system only:
Haemophilus
,
Veillonella
,
Staph. aureus
, diphtheroids (harmless g(+) that resemble
C. diphtheriae
), other g(-) cocci, and alpha-hemolytic streptococci
including
Strep. pneumoniae |
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Streptococcal Respiratory Diseases | back 17 -
What?- sore throat, difficulty swallowing,
can progress to scarlet or rheumatic
fever
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Who?- group A strep-
Strep. pyogenes
: g(+) cocci, beta-hemolytic, many virulence factors;
occurs when microbiota depleted, large inoculum introduced, or
adaptive immunity impaired
-
How?- respiratory droplets; often in winter or
spring
-
Diagnosis?- often confused with viral pharyngitis;
streptococci in throat not diagnostic b/c normal part of pharynx
microbiota; must verify species
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Treatment?- penicillin
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| back 18 -
What?- sore throat, fever, oozing intracellular fluid
thickens into thick pseudomembrane that can
obstruct airways
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Who?-
Corynebacterium diphtheriae
: High G+C, pleomorphic; diphtheria toxin stops
protein synthesis = cell death
-
How?- respiratory droplets or skin contact with
non-immunized (100,000s/yr to 2/yr today) or
immunocompromised
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Diagnosis?- presence of pseudomembrane
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Treatment?- antitoxin and Abx; immunize!
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Sinusitis and Otitis Media | back 19 -
What?- sinusitis: pain and pressure
in affected sinus (common in adults); otitis
media: severe ear ache (common in kids)
-
Who?- various microbiota (ie
Strep. pneumoniae, Strep. pyogenes, Haemophilus,
Moraxella, Staph. aureus)
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How?- bacteria in pharynx spread into sinuses via
throat
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Diagnosis?- symptomatic
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Treatment?- penicillin; no prevention
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| back 20 -
What?- sneezing, runny nose, congestion, malaise,
sore throat, and cough; lasts ~week; usually no
fever
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Who?- over 200+ strains;
Rhinovirus
most common cause: ssRNA+ naked polyhedral; attaches
to ICAM-1 protein in nasal cavity cell cytoplasmic membranes;
grows best at 33C and neutral pH; lytic;
infected cells lose ciliary action, slough off, trigger
inflammatory cytokines; stimulated nerves trigger mucus production
and sneezing; localized inflammation = congestion
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How?- aerosols via sneezing/coughing, fomites,
contact
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Diagnosis?- symptomatic
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Treatment?- symptom relief
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| back 21 -
lobar; 85% of pneumonia cases; short, rapid
breathing; rust colored sputum; neutrophils in sputum
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Who?-
Strep. pneumoniae
: g(+); adhesins, capsule, and toxin pneumolysin
(binds cholesterol in PM of ciliated cells, creates pores that
lyses them; neutralizes lysosomes in phagocytes)
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How?- inhalation into (usually damaged) lungs;
bacteria endocytosed by lung cells, replicate and lyse, damages
lining which allows fluid from blood into alveoli, WBC
attack bacteria causing inflammation and more
fluid
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Diagnosis?- streptococci in sputum smears
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Treatment?- penicillin; vaccine given to
kids
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Primary Atypical (Mycoplasmal) Pneumonia | back 22 -
pneumonia + mild symptoms including fever, malaise,
sore throat, excessive sweating
-
Who?-
Mycoplasma
: low G+C obligate aerobe, encapsulated, no cell
wall, sterols in PM, small; adhesion protein allows attachment to
base of cilia on epithelial cells
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How?- by nasal secretions
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Diagnosis?- difficult
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Treatment?- tetracycline or erythromycin
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Klebsiella Pneumonia (Nosocomial Pneumonia) | back 23 -
normal symptoms plus thick bloody sputum (destroys
alveoli) and recurrent chills; often
nosocomial
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Who?-
Klebsiella
: g(-) bacillus w/prominent capsule,
endotoxin
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Diagnosis?- symptomatic and culture from
sputum
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Treatment?- supportive; abx available but endotoxin
creates severe and permanent damage to lungs, sometimes
fatal.
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| back 24 -
What?- pneumonia symptoms, pulmonary fxn rapidly
decreases, 50% mortality if untreated
-
Who?-
Legionella
: g(-), aerobic, pleomorphic; nutrient
needy; intracellular parasite of freshwater
protozoan phagosomes, protozoa release bacteria-filled
vesicles that are inhaled by human host, into
macrophages
-
How?- survives in domestic water sources (showers,
hot tubs, AC) kills human cells, causes tissue damage and
inflammation, rarely spreads outside lungs
-
Diagnosis?- fluorescent Ab staining,
serological
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Treatment?- quinolone, macrolides; reduce bacteria in
water
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| back 25 - What?- fever, cough, fatigue, chest pain, wheezing, coughing up
blood, tubercles in lungs
- Who?-
Mycobacterium tuberculosis : mycolic acid =
slow growth and resistances, viable in aerosols for long time;
replicate freely in macrophages. Primary tb: can
develop tubercles (caseous necrosis in center). Secondary
tb: reactivation by escaping tubercle. Disseminated
tb: systemic infection (macrophages carry to other parts of
body)
- How?- inhaled; alveolar macrophages endocytose;
bacteria divide freely in macrophage; more macrophages come, get
infected or sequester into tubercle; center macrophages die =
caseous necrosis = stalemate; 10% people lose
stalemate, often decades later = reactivation
- Diagnosis?-
Tuberculin skin test, chest x-ray for tubercles,
- Treatment?- combo of drugs for months; resistant strains
emerging, BCG vaccine sometimes available (effective?)
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| back 26 -
What?- initially cold-like symptoms, then persistent
powerful cough that fatigues, turning blue, ruptured eye
vessels
-
Who?-
Bordetella
: small, aerobic, nonmotile, g(-) coccobacillus;
numerous virulence factors; bind cilia in trachea, stop ciliary
elevator, invade neutrophils, survive in phagosomes, invade
respiratory epithelial cells
-
How?- highly contagious via airborne respiratory
droplets, life threatening in children
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Diagnosis?- symptomatic
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Treatment?- supportive, prevent with DTaP
vaccine
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| back 27 -
What?- initially resembles cold or flu, then severe
coughing, lethargy, shock, and death
-
Who?-
Bacillus anthracis
: g(+), endospore forming, hemolytic, aerobic;
capsule and anthrax toxin kills human cells and edema
-
How?- contact or inhalation of anthrax, most
die
-
Diagnosis?- identify in sputum
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Treatment?- aggressive abx; vaccine for select
individuals
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| back 28 -
What?- sudden fever, pharyngitis, fatigue,
congestion, cough
-
Who?- Influenza virus A and B:
ssRNA(-), enveloped, HA and NA glycoprotein spikes.
NA hydrolyzes mucus to give access to cell
surface; HA attaches to host epithelial cells and
triggers endocytosis; symptoms are immune response to virus
(cytokines and inflammation); damages lung epithelium, secondary
bacterial infection possible (ie.
Haemophilus
)
-
How?- inhalation or self-inoculation; complications
most often in elderly, kids, weak immune system
-
Diagnosis?- symptomatic with community
outbreak
-
Treatment?- supportive care; yearly multivalent
vaccine
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SARS (severe acute respiratory syndrome) | back 29 -
What?- high fever, shortness of breath, difficulty
breathing; 10% mortality
-
Who?- a
Coronavirus
called SARS Virus: ssRNA(+),
enveloped, helical capsid
-
How?- via respiratory droplets
-
Diagnosis?- via signs/symptoms
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Treatment?- supportive treatment
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RSV (respiratory syncytial virus) | back 30 -
What?- most common respiratory disease in
newborns and young children; fever, runny nose,
cyanosis (blue cast to skin), coughing, sometimes
wheezing. Causes inflamed bronchioles
(bronchiolitis) and pneumonia in infants,
#1 respiratory killer of infants
worldwide
-
Who?- Respiratory Syncytial Virus
: ssRNA(-), enveloped; causes syncytia to form in
lungs, immune responses to RSV damages lungs
-
How?- via close contact (kissing, touching), fomites,
and sometimes respiratory droplets (less common)
-
Diagnosis?- symptoms and immunoassay
-
Treatment?- supportive care in young children; Ab
against RSV and inhaled ribavirin in severe cases
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Hantavirus Pulmonary Syndrome | back 31 -
What?- cough, shock, and labored breathing;
4-10 days after infection 50% die
-
Who?-
Hantavirus
: segmented (3 pieces) ssRNA(-), enveloped; invades
blood capillary walls and lungs, then widespread inflammation and
shock
-
How?- inhalation of mouse excrement;
not contagious by contact
-
Diagnosis?- based on symptoms
-
Treatment?- none; control rodents
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Coccidioidomycosis (Valley Fever) | back 32 -
What?- resembles pneumonia or TB, may become
systemic
-
Who?-
Coccidioides
: dimorphic soil Ascomycota
fungus; grow as mycelial filaments and produce spores in
soil
-
How?- inhalation of conidia by mammals,
converts to yeast form at body temp, germinate
in alveoli into spherules with lots of spores;
almost exclusive to southwestern US and northern
Mexico
-
Diagnosis?- presence of spherules in clinical
specimens
-
Treatment?- amphotericin B; masks reduce to conidia
exposure
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Histoplasmosis *** (Prof's fave) | back 33 -
What?- most common fungal systemic disease in humans;
asymptomatic in 95% of cases, otherwise coughing with bloody
sputum or skin lesions, splenomegaly, hepatomegaly
-
Who?-
Histoplasma capsulatum
: dimorphic soil ascomycete; in moist soils
with bird or bat droppings; yeast form pathogenic at
body temp
-
How?- inhalation, then intracellular in alveolar
macrophages, then spread systemically via blood/lymph; prevalent
in eastern US
-
Diagnosis?- identification from clinical
samples
-
Treatment?- no treatment needed in
immunocompetent
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Respiratory fungal pathogenesis | back 34
(1)Aerosolization of conidia;
(2)Inhalation of conidia by host;
(3)Travel into deep lung (alveoli);
(4)Encounter innate immune cells
- Fungal cell wall components: alpha and beta-glucan, specific
glycoproteins/polysaccharides
- Complement can bind wall;
macrophage complement receptor 3 (CR3) recognizes complement and
cell wall proteins
- Macrophage Dectin-1 recognizes
beta-glucan
- Macrophage TLR-2 and -4 recognize glycoproteins
and polysaccharides
(5) Conidia phagocytosed by macrophages; Two
options: some degraded by macrophages/ other immune cells,
some survive and replicate inside innate immune cells
(6) Dissemination to other organs: either degraded by
cell-mediated response in 7-10 days OR overwhelm
immune system=fungal sepsis |