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234 Cards in this Set
- Front
- Back
How many types of Hepatitis
|
6: A-E and G
|
|
Hepatitis A
|
Picrona virus
called Heprna acute |
|
Hep B
|
Hepadna
chronic |
|
Hep C
|
flavivirus (rna)
chronic |
|
Hep D
|
Delta virus (rna)
needs Hep B |
|
Hep E
|
Rna virus
resembles Hep A |
|
Hep G
|
Flavivirus (rna)
chronic |
|
Hepatitis similarities (3)
|
less similar than different
- all liver - cause icteric jaundice - can be asymptomatic, causing transmission from one person to another |
|
Hepatitis difference (6)
|
- structures
- mode of replication - transmission - timing - disease course -sequelae |
|
HAV known as
old term basics of infection |
infectious hepatitis
Enterovirus 72 asympt. 1 mo.--> abrupt sx. --> rarely fatal |
|
HBV- aka
structure infection transmission infection basics |
Serum hepatitis
hepadna virus blood, sexual activity, dirt needle, perinatal infection 3 mo incubation, insidious onset of jaundice. |
|
% of HBV --> chronic
can lead to Fraction of people CDC estimates have/ had HBV |
5-10%
PHC 1/3 |
|
PHC
|
primary hepatocellular carcinoma
|
|
HCV
how many people have it route of infection |
flavivirus-- often goes chronic
~170 million carriers blood, needles, sex, perinatal |
|
HGV
|
flavivirus
similar to HCV chronic |
|
HEV unique because
structure resembles |
own family
RNA virus HAV, but enteric encapsulated |
|
HDV called
unique because |
Delta hepatitis
- needs HBV to infect -- envelope from HBV |
|
HAV acquired through
|
contaminated h20
- shellfish bivalves, filter feeders, other food |
|
structure of HAV
|
naked
icosaherdral capsid only 1 serotype |
|
Replication of HAV occurs
|
in liver, few other cells
slow released through exocytosis |
|
Disease process of HAV
|
presympt. ingestion-- > oropharynx --> gut --> blood --> liver --> rep --> released in bile and stool
sx. show after stool |
|
Outbreaks of HAV occur in
|
restaurants, daycares, poor hygiene and overcrowding
|
|
Sx. of hAV
|
acute onset of sx.
15-20 days post exposure--> prodrome 4-6 days later intensify --> jaundice dark urine and pale stools with increasing bilirubin abdominal pain itching |
|
HAV affects age worse
|
adults
70% --> jaundice kids, 10% --> jaundice |
|
HAV viral particle shed when
|
~ 14 days pre sx. until before sx. disappear
|
|
Danger of HAV
|
fulminant hepatitis (80% mortality)
|
|
Unique thing of HAV sx.
|
no rash or arthritis
|
|
Dx. of HAV
treatment prevention vaccine |
serologically
normally self limiting (IgG if exposed pre sx) wash hands, good hygiene killed HAV vaccine for travelers HAV only infects HUMANS!! |
|
HBV basics
|
concerned for transfussions and health care workers
only infects humans and chimps can also attack kidney and pancreas |
|
Structure of HBV
|
enveloped small DNA virus
retroviral-like, can't insert genome because lacking integrase codes via rtase with rna intermediate |
|
Dane particle
has (4) |
virion of HBV
protein kinase, polymerase with Rtase, ribonuclease H, P protein |
|
What is important for dx in HBV
|
antigens
HBcAg HBsAg HBeAg |
|
HBsAG called
has |
Australian Ag
surface antigen 3 glycoproteins (L,M,s) group/ type specific (a: d or y: w or r) |
|
HBcAg
|
core antigen
|
|
HBsAg- L glycoprotein
|
binds
sandwiches between liver and virion |
|
HBsAG s glycoprotein
|
major component of surface Ag
|
|
Group of HBV
|
a
|
|
Type of HBV
|
d or y
and w or r |
|
Which two antigens of HBV share structure properties
|
HBcAg and HBeAg
|
|
HBV replication
|
via rna intermediate
process and release Ag decoy mlcls (HbsAg) |
|
3 mrnas of HBV
|
3500- Hbc and HBe, polymerase and DNA primer
2100- S and M glycoproteins 2400- L glycoproteins |
|
Pathogenesis of HBV
|
acute or chronic
sympt. or asymptom. |
|
different stages of HBV
|
active- HBsAg and HBeAg found
3 days until replication sx. occur within 45 days HBsAg shows active defense |
|
sx of virus depends on (3)
|
dose
route health |
|
HBV can go latent by
|
incorportaion into hepatocytes
|
|
"ground glass" appearance
|
HBV when filamentous surface Ag clump
|
|
HBV can cause type 3 _______
|
hypersensitivity reaction
arthralgia, rash, renal inv. |
|
% infants get HBV
|
90 are chronic carriers, no sx.
|
|
% HBV --> chronic
- % develop chronic active hepatitis % of HBV --> fulminant |
5-10%
- 1/3 1% |
|
PHC process
|
damage to cells --> repair --> damage --> repair
genetic rearrangement-- oncogenic mutation |
|
Chronic Ag of HBV
|
HBcAg
|
|
treatment of HBV
|
HBIgG
drugs inhibiting reverse transcriptase |
|
Vaccines of HBV for
made of |
health care workers, infants/ children
plasmid to yeast (not killed) 3 injections (0, 1mo, 6 mo) 5% don't seroconvert |
|
HBVirus is immune to
|
detergents!
|
|
HCV first found in
first called |
1989- chimp infected with person blood
NANBH |
|
NANBH
HCv also called |
nonA nonB hepatitis
Hepacivirus |
|
HCv bad rap because
|
major cause of post-transfusion hepatitis
|
|
HCV is mainly ____ which can lead to ___ and ____
|
chronic
cirrhosis cancer |
|
Structure of HCV
|
enveloped flavivirus
no vaccines --> extremely variable 2 glycoproteins |
|
glycoproteins of HCV characteristics
|
mutations, antigenic variablitis, 6 clades
|
|
process of transmission in blood (HCV)
|
binds to hepatocytes and B lymph
coated with lipoproteins LDL and VLDL - enters via lipoprotein reveptors of cell |
|
HCV causes
|
persistent infection --> no cell apoptosis --> cancer
|
|
transmission of HCV
highest risk |
blood, sex
iv drugs, tatuoos, transfusion/ organ transplants, hemophiliacs (factors Viii and Ix) |
|
clinical sx of HCV
|
15%recover fully
15% cirrhosis rapid onset 70% persistent -- 40% asx. --> chronic 60% chronic -- 6% liver fail, 20% cirrhosis, 4$ carcinoma |
|
timeline of HCV
|
1-3 wks viremia
acute--> 4-6 mo persistent >10 yrs |
|
Dx of HCV
treatment |
anti-HCV shows exposure
RtPCR interferon alpha and/or regylated interferon and/or riboviran 50% recovery |
|
HDV is mainly a
needs because |
fulminant hepatitis
HBV to infect can't replicate all proteins |
|
Structre of HDV
|
circular ssRNA
-looks like rods delta Ag core with HBsAg envelope |
|
replication of HDV
|
host RNA pol --> repl. RNA genome
forms ribozyme cleaves RNA circle --> small Delta Ag infect host and mutates D Ag - makes large D Ag inorporates with HBsAg --> virion formed and released |
|
enxyme used to mutate Small Delta Ag
|
ds-RNA activated adenosine deaminase
|
|
Transmission of HDV
|
blood, body fluids
needs active HBV donor |
|
super infection of hepatitis
|
HBV in host --> then infected with HDV
|
|
Epidemiology of HDV
|
world wide
most prevelent in drug users |
|
clinically HDV (and HBV)
|
most severe form of hepatitis
- hepatitis encephalopathy -extreme jaundice -massive liver necrosis (80% fatal) |
|
Dx of HDV
treatment vaccine |
Anti-HDV
serology and RtPCR none HBV vaccine protects against HDV |
|
HEV aka
|
Enteric or epidemic hepatitis
similar to HAV fecal/oral transmission |
|
HEV resembles
Sx. mortality |
calcivirus
only acute similar to HAV-- sx appear later 10x mortality compared to HAV -- very serious in pregnancy |
|
4 classes of fungi known to cause human disease
|
zygomycetes
basidiomycetes archiascomycetes hemiascomycetes |
|
Taxonomy of fungi based on
|
morphology and mode of spore production
|
|
taxonomy of fungi will change based on
|
ultrastructural functions
biochem characteristics molecular characteristics |
|
yeast definition
|
cell that reproduces by budding or fission
bud can elongate and form pseudohyphae generally round, pasty or mucoid |
|
Mold classified as
|
multicellular
true hyphae - elongate by apical extensions |
|
types of hyphae
|
coenocytic- hollow
septate- cross wall partitions |
|
mycelium
|
many hyphae in mat form
|
|
different types of hyphae on plates
|
vegetative- on or under media
aerial- extend/ project from surface |
|
molds produce by
|
budding (blastic)
thallic (hyphal segments fragment into arthroconidia) |
|
thallic
|
hyphal segments fragment into arthroconidia (form of replication in molds)
|
|
Medically important fungi have 5 characteristics
|
dimorphic (temp dependant)
aerobic (most) primary metablites- citric acid, ethanol, glycerol secondary metabolits- antibiotics slow relplication (hours) |
|
Reproduction of fungi
|
spore form:
- sexual: meiosis -- called telemorphs - asexual: mitosis -- called anamorphs |
|
difference between telemorphs and anamorphs
|
tele- sexual repro
ana- asexual repro |
|
conidia means
|
"born naked"
|
|
different names for same fungi because
|
different forms (a/sexual)
-use asexual designation |
|
Zygomycetes highlighs
|
molds
- broad, sparsely septae, hollow hyphae, sexual zygospores |
|
most clinically sig. order of zygomycetes
other important order |
mucorale
has columella and rhizoids (roots) entomophthorales |
|
entomophthorales causes
diseases calles |
tropic subacute zyomycosis
called basideobolus and conidiobolus |
|
ending for KPCOFGs
|
kingdom- fungi
phylum- -mycota class- -mycetes order -ales family- -aceae |
|
Basidiomycetes
|
sexual repro- basidiospores
anamorphic phase of yeast = pathogens |
|
3 types of basidiomycetes pathogens
|
cryptococcus, malassezia, trichosporon
|
|
Archiascomycetes
- most well known |
newly discovered
pneumocystis jirovecii |
|
Hemiascomycetes has
anamorphic stage is # of teleomorph genera |
ascomycetous yeasts
candida 10 |
|
Euascomycetes
|
produce ascus
12 oders - onygenales, histoplasma and blastomyces eurotailes - aspergillus and penicilin |
|
ascus
|
thin walled sack with haploid ascospores
|
|
Classification of fungi based on
|
taxonomy
tissue infected group characteristics |
|
5 different human mycoses
|
superficial
cutaneous subcutaneous endemic opportunistic |
|
Superficial mycoses (3 things)
|
on skin and hair
non destructive cosmetic |
|
3 examples of superficial mycoses
|
pityriasis versicolor
tinea nigra piedra (black and white) |
|
cutaneous mycoses found in
causes (5) |
keritinized layer (skin, hair, nails)
intching, scaling, broken hair, ring-like patches, thickened discolored nails |
|
3 examples of cutaneous mycoses
|
dermatophytes
tinea unguium onchomyosis |
|
Subcutaneous (4) characteristics
|
affects cornea, muscle, connective tiss
caused by traumatic inoculation remains localized can get abscesses, ulcers, draining of sinus tract |
|
Systemic mycosis (aka)
3 characteristics |
endemic
thermal dimorphism has niches (geographical and ecolog) true pathogens --> lungs can spread |
|
3 examples of systemic mycosis
|
blastomycetes, histomycetes, coccidiomycetes
|
|
Opportunistic mycoses
|
normally avirulent
immunocomp |
|
4 examples of opportunistic mycoses
|
candida
cryptococcus neoformans aspirgillus pneumocystis jirovecii |
|
4 things used to dx fungi
|
10% KOH
calcufluor white H&E, PAS stains Wood's lamp |
|
H&E
PAS |
hematoxylin and eosin
periodic acid schiff |
|
Superficial mycosis are ____ because
|
asx. because no immune response
non- destructive |
|
Pityriasis versicolo (old name)
is a ____ yeast found transmission |
tinea
lipophilic worldwide (young adults in tropics) person to person |
|
Malassezia furfur
|
bowling-pin like
thick walled short hyphae, not branched |
|
phialoconidia or collarette
|
line between mother and bud
|
|
clinical sx. of superficial
|
small pigmented macules covered by scales
hypo/er pigmentation-- affects melanin production mainly on trunk, arms, chest, shoulders face and neck |
|
Sx. of p. versicolor
increased severity in |
chronic and persistent
pt. with perienteric tube feeding, low birth weight infants and debilitated pts. |
|
treatment of P. versicolor
|
self-resolution (rare)
need azole or selenium sulfide shampoo oral if topical doesn't work |
|
Tinea nigra causes
caused by |
Black fungus
hortaea werneckii |
|
morphology of tinea nigra
|
septate hyphae, with spores
pigmented branched arthroconidia |
|
culture of tinea nigra
|
black mold
produces rings |
|
anelloconidia means
|
ringed
|
|
location if tinea nigra
|
tropics
inoculation via traumatic poke typically in children and young adults -females |
|
clinicals of tinea nigra
|
brown to black singl irregular macule
on palms/ soles not contagious looks like malignant melanoma |
|
dx. of tinea nigra
|
skin scraping
10% KOH see hyphae and yeast H&E stain colony top: olive/black bottom: black |
|
treatment of tinea nigra
|
azoles
|
|
White piedra is a
infects main causative agent |
superficial mycoses
hair trichosporon |
|
white piedra colonies
|
white top, cream bottom
aerial mycelium dried and wrinkled |
|
white piedra found in
|
tropics
temp and poor hygiene - hairs of armpits and groin - see white-->brown color swelling around hair shaft |
|
dx. of white piedra
|
culture hair
inhibited by cycloheximide |
|
treatment of white piedra
|
improve hygiene, shave, topical
|
|
Black piedra affects
causitive agent |
scalp hair
piedra hortae |
|
pigment of black piedra
|
red-black
contains ascus with spindle shaped ascospores |
|
black piedra does what to hair
|
causes hyphae mass--> rock hard hair
ascocarp |
|
Treatment of black piedra
|
cut hair
|
|
Cutaneous mycosis are called
|
dermatophytic fungi "skin loving"
and non-dermatophytic fungi |
|
dermatophytic fungi cause
linked to 3 organisms refered to as |
dermatophytosis
trichophytons, epidermophytons, microporums "the Tineas" |
|
Tineas aka
classified according to |
"ring worm"
site of infection |
|
6 tineas and location
|
capitis- head
barbae- beard corporus- smooth skin cruris- groin pedis- foot unguium/ onychomycosis- nails |
|
taxonomy of tineas based on (4)
|
growth pattern in culture, colony morphology, spore production, nurtitional requirements
|
|
microscopically tineas
|
have different dermatophytes
- only look different in culture |
|
3 patterns of infection
|
ecothrix- wrapped around
endothrix- inside hair flavid- honeycomb patter, with empty space |
|
GMS
|
gomori methenamine silver stain
|
|
Ecology of tineas
|
geographic types- soil
zoophilic- hair/skin of animals anthropophilic- human pathogens |
|
nondematophytic causes
|
dermatomycoses
|
|
Dermatophytes are found
spreads via |
worldwide
host--> host, arthroconidia, hyphae or kerotinized material |
|
host Ages of tinea
examples |
all ages
capitis- young pedis and cruris- adult males |
|
species of tinea depend on
most prevelant |
geographic location
80-90% T. rubrum and metagraphytes |
|
severity of sx. in tinea depend on (4)
|
species, dosage, site, immune status
|
|
Dx. of tinea
|
KOH, calcofluor white, culturing
different speies have different look |
|
Treatment of tinea
|
topical, oral
|
|
Non-dermatophytic fungi
|
onyomycoses
candida may need surgical removal if no response to treatment |
|
Subcutaneous mycoses
has a very need ____ to acquire infection mainly is ____ but can ____ |
low pathogenic potential
traumatic introduction localized, but can spread (rarely) |
|
which mycoses is refractory
|
subcutaneous
|
|
5 different conditions of subq mycoses
|
lymphocutaneous soprotrichosis
chromoblastomycosis eumycotic mycetoma subq zygomycosis subq phaeohphomycosis |
|
lymphocutaenous sporotrichosis called
caused by |
rose handler's disease
sporothrix schenckii |
|
Rose handler's disease caused by
looks like |
sporothrix, lymphocutaneous sporotrichosis
daisy petals (oval conidia) |
|
sporothrix found in
causes |
soil and decaying vegetative matter
nodular/ ulcerative lesions lymph action--> spreads linearly |
|
what disease causes a linear infection that drains, following lymph node
|
rose handler's disease
|
|
rose handler's disease can be spread via
|
soil, detritus, armadillo and cats
|
|
clinically- Rose handler's disease
|
causes ulcerations
2 weeks post infection, nodules along lymphatic system - linear chain of ulcers, painless |
|
sporothrix looks like (sx. wise)
|
nocardia and mycobacterium, carcinoma
|
|
Dx of sporothrix
|
culture pus or tissue
- see asteroid body |
|
Splendore- Hoeppli material
|
spherical fungus with star around it
rose handler's disease |
|
treatment for sporothrix
|
KI
itraconazole* treatment of choice* |
|
Chromoblastomycosis
|
chronic
slow gorwing nodule or plaques tropics, traumatic inoculation |
|
chromoblastomycosis caused by
|
colored fungi
|
|
dematiaceous
|
pigmented
|
|
muriform
|
medlar body
-seen in chromoblastomycosis cells full of melanin, internal septation (.5 or .25, then split) |
|
Saprobic form vs parasitic form
|
saprobic- mold
parasitic- yeast |
|
Chromoblastomycosis epidemiology
|
tropics, rural, occupational hazars
rainfall determines lower extremities |
|
syndrome of chromoblastomycosis (6)
causes |
chronic, pruritic, progressive, indolent, resistant, refractory
warty papules, lymphadema, fibrosis |
|
Dx. of chromoblastomycosis
|
presentaiton
muriform cells culture KOH prep and H&E stain NO serology |
|
Treatment of chromoblastomycosis
|
antifungals are ineffective
-cocktail of antifungals |
|
Eumycotic mycetoma id
|
differentiate from actinomycoses
|
|
mycetoma
|
localized chronic granulomatous inf. process that involves cutaneous and subq tissue
|
|
mycetoma causes
|
granules, grains in fluis
aggregation of hyphae lessions destruction of muscle, fascia and bone |
|
morphology of mycetoma
|
granules with fungal hyphae, black grains, hyaline, color
|
|
hyphae of mycetoma is
|
distored and in different forms/sizes
|
|
epidemiology of mycetoma is
|
low rainfall tropics
puncture (normally foot/ hand) more common in men |
|
clinical presentation of mycetoma
|
long infections
nodules --> disfigurations draining sinuses can spread locally |
|
Dx. of mycetoma
treatment |
KOH, H&E, grains
amputation-- important to distinguish from bacteria |
|
subq zygomycosis causes
caused by prevelance |
entomophthomycosis
zygmycetes rare |
|
two types of infections by two types of zygomycetes
|
conidiobolus coronatus--> facial infections from inhal., swelling of nose and upper lip --> painless
Basidiobolus ranaram--> proximal limb infection (children) --> ulceration |
|
dx of zygomycosis (4)
|
biopsy
look for eosinophils splendore-hoeppli material culture |
|
subq phaeohyphomycosis caused by
that are live in |
many organisms
pigmented and have irregular hyphae dead things |
|
in culture phaeohyphomycoses are
# of organisms that can cause this |
black molds, with bizare hyphal forms
20 different fungi can cause |
|
sx. of phaeohyphomycoses
treatment |
lesions on feet and lefs
excise cyst antifungals |
|
Important in systemic mycoses
|
AIDS
get recurrent infection can disseminate to deep viscera |
|
5 major fungi that can go systemic
|
blastomyces dermititidus
coccidiodes immitis or posadasii histoplasma capsulatum capsulatum or duboisii paracoccidiodes brasiliensis penicilium marneffei |
|
blastomycoses
|
easter us
- mississippi river valler -ohio river basin great lakes SE US |
|
blastomycosis appearance
|
must stain to see well (GMS, PAS)
- yeast form- thick and double contoured |
|
Blastomycosis found in
|
decaying matter
aerosolized get via inhalation not spread person to person dogs get 10x more than people |
|
symptoms of blastomycosis
|
depend on exposure and immune statue
<50% get sx. - flu-like sx. --> extrapulmonary siddeminated disease --> 2/3 bone/ skin --> respiratory pneumonitis --> fulmonate form |
|
organs affected by blastomycosis
|
lungs
prostate, liver, spleen, kidney |
|
classic form of blastomycosis involves
|
lesions, painless but look like carcinoma
|
|
dx of blastomycosis
|
biopsy, culture at diff. temps
takes up to 4 weeks to grow NO serological test |
|
Coccidio mycosis called
found in |
"the great imitator"
SW US and north mexico |
|
immitis found in
posadasii |
CA desert
everywhere else |
|
coccidio mycosis caused by
causes |
inhilation
mostly asx --> can progress to cause lesions |
|
primary disease of coccidio mycosis
|
coccidiodal granuloma
called Valley fever in san joaquin |
|
unique morphology of coccidio mycosis
|
conidia are barrel shaped with annular frill at both ends
|
|
inhalation of coccidio mycosis causes
|
conversion to sperules (filled with endospores) ---> cleavage until rupture
|
|
coccidio mycosis likes
|
dirt and soil, high nitrogen content (bat/rodent droppings)
dry seasion -->aerosolized wet season --> grows |
|
dissemination of coccidio mycosis causes
|
secondary coccidiodes --> nodules
- progressed in 5% of cases --- 1-5% get disseminated form ------ multisx. soft tissue, skin, bone, joints |
|
people more affected by coccidio mycosis
|
filipino> af. am> nat. am> hispanic> asian
infants and elderly 9:1 male:femal |
|
dx. of cocciodes
treatment |
histopathology
--barrel shaped yeast serologically whatever is necessary -pregnancy--> amphotericin B |
|
Histoplasma capsulatum
|
SE US, SA, Wafrica
|
|
subspecies found in US
other one |
capsulatum
duboisii |
|
morphology of histoplasma
|
large conidia-- spike-like projections (tuberculate)
|
|
geology of histoplasma
|
soil with high N content
-bat caves, soil disturbance |
|
Sx. of histoplasma
|
asx.
serious in children and immunocomp |
|
clinically of histoplasma
|
local or disseminates (via lymph system and pulmonary macrophages)
|
|
H. capsulatum capsulatum
cause |
90% have low dose and asx. --> mild sx.
acute pulmonary histoplasmosis--> acute respiratory distress syndrom |
|
acute respiratory distress syndrom causes
|
inflam-- lymphadenopathy, brondhial iss., arthritis, pericarditis
--> mediastina fibrosis (fibrosis of heart and great vessels |
|
other affects of acute resp. distress
|
- progressive pulmonary histoplasmosis
-disseminated histoplasmosis subacute diss. histo-- death w/in 2-24 mo acute diss. histo-- death w/in days weeks |
|
H.c. duboisii
causes |
not usually pulmonary lesions
-chronic disease of lymphs, skin and bone -ulcers --can go fulminant (death quickly) |
|
dx. of H.capsulatum
issues of dx. |
microscopy (tuberculate)
culture serological yeast in sputum, blood, tissue need biosafety precautions... slow growers |
|
Treatment of H. capsulatum
|
patient by patient
-- not treatment mainly |
|
Paracoccidiomycosis caused by
found in (8) |
P. basilliensis
brazil, younger, lungs (mainly), humid regions, rich in vegetation, moderate temp, acidic soil, armadillo |
|
morphology of paracoccidiomycosis
|
mycelial non descript
yeast- refractile -- look like pilot or mariner wheel |
|
sx. of paracoccidiomycosis
|
subclinical--> progressive
acute--> chronic usually self-resolving disseminated--> lesions on mouth (painful) can spread to lymph, liver, spleen, CNS |
|
Dx. of paracoccidiodes
treatment |
look at yeast
DO NOT CULTURE serological test can be done antifungals |
|
Peniciliosis caused by
|
peniciliosis marneffei
-- only penicillium pathogen -- only dimorphic penicillium |
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UNique morphology of penicilliosis marneffei
invivo can resemble |
red
H. capsulatum -- except buddng morph |
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Penicilliosis has become a marker for
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HIV--> AIDS
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location of Peniclliosis
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SE asia
HIV people dirt, rats (bamboo rats) |
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clinically penicilliosis
causes (9) |
mimics other AIDs infections (TB)
fever, cough, pukmonary infiltrates, lymphadenopathy, organomegally, anemia, leukopenia, thrombocytopenia, skin lesions |
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Dx. of penicilliosis
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look at tissue for red pigment
yeast- elipitcal with septate, phagocytized no serologial |
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treatment of penicilliosis
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antifungals-- >for life (AIDS pts)
recurrent infection |