infectiont5 Flashcards
multi system infection, NS infections
akiThe primary target cells of the Flaviviruses are, where do they replicate
what happens after target is reached
monocyte-macrophages inc dendritic cells, esp suffer cells. will replicate in lymphnodes first and then infect macrophages to send virus into system/organs
induce INFa and cytokine production= prodromal sx
neutralizing vs non neutralizing antibodies
NON-NEUTRALIZING ANTIBODIES PROMOTE INFECTION.-Fc receptors on cell attach Flavivirdae and will enhance the infection(encourage macrophage uptake and induce more cytokine release and will recruit T lymphocytes
NEUTRALIZING ANTIBODIES CAN BLOCK DISEASE. -these will tag a micro for immune destruction
yellow fever endemic countries
vector and resovior
South America, Africa
vector is mosquito but the resovior is non human promates
what gets the most damage in yellow fever
hepatocellular apapotosis and necrotic cells make the councilman bodies
mucosa surfaces have massive hemmorages
jaundice hurts kidney-all scene in severe form
other notable sx: conjunctival injection, bradycardia
dengue endemic countries
asia, africa, South America, US
same for zika
positive torniquette test
dengue
rash on palms and soles
Zika, Ricketsia(both also have conjunctivitis)
The virus replicates in the fibroblasts of the dermis and disseminates through the bloodstream to several tissues.
chikungonia
saddleback fever
chikungonia
along with severe distal joint pain
obligate intracellular
bacteria:
ricketsia, chlamydia
protozoa: leishmania, brucella
(both for the reticuloendothelial system[MAC], toxoplasma
obligate, intracellular bacteria
Small, Gram –ve rod, non-motile, pleomorphic coccobacilli
ricketsia
Gems stain
ricketsia, borellia
target cells of ricketsia…who has similar target
what happens after the target is reached
Infect vascular endothelium (systemic and pulmonary circulation)…similar target is lepto
inc vascular permeability, T cell mediated immunity, INFg, TNFa, cytokines= edema, hypovolemia, vasculitis, digital necrosis
indirect FA (IFA) and enzyme immunoassays (EIA) used for
ricketskia testing and borellial
should follow with confirmatory western blot assay
spirochete
borellia, lepto, trep palledum(syphillus)
adheres to integrins, proteoglycans, glycoproteins on host cells or tissue matrices
disseminated borellia
at first will multiply locally at bite sight and induce inflammation locally
protozoan from snad fly
leishmania
endemic visceral leishmania
india, africa
promastigote injected into skin, pages by macrophages, transform to amastigote which will go infect other cells(which cells?). Vector takes in amastigote and will change back to promastigotes
leishmania
likes to go for the reticuloendothelial system, sleen, liver, and bone marrow
parasitophorous vacuoles
helps leishmania survive intracellularly( blocks phase lysosomal formation in macrophages)
Leishmanolysin fuction
Facilitates complement and NATURAL KILLER CELL inactivation
Prevents antigen cross-presentation to T cells
G –ve, short rods “Coccobacilli”
* Aerobic, facultative, non-spore forming and catalase +ve
* Nutritionally fastidious: will not grow on blood or other common media; requires supplemental compounds (Fe2+, cysteine)
Francisella tularensis
tularemia sx
if via injection there will be an ulcer on the skin.
if via inhalation will present like pneumonia(like tb pneumonia- dry could, pleuritic chest pain)
if ingested-exudative tonsillitis, bloody diarrhea. of typhoidal fever sx
if inoculated into eyes -purulent conjunctivitis, corneal ulceration, lymphadenopathy
intermittent fever, abdonimal enlargement, pancytopenia
leishmania(visceral)
if cutaneous form will present with huge lesion
intermittent fever also seen with brucella
development of depigmented, granulomatous eruptions on the skin (primarily on the face, arms and upper trunk)
post-kala-azar dermal leishmaniasis
happens after successful tx
trypomastigotes enter (how), invades macrophages, fibroblasts, and muscle tissue, transforms to amastigots, once the cell is full will turn back to trypomastigo before the cell bursts
trypomastigotes enter when bug bites face and shits on you(actually comes from the shit)
s American
Shed in rodent’s urine and inject through
lepto
infect through skin abrasion or conjunctiva
chronic phase of chugs sx
cardiac sx bc of conduction abnormalities, can have sudden death
digestive sx: constipation, megacolon
esp happens if the
trypanosomes multiply in subcutaneous tissues, blood and lymph.
then what
african sleeping
parasite can cross the BB and that when will effect sleep
tularemia target cell and forms of inoculation
who has similar pattern of inoculation
inhalation, ingestion, or injection
will go for macrophaes to multiply then breaks out and goes to organs(spleen, liver BM) and can produce granulomas…this is similarly seen in brucella
resoviors in 2 different African sleepies
(East)T. b. rhodesiense → 1° reservoir: animals
(West)T. b. gambiense → 1° reservoir: humans,
lepto sx
-jaundice
-retroorbital pain
-Conjunctival suffusion (redness without exudate)
-intense muscle pain esp of back nd calves(NOT JOINT pain)
leads to weils dz(hemmorage, jaundice, acute kidney injury_
darkfield microscopy on urine and blood specimens to microscopic agglutination test (MAT)
lepto
possible injections from unpasteurized milk vs contaminated milk
unpasteurized: brucella and listeria
contaminated: echinococcus
- Small (0.5 x 0.6-1.5um)
- Nonmotile
- Non-encapsulated
- Gram-negative coccobacilli - Aerobic
-facaultative intracellular - Requires complex growth media: Cx
brucella
Bacterium can form smooth or rough colonies →
determined by the O antigen of the cell wall LPS…dont use same antibodies but O is used as virulence marker
brucella
BMAT
brucella testing
A slow-growing, tumor-like, and space-
occupying structure enclosed by a
laminated germinative membrane.
headed cyst by echinococcus granulomatous
-tapeworm heads develop in the brood capsules in these membranes
a parasite than can induce anaphylaxis
echino granulomatous
definitive hosts of ecchino g. vs ecchino m
Echino g:dogs. intermediate hosts: intermediate hosts: sheep and herding animals. humans dead end after fecal oral injection
Echino m: foxes. intermediate hosts: small rodents
After ingestion, egg hatches insmall intestine & releases an oncosphere
2. Oncosphere penetrates intestinal wall,
migrates → circulatory system into various organs (liver & lungs)
3. Oncosphere develops into a cyst that enlarges producing protoscolices & daughter cysts that fill cyst interior
echino granulomatous
can make granulomas anywhere(liver, lungs, brain, heart)
cancer like growth in the liver
echino multiocularis
“rosette-like honeycomb” cyst
echino
“CR2”/ “CD21” are The primary receptor
EBV
- goes for th B cells
replicates in epithelial cells of the oropharynx which causes and
EBV
bc in oropharynx will shed in saliva and cause exudative tonsils
will also inject the B cells which will cause mononucleosis, uncontrolled B cell proliferation(lymphoma) and T cell activation causing organomegaly and atypical lymphocytes (downey cells)]
can also somehow cause GBS
Heterophile AB
EBV diagnosis seen on mono spot test(positive)
if mono sx and negative heterophil AB on mono spot test = CMV
which pathogen causes rash after ampicillin Tx
EBV
Establishes latency in the bone marrow and monocytes.
CMV
Prevent expression of both MHC I and II. Blocks NK cell attach
Encodes an IL-10 analog that would inhibit TH1 protective
immune responses.
CMV
NK block also seen in leishmania
owl eye
CMV
Binding receptors are primarily ICAM-1 and CD55
enterovirus
Fetal alcohol synd vs nicotic exposure
alcohol: growth obstruction-microcephaly/short palpable tissue/maxillary hypoplasia,
nicotine: premature, placental abnormalities, spont abortion, low birth weight, sudden infant death syndrome
risk factor for trisomy 21 and what are features of baby
inc maternal age, disjunction happens in ovum
-flate face, epicentral folds, AV septal defect, duodenal/esophgeal atresia’s, leukemia, APP gene, umbilical hernia
turner syndrom sx
short and webbed neck, cubits valves, coarctation of aorta/ bicuspid aortic valve, horseshoe kidney, amenorrhea/streak ovaries
22q11 deletion
diagnose with FISH
Velocardiofacial (congenital heart disease, facial/palate abnormalities, developmental delay)
Di George-thymic hypoplasia- impaired T cell immunity, parathyroid hypoplasia - hypocalcemia
both have psychosis
malformation vs disruption vs deformities
dIsruption: formed normally then an outside factor deformed - amnIotIc band
malformation: never formed right for intrinsic/genetic reasons-trisomy, ASD
dEformity: never formed right for external reasons- uterus too small, twins(comprEssion issue)
potter sequence
maternal htn causes placental insufficiency leading to oligohydramnios (decrease in amniotic fluid) or can be from fetal renal agencies/ urinary tract obstruction which causes no urination(major component of amniotic fluid), too little amniotic fluid wall cause compression of the fetus and cause a flattened face, *low set ears, hypoplastic lungs(dec chest expansion) and dislocated hips
premature complications
RDS(surfactant deficiency) and NEC(inflammatory damage to intestines after starting oral feeding inducing vomitting, bloody diahrea and distended abdominal), intraventricular and germinal matrix hemorrhage
nasal flaring, grunts, ground glass
RDS
-develops within a few hours of birth. lungs resemble liver. will see thick hyaline membrane
amniotic fluid phospholipids measures what
level of surfactant
RDS complications
often from too much oxygen
retrolental fibroplasia
bronchopulmonary dysplasia
Pneumatosis intestinalis
gas within the intestinal wall . present in NEC babies in the 2/3rd week of life or when starting formula. will see dialated loops of bowel. will have air below the mucosa
early and delated complications of NEC
early- preformation, shock, DIC, acute tubular necrosis
late-short gut syndrome, strictures, malabsorption
bulging anterior fontanelle and anemia
neonatal intraventricular hemorrhage- bleeding into the germinal matrix. if they survive, hydrocephalus, hemosiderin laden macrophages and gloss
Erythroblastosis fetalis
hemapoetic disease causing unconjugated hyperbilirubin. caused by blood group antigen incompatibility between mother
and fetus
bone marrow hyperplasia, extramedullary hemapoisis
Human antiglobulin test (Coombs test)
positive on fetal chord blood for Erythroblastosis fetalis
Crigler Najjar Syndrome
unconjugated hyperbilirubin.
type 1: complete absence of UDP-gluconyltransferase
type 2: partial absence . can be managed with phenobarbital
idiopathic neonatal hepatitis
causes conjugated hyperbilirubinemia and diagnosed when you have ruled out extra hepatic biliary atresia and 1 AT.
cholistasis causes giant cell transformations, ballooning and acidification degradation
Rotor syndrom
causes conjugated hyperbilirubinemai
mutation is transport proteins for bilirubin Into the caniliculi so absorbed back into blood
presents with jaundice and intermittent gastric pain and distention
Dubin Johnson Syndrom
black liver and causes conjugated hyperbilirubin. defective transfer of bile from hepatocytes to canaliculi. Associated defect in hepatic excretion of coproporyphrins
presents in early adulthood with jaundice
pigment in the lysosomes made of EPI in hepatocytes and suffer cells
nasal polyp and rectal prolapse
CF
immunoreactive trypsinogen
CF
Which meningitis orgs need serology testing instead of CSF
arbovirus
-no PCR which is what you would normally do to the CSF
meningitis septic orgs
Strep pneumo
Group B strep
E coli
N. meninigitis
Hib
-all have vaccines made from the polysaccharide capsule except coli(does have capsule but not vaccine), most are nasopharynx origin which will also have IgA protease
most common accumity acquire and hospital acquired meningitis
community: neisseria meningitiis, and strep pneumo
hospital: staph aureus, something gram negative
Gram -/+
pilli?
endotoxin?
cytotoxin?
purple?
pink?
lipoteic acid
teiochic acid
LOS/LPS
Pilli Gram -
endotoxin G-
cytotoxin G+
Purple G+
Pink G-
L acid G+
T acid G+
LOS/LOS G-
1 neonate meningitis
-shape
-how do they acquire
-hemolysis
Streptococcus agalactiae(group B strep) *type 3 is most virulent
-G+ cocci chains
-acquired while passing through the vagina
-complete beta hemolytic(like pyrogens)
1.Group B strep
2. Strep pyrogenes
3. Strep Pneumo
4. Strep viridian
5. enterococcus
1.neonatal meningitis
2. strep throat, cellulitis
(both beta hemolytic)
3. pneumonia, otitis media/ adult meningitis
4. endocarditis/ dental
(both alpha hemolytic, green)
5. hospital acquired UTI, endocarditis of prosthetic valve (gamma, none)
2 causal agent of neonatal meningitis
-shape
-strain
-agar
-ferments(dos/donts
-special products
e.coli
-G- bacilli
-K-1 stain has the
capsule to cause the meningitis
-MacConkey - pink = ferments lactose, not sorbitol
-siderophore production
meningitis #3 cause in neonates, in immunosuppressed, older adults, and
pregnant women
-shape
-mobility
-conditions
-virulence
listeria
-G+ rod
-tumbiling
-cold conditions/ food associate
virulence: intracellular, Internalin A/B
Gram negative rod
▪ Oxidase positive
major virulence is a capsule
Hib
PRP capsule however nonencapsulated!
prone with URTI
Most common bacterial meningitis in adults
▪ Gram
▪ shape
hemolytic?
vaccine
strep pneumonia
▪ Gram-positive, alpha-hemolytic
▪ Diplococci-lancet shape
two vaccines
Tb virulence
Mycolic acid,
Cord Factor
“lipids on outer membrane”
Intracellular
catalase +
basal meningital enhancement
presents as
TB meningitis
present as hydrocephalus, cranial nerve defects, vasculitis
CSF= fibrin web, lymphocytes, low glucose
papilledema
Lyme, brain access
syphillus test
RPR or VDRL
confirmatory treponemal
test (e.g., the FTA-ABS
1 Aseptic Viral Meningitis
family
class
stable with
transmission
enterovirus
-picorna
naked +ssRNA
acid stable
fecal oral
polio, echino, coxasackie A/B
if IC #1 is CMV-HHV5
which herpes causes vertical transmission
hsv 2
Hospital-acquired opportunistic infection that occurs in patients with
neutropenia via artificial introduction on foreign objects (shunts,
catheters, surgerical tools), leading to blood-stream infection BSI
candida
Polymorphic/Pseudohyphae – C. albicans
* Monomorphic Yeast - C. auris(doesn’t form in germ tube or hyphae)
neutropenia is key
pre and post exposure to rabies
Human Rabies Immune Globulin (HRIG) – passive immunit followed by Inactivated Vaccine – active immunity
Neurotropic, targets Acetylcholine receptor
classification
shape
rhabies
E -ssRNA
bullet helical
positive CHROMagar
Candida auras
Confirmation: MALDI-TOF, ITS sequencing
endemic in Afghanistan, Nigeria and Pakistan
pilovirus
enterovirus
reaches the CNS by direct neuronal
transmission through peripheral nervous system and the olfactory tract
rhabies
▪Animal reservoir = Bird
▪Arthropod vector = Culex mosquito
West Nile virus
- Monomorphic Yeast
- Encapsulated- polysaccharide capsule
crypto neo
severe pain when swallowing, hydrophobia
due to neck and pharyngeal spasm
rhabies
positive serum CrAg
shows what on imaging
crypto neo
no patterns on imagine
▪ Arenaviridae Enveloped ss(-)RNA
▪ Rodent transmission
sx
Viral Encephalitis: LCMV
Lymphocytic Choriomeningitis Virus
headache, fever, nausea,
confusion, partial paralysis, coma, and
seizures
fresh urine, feces, saliva from rodent
unicellular parasite
Transmission occurs via exposure to warm freshwater source (swimming/diving
in lakes, rivers,
Naegleria fowleri ameba
Cysticercosis is caused by the what
stage of the what org
presents
larval stage / metacestode
pork tape worm tenia solium
presents with seizures (intraparenchymal) and often inc ICP(extra parenchymal)
starry sky on head ct
neurocytocerosis
labs, stool, and everything else is normal
Sporozoan unicellular parasite
* Obligate intracellular
presents
toxoplasma
presents with intracranial calcification/seizures, hydrocephalus, chorioretinitis/cataracts
what infections cause ring enhancing lesions
toxoplasma
tb
neurocystocerosis
brain abyss
most common agents for encephalitis in usa
1.HSV1, HSV2, arbovirus ex. west nile, enterovirus
what kind of encephalitis with:
1. parotitis
2. flaccid paralysis
3. face/body tremors
4. temporal lobe involve
5. basal gangli/thalamus involv
6. hydrocephalus
- parotitis= mumps encephalitis(paramyxovirus)
- West Nile virus
- WNV or St. Louis E
- HSV
- tb, cretuz-jacob dz, arbovirus
- definitely not viral
pathology with photophobia
meningiits
temporal and frontal brain abcess origin
frontal: dental, sinuses
temporal: otitis media
or both can be from blood
common agents of myelitits
presentation
polio(abortive with flu sx, nonparalytic which is meningitis, paralytic- asymmetrical flaccid paralysis
Salk vaccine and Sabin
vaccine
Inactivated polio vaccine (IPV) or Salk vaccine
▪ Most commonly used in countries without wild-type
virus transmission
Live oral attenuated polio vaccine (OPV) or Sabin vaccine comes with he risk of getting polio
clostridium botulism
gram
conditions
virulence
gram + anaerobic
spore botulism A/B toxin
DTap
when given
tetanus
can be administered post exposure,
booster important for pregnant moms for passive immunity
Bulging and drooping of
the ear
common causal agents
mastoiditis
strep pneumo, Hib, maxorella cat or virus
what orgs block ach release and what block gaba release
where and what happens
ach blocked presynpatically= botulism causing descending flaccid paralysis
gaba blocked presynaptically = tetanus causing rigid paralysis
Creutzfeldt-Jakob
Disease
prion disease can be sporadic, familial, latrogoenic
will see more glial cells and vacuoles in the brain
common causes of conjunctivitis vs keratitis
conjuct: staph aureus, any of the middle ear orgs, adenovirus, neisseria gonoreah(squires intrapartum)
kert:: staph, hsv1/cmv, acanthameboae
Trachoma
Chronic Keratoconjunctivitis
Chlamydia trachomatis
EB form spread via eye
phase 1 in childhood with limited conjunctivitis and phase 2(cicatricial) in adult with chronic infection leading to inflammation and scarring of eyelids also causing in grown eyelashes, ulcerations, and edema
*Periventricular calcifications
* Enlarged ventricles
* Polymicrogyria
CMV
and hearing loss and microcephaly
Naked dsDNA
adenovirus
how to get CMV
mother exposure to urine, saliva, or sexual liquids
transplacenta transmission to fetus
proteinase
candida auras
prenatal and post natal CMV testing
prenatal serum blood screening
postnatal is urine or saliva(think how mom get it)
early and late presenting congenital syphillus
early: snuffles(thick and bloody nasal discharge), rash on palms and soles, osteochondritis, hepatosplenomegaly, blood and liver counts are fucked
late: Hutchison incisors, saber shins, hearing loss, ulcers
eyes, hearing, heart
family
classification
rubella
togaviridae
Enveloped +ssRNA
T argets neural progenitor cells
* Reduces neural proliferation, migration and maturation.
* Decreases brain growth
family
class
features
ZIKA
flaviviridae
Enveloped +ssRNA
microcephaly, facial distortions, hearing loss, seizures
HIV classification
Enveloped +ssRNA
acid fast bacillus ubiquitous in nature
transmission?
presentation?
MAC
transmission via inhalation or injection
-pulmonary type presents like TB
-localized type has lymphadenopathy
-disseminated MAC is fever, night sweats, weight loss with organ specific sx
bacillary angiomatosis
gram
conditions
transmitters
presents
bartonella
gram -, facultative intracellular rod, fastidious
B.H from cats and affects the immunocompromised
presents with purple pappules that resemble karposi sarcoma but will grow more over time
reactive arthritis
samonellitis(HIV)
viruses
intranuclear inclusions
intracytoplsmic
nuclear: CMV[owl eye]
cytoplasmic: Rabies[negri]
lacks ergosterol
presents
PCP fungus
presents chronic dry cough, weight loss, fever
AIDS and severe chronic diahrea
cryptosporidosis- intracellular protozoan parasite
LC virus
classification
name when reactivates
where is it latent
non enveloped dsDNA
primery in childhood and ask reactivation as immune comp causes Progressive Multifocal Leukoencephalopathy cause demyelination by infecting the oligodendrocytes
latent in kidney and lymph organs
sand fly releases
where do they replicate
sx
leishmania promastigotes
replicate in spleen, liver, bone marrow / inside macrophages as amastigotes
sx reflect this
also can have black fever-darkening of the skin
1.Failure to thrive, vomiting, seizures, skin rashes, microcephaly (small head size), developmental delays.
- Dislocation of the lens in the eye (ectopia lentis), skeletal abnormalities (long limbs, marfanoid features), developmental delays, intellectual disability, seizures, blood clots.
- Vomiting, diarrhea, lethargy, failure to thrive, jaundice, liver enlargement, cataracts.
- Ochronosis develops later in life (20s-40s): Blackish discoloration of urine turning dark upon standing, ochronotic pigment deposits in cartilage (leading to arthritis), ear cartilage discoloration, eye problems (pigmentation, cataracts).
1.PKU
- homocystinuria
- galactosuria
- alkaptouria
cryptospridiosis complications
dehydration, malnutrition, calculus chloesistitis
terminal spine vs lateral spine
terminal spine = schistosomes H/bladder
lateral spine = shistosomas m or j/ liver, gallbladder
parasite that causes hematuria
complications
schistosomes H
bladder fibrosis and carcinoma
schistosomes m and j have portal vein and liver involvement
name and mech of infection
Can range from asymptomatic to severe bloody diarrhea, abdominal pain, dehydration, tenesmus
vs
Rapidly progressing headache, fever, stiff neck, nausea, vomiting, confusion, seizures, coma
entamebao histolytic
fecal oral inject cyst, forms trophozyte and burrow into intestinal wall, systemic invasion
naegrali fawli
swims up your nose into the brain
2 copies of ssRNA (- stranded), not directly infectious,
integrates into host genome
HIV
cough that was initially dry and is now productive, mild fever,
night sweats and weight loss.
tb
skirrow agar
campy jejune
