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infectiont5 Flashcards

multi system infection, NS infections

1
Q

akiThe primary target cells of the Flaviviruses are, where do they replicate

what happens after target is reached

A

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

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2
Q

neutralizing vs non neutralizing antibodies

A

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

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3
Q

yellow fever endemic countries

vector and resovior

A

South America, Africa

vector is mosquito but the resovior is non human promates

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4
Q

what gets the most damage in yellow fever

A

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

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5
Q

dengue endemic countries

A

asia, africa, South America, US

same for zika

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6
Q

positive torniquette test

A

dengue

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7
Q

rash on palms and soles

A

Zika, Ricketsia(both also have conjunctivitis)

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8
Q

The virus replicates in the fibroblasts of the dermis and disseminates through the bloodstream to several tissues.

A

chikungonia

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9
Q

saddleback fever

A

chikungonia
along with severe distal joint pain

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10
Q

obligate intracellular

A

bacteria:
ricketsia, chlamydia

protozoa: leishmania, brucella
(both for the reticuloendothelial system[MAC], toxoplasma

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11
Q

obligate, intracellular bacteria
Small, Gram –ve rod, non-motile, pleomorphic coccobacilli

A

ricketsia

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12
Q

Gems stain

A

ricketsia, borellia

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13
Q

target cells of ricketsia…who has similar target

what happens after the target is reached

A

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

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14
Q

indirect FA (IFA) and enzyme immunoassays (EIA) used for

A

ricketskia testing and borellial
should follow with confirmatory western blot assay

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15
Q

spirochete

A

borellia, lepto, trep palledum(syphillus)

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16
Q

adheres to integrins, proteoglycans, glycoproteins on host cells or tissue matrices

A

disseminated borellia

at first will multiply locally at bite sight and induce inflammation locally

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17
Q

protozoan from snad fly

A

leishmania

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18
Q

endemic visceral leishmania

A

india, africa

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19
Q

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

A

leishmania

likes to go for the reticuloendothelial system, sleen, liver, and bone marrow

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20
Q

parasitophorous vacuoles

A

helps leishmania survive intracellularly( blocks phase lysosomal formation in macrophages)

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20
Q

Leishmanolysin fuction

A

Facilitates complement and NATURAL KILLER CELL inactivation

Prevents antigen cross-presentation to T cells

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20
Q

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)

A

Francisella tularensis

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20
Q

tularemia sx

A

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

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20
Q

intermittent fever, abdonimal enlargement, pancytopenia

A

leishmania(visceral)

if cutaneous form will present with huge lesion

intermittent fever also seen with brucella

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20
Q

development of depigmented, granulomatous eruptions on the skin (primarily on the face, arms and upper trunk)

A

post-kala-azar dermal leishmaniasis

happens after successful tx

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20
Q

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

A

trypomastigotes enter when bug bites face and shits on you(actually comes from the shit)

s American

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20
Q

Shed in rodent’s urine and inject through

A

lepto

infect through skin abrasion or conjunctiva

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21
Q

chronic phase of chugs sx

A

cardiac sx bc of conduction abnormalities, can have sudden death

digestive sx: constipation, megacolon

esp happens if the

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21
Q

trypanosomes multiply in subcutaneous tissues, blood and lymph.

then what

A

african sleeping

parasite can cross the BB and that when will effect sleep

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21
Q

tularemia target cell and forms of inoculation

who has similar pattern of inoculation

A

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

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21
Q

resoviors in 2 different African sleepies

A

(East)T. b. rhodesiense → 1° reservoir: animals

(West)T. b. gambiense → 1° reservoir: humans,

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22
Q

lepto sx

A

-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_

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23
Q

darkfield microscopy on urine and blood specimens to microscopic agglutination test (MAT)

A

lepto

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24
Q

possible injections from unpasteurized milk vs contaminated milk

A

unpasteurized: brucella and listeria

contaminated: echinococcus

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25
Q
  • Small (0.5 x 0.6-1.5um)
  • Nonmotile
  • Non-encapsulated
  • Gram-negative coccobacilli - Aerobic
    -facaultative intracellular
  • Requires complex growth media: Cx
A

brucella

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26
Q

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

A

brucella

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27
Q

BMAT

A

brucella testing

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28
Q

A slow-growing, tumor-like, and space-
occupying structure enclosed by a
laminated germinative membrane.

A

headed cyst by echinococcus granulomatous

-tapeworm heads develop in the brood capsules in these membranes

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29
Q

a parasite than can induce anaphylaxis

A

echino granulomatous

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30
Q

definitive hosts of ecchino g. vs ecchino m

A

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

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31
Q

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

A

echino granulomatous

can make granulomas anywhere(liver, lungs, brain, heart)

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32
Q

cancer like growth in the liver

A

echino multiocularis

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33
Q

“rosette-like honeycomb” cyst

A

echino

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34
Q

“CR2”/ “CD21” are The primary receptor

A

EBV
- goes for th B cells

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35
Q

replicates in epithelial cells of the oropharynx which causes and

A

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

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36
Q

Heterophile AB

A

EBV diagnosis seen on mono spot test(positive)

if mono sx and negative heterophil AB on mono spot test = CMV

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37
Q

which pathogen causes rash after ampicillin Tx

A

EBV

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38
Q

Establishes latency in the bone marrow and monocytes.

A

CMV

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39
Q

Prevent expression of both MHC I and II. Blocks NK cell attach
Encodes an IL-10 analog that would inhibit TH1 protective
immune responses.

A

CMV

NK block also seen in leishmania

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40
Q

owl eye

A

CMV

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41
Q

Binding receptors are primarily ICAM-1 and CD55

A

enterovirus

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42
Q

Fetal alcohol synd vs nicotic exposure

A

alcohol: growth obstruction-microcephaly/short palpable tissue/maxillary hypoplasia,

nicotine: premature, placental abnormalities, spont abortion, low birth weight, sudden infant death syndrome

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43
Q

risk factor for trisomy 21 and what are features of baby

A

inc maternal age, disjunction happens in ovum

-flate face, epicentral folds, AV septal defect, duodenal/esophgeal atresia’s, leukemia, APP gene, umbilical hernia

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44
Q

turner syndrom sx

A

short and webbed neck, cubits valves, coarctation of aorta/ bicuspid aortic valve, horseshoe kidney, amenorrhea/streak ovaries

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45
Q

22q11 deletion

A

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

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46
Q

malformation vs disruption vs deformities

A

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)

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47
Q

potter sequence

A

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

48
Q

premature complications

A

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

49
Q

nasal flaring, grunts, ground glass

A

RDS

-develops within a few hours of birth. lungs resemble liver. will see thick hyaline membrane

50
Q

amniotic fluid phospholipids measures what

A

level of surfactant

51
Q

RDS complications

A

often from too much oxygen

retrolental fibroplasia
bronchopulmonary dysplasia

52
Q

Pneumatosis intestinalis

A

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

53
Q

early and delated complications of NEC

A

early- preformation, shock, DIC, acute tubular necrosis

late-short gut syndrome, strictures, malabsorption

54
Q

bulging anterior fontanelle and anemia

A

neonatal intraventricular hemorrhage- bleeding into the germinal matrix. if they survive, hydrocephalus, hemosiderin laden macrophages and gloss

55
Q

Erythroblastosis fetalis

A

hemapoetic disease causing unconjugated hyperbilirubin. caused by blood group antigen incompatibility between mother
and fetus

bone marrow hyperplasia, extramedullary hemapoisis

55
Q

Human antiglobulin test (Coombs test)

A

positive on fetal chord blood for Erythroblastosis fetalis

56
Q

Crigler Najjar Syndrome

A

unconjugated hyperbilirubin.
type 1: complete absence of UDP-gluconyltransferase

type 2: partial absence . can be managed with phenobarbital

56
Q

idiopathic neonatal hepatitis

A

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

56
Q

Rotor syndrom

A

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

56
Q

Dubin Johnson Syndrom

A

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

57
Q

nasal polyp and rectal prolapse

A

CF

58
Q

immunoreactive trypsinogen

A

CF

59
Q

Which meningitis orgs need serology testing instead of CSF

A

arbovirus
-no PCR which is what you would normally do to the CSF

60
Q

meningitis septic orgs

A

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

60
Q

most common accumity acquire and hospital acquired meningitis

A

community: neisseria meningitiis, and strep pneumo

hospital: staph aureus, something gram negative

61
Q

Gram -/+
pilli?
endotoxin?
cytotoxin?
purple?
pink?
lipoteic acid
teiochic acid
LOS/LPS

A

Pilli Gram -
endotoxin G-
cytotoxin G+
Purple G+
Pink G-
L acid G+
T acid G+
LOS/LOS G-

62
Q

1 neonate meningitis

-shape
-how do they acquire
-hemolysis

A

Streptococcus agalactiae(group B strep) *type 3 is most virulent

-G+ cocci chains
-acquired while passing through the vagina
-complete beta hemolytic(like pyrogens)

63
Q

1.Group B strep
2. Strep pyrogenes
3. Strep Pneumo
4. Strep viridian
5. enterococcus

A

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)

64
Q

2 causal agent of neonatal meningitis

-shape
-strain
-agar
-ferments(dos/donts
-special products

A

e.coli
-G- bacilli
-K-1 stain has the
capsule to cause the meningitis
-MacConkey - pink = ferments lactose, not sorbitol
-siderophore production

65
Q

meningitis #3 cause in neonates, in immunosuppressed, older adults, and
pregnant women
-shape
-mobility
-conditions
-virulence

A

listeria
-G+ rod
-tumbiling
-cold conditions/ food associate
virulence: intracellular, Internalin A/B

66
Q

Gram negative rod
▪ Oxidase positive
major virulence is a capsule

A

Hib
PRP capsule however nonencapsulated!

prone with URTI

67
Q

Most common bacterial meningitis in adults
▪ Gram
▪ shape
hemolytic?
vaccine

A

strep pneumonia
▪ Gram-positive, alpha-hemolytic
▪ Diplococci-lancet shape
two vaccines

68
Q

Tb virulence

A

Mycolic acid,
Cord Factor
“lipids on outer membrane”

Intracellular
catalase +

69
Q

basal meningital enhancement

presents as

A

TB meningitis

present as hydrocephalus, cranial nerve defects, vasculitis

CSF= fibrin web, lymphocytes, low glucose

70
Q

papilledema

A

Lyme, brain access

71
Q

syphillus test

A

RPR or VDRL
confirmatory treponemal
test (e.g., the FTA-ABS

72
Q

1 Aseptic Viral Meningitis

family
class
stable with
transmission

A

enterovirus
-picorna
naked +ssRNA
acid stable
fecal oral

polio, echino, coxasackie A/B

if IC #1 is CMV-HHV5

73
Q

which herpes causes vertical transmission

A

hsv 2

73
Q

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

A

candida

Polymorphic/Pseudohyphae – C. albicans
* Monomorphic Yeast - C. auris(doesn’t form in germ tube or hyphae)

neutropenia is key

73
Q

pre and post exposure to rabies

A

Human Rabies Immune Globulin (HRIG) – passive immunit followed by Inactivated Vaccine – active immunity

73
Q

Neurotropic, targets Acetylcholine receptor

classification
shape

A

rhabies

E -ssRNA
bullet helical

73
Q

positive CHROMagar

A

Candida auras

Confirmation: MALDI-TOF, ITS sequencing

74
Q

endemic in Afghanistan, Nigeria and Pakistan

A

pilovirus

enterovirus

74
Q

reaches the CNS by direct neuronal
transmission through peripheral nervous system and the olfactory tract

A

rhabies

74
Q

▪Animal reservoir = Bird
▪Arthropod vector = Culex mosquito

A

West Nile virus

75
Q
  • Monomorphic Yeast
  • Encapsulated- polysaccharide capsule
A

crypto neo

75
Q

severe pain when swallowing, hydrophobia

A

due to neck and pharyngeal spasm

rhabies

75
Q

positive serum CrAg
shows what on imaging

A

crypto neo

no patterns on imagine

75
Q

▪ Arenaviridae Enveloped ss(-)RNA
▪ Rodent transmission

sx

A

Viral Encephalitis: LCMV
Lymphocytic Choriomeningitis Virus

headache, fever, nausea,
confusion, partial paralysis, coma, and
seizures

fresh urine, feces, saliva from rodent

75
Q

unicellular parasite
Transmission occurs via exposure to warm freshwater source (swimming/diving
in lakes, rivers,

A

Naegleria fowleri ameba

75
Q

Cysticercosis is caused by the what
stage of the what org

presents

A

larval stage / metacestode

pork tape worm tenia solium

presents with seizures (intraparenchymal) and often inc ICP(extra parenchymal)

76
Q

starry sky on head ct

A

neurocytocerosis
labs, stool, and everything else is normal

77
Q

Sporozoan unicellular parasite
* Obligate intracellular

presents

A

toxoplasma

presents with intracranial calcification/seizures, hydrocephalus, chorioretinitis/cataracts

78
Q

what infections cause ring enhancing lesions

A

toxoplasma
tb
neurocystocerosis
brain abyss

79
Q

most common agents for encephalitis in usa

A

1.HSV1, HSV2, arbovirus ex. west nile, enterovirus

80
Q

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

A
  1. parotitis= mumps encephalitis(paramyxovirus)
  2. West Nile virus
  3. WNV or St. Louis E
  4. HSV
  5. tb, cretuz-jacob dz, arbovirus
  6. definitely not viral
81
Q

pathology with photophobia

A

meningiits

81
Q

temporal and frontal brain abcess origin

A

frontal: dental, sinuses
temporal: otitis media
or both can be from blood

82
Q

common agents of myelitits

presentation

A

polio(abortive with flu sx, nonparalytic which is meningitis, paralytic- asymmetrical flaccid paralysis

83
Q

Salk vaccine and Sabin
vaccine

A

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

84
Q

clostridium botulism
gram
conditions
virulence

A

gram + anaerobic
spore botulism A/B toxin

85
Q

DTap

when given

A

tetanus

can be administered post exposure,
booster important for pregnant moms for passive immunity

86
Q

Bulging and drooping of
the ear

common causal agents

A

mastoiditis

strep pneumo, Hib, maxorella cat or virus

86
Q

what orgs block ach release and what block gaba release

where and what happens

A

ach blocked presynpatically= botulism causing descending flaccid paralysis

gaba blocked presynaptically = tetanus causing rigid paralysis

87
Q

Creutzfeldt-Jakob
Disease

A

prion disease can be sporadic, familial, latrogoenic

will see more glial cells and vacuoles in the brain

87
Q

common causes of conjunctivitis vs keratitis

A

conjuct: staph aureus, any of the middle ear orgs, adenovirus, neisseria gonoreah(squires intrapartum)

kert:: staph, hsv1/cmv, acanthameboae

87
Q

Trachoma

A

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

87
Q

*Periventricular calcifications
* Enlarged ventricles
* Polymicrogyria

A

CMV
and hearing loss and microcephaly

88
Q

Naked dsDNA

A

adenovirus

88
Q

how to get CMV

A

mother exposure to urine, saliva, or sexual liquids

transplacenta transmission to fetus

88
Q

proteinase

A

candida auras

89
Q

prenatal and post natal CMV testing

A

prenatal serum blood screening

postnatal is urine or saliva(think how mom get it)

90
Q

early and late presenting congenital syphillus

A

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

91
Q

eyes, hearing, heart

family
classification

A

rubella
togaviridae
Enveloped +ssRNA

92
Q

T argets neural progenitor cells
* Reduces neural proliferation, migration and maturation.
* Decreases brain growth

family
class

features

A

ZIKA

flaviviridae
Enveloped +ssRNA

microcephaly, facial distortions, hearing loss, seizures

93
Q

HIV classification

A

Enveloped +ssRNA

94
Q

acid fast bacillus ubiquitous in nature
transmission?
presentation?

A

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

95
Q

bacillary angiomatosis

gram
conditions
transmitters
presents

A

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

96
Q

reactive arthritis

A

samonellitis(HIV)

97
Q

viruses
intranuclear inclusions
intracytoplsmic

A

nuclear: CMV[owl eye]

cytoplasmic: Rabies[negri]

98
Q

lacks ergosterol

presents

A

PCP fungus

presents chronic dry cough, weight loss, fever

98
Q

AIDS and severe chronic diahrea

A

cryptosporidosis- intracellular protozoan parasite

99
Q

LC virus
classification
name when reactivates
where is it latent

A

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

100
Q

sand fly releases

where do they replicate

sx

A

leishmania promastigotes

replicate in spleen, liver, bone marrow / inside macrophages as amastigotes

sx reflect this
also can have black fever-darkening of the skin

101
Q

1.Failure to thrive, vomiting, seizures, skin rashes, microcephaly (small head size), developmental delays.

  1. Dislocation of the lens in the eye (ectopia lentis), skeletal abnormalities (long limbs, marfanoid features), developmental delays, intellectual disability, seizures, blood clots.
  2. Vomiting, diarrhea, lethargy, failure to thrive, jaundice, liver enlargement, cataracts.
  3. 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).
A

1.PKU

  1. homocystinuria
  2. galactosuria
  3. alkaptouria
102
Q

cryptospridiosis complications

A

dehydration, malnutrition, calculus chloesistitis

103
Q

terminal spine vs lateral spine

A

terminal spine = schistosomes H/bladder

lateral spine = shistosomas m or j/ liver, gallbladder

103
Q

parasite that causes hematuria

complications

A

schistosomes H

bladder fibrosis and carcinoma

schistosomes m and j have portal vein and liver involvement

104
Q

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

A

entamebao histolytic

fecal oral inject cyst, forms trophozyte and burrow into intestinal wall, systemic invasion

naegrali fawli
swims up your nose into the brain

105
Q

2 copies of ssRNA (- stranded), not directly infectious,
integrates into host genome

A

HIV

106
Q

cough that was initially dry and is now productive, mild fever,
night sweats and weight loss.

A

tb

107
Q

skirrow agar

A

campy jejune

term 4 (13 decks)

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