Micro Flashcards
P. jiroveci
CD4 count, risk factor, prophylaxis
CD4 <200/mm3
oropharyngeal candidiasis increases risk
TMP-SMX
Toxoplasma gondii
CD4 count, risk factor, prophylaxis
CD4 <100/mm3
positive Toxoplasma IgG is a risk factor
TMP-SMX
Mycobacterium avium complex
CD4, prophylaxis, pathogenesis in HIV, signs/symptoms, biopsy
CD4 <50/mm3, prevent with Azithromycin
ingestion/inhalation > prevents phagolysosome formation > insufficient IFN-y to activate macrophages in CD4 defic.
nonspecific sx (fever, weight loss, D); anemia, HSmegaly, high ALP/LDH with RES involvement
dx by blood culture (but slow); biopsy shows granulomas of foamy epitheliod cells + giant cells with IC acid-fast bacilli
Congenital Toxoplasmosis: when does baby get it and what it do
in utero transplacental infection
triad = intracranial calcifications, chorioretinitis, hydrocephalus
also hepatosplenomegaly, neuro issues (seizure, eye movement problems, altered muscle tone) and rash
Congenital HSV: when does baby get it and what it do
intrapartum infection
causes ophthalmia neonatorum (also via Chlamydia or Neisseria, conjunctivitis)
Clostridium septicum
what does it cause? in whom specifically?
gram-pos, spore-forming, exotoxin-producing normal flora
spontaneous gas gangrene in patients with underlying COLON CANCER, IBD or immunosuppression (is normal gut flora that can get into circulation when mucosa is compromised
RAPID ONSET MUSCLE PAIN, fever, HEMORRHAGIC BULLAE, dusky skin, edema + CREPITUS
Vibrio vulnificus
gram-negative
increased risk for fulminant infection in HEMOCHROMATOSIS b/c needs free iron for growth
rapid-onset sepsis and bullous skin lesions
shellfish consumption or wound infection with seawater
fungal infection from indwelling catheter
what microbe + what sx?
candidemia
sepsis, abscess, and pustular skin lesions with red base
multiple myeloma-related common infections
lung - S. pneumo or H. flu
UTI - E. coli
differentiation of EBV vs. non-EBV infectious mononucleosis
causes of non-EBV IM
non-EBV IM often does NOT have sore throat or lymphadenopathy or heterophile Ab positivity
CMV IM can come from blood transfusions (irradiation of blood products reduces risk)
other causes of IM-like syndromes are HHV-6, HIV and toxoplasmosis
a glycosylated HIV polyprotein that is cleaved into 2 smaller proteins
what is it? what are the 2 smaller proteins? functions of resulting proteins and why are they glycosylated?
GP160 is cleaved into GP120 and GP41 (Gp160 glycosylated in rER and Golgi)
gp120 is an envelope protein that mediates viral attachment
gp41 is an envelope protein that mediates fusion
glycosylation helps with immune evasion (masks antigens), host cell binding + proper protein folding
main mechanism of aminoglycoside resistance
how does this mechanism arise in microbes?
antibiotic-modifying enzymes (acetylases, kinases, etc.)
aminoglycosides altered by acetylation, etc. have reduced binding of the 30S ribosomal subunit (16S component)
usually via PLASMID or TRANSPOSON transfer, not chromosomal mutation
3 infections assoc. with acute pancreatitis
mumps
Coxsackie
Mycoplasma
Staph epidermidis
biochem tests + microbiological characteristics
catalase-positive (as are all Staph)
coagulase negative (differentiates it from aureus)
gamma-hemolytic (no hemolysis)
novobiocin sensitive (diff from saprophyticus)
gram-positive cocci in clusters
adhesion + biofilm proteins > infects prosthetics
Histoplasma capsulatum
general characteristics, transmission + pathogenesis
dx (culture, labs + characteristic signs)
dimorphic, transmitted by inhalation > transforms to yeast in lungs
replicates in phagosomes of macrophages > oval/round yeast cells in macros
intact immunity > asymptomatic or self-limited pulmonary infection (cell-mediated immunity)
impaired immunity > RES dissemination with HSmegaly, LAP, and PANCYTOPENIA
dx by BLOOD/URINE Ags, hyphae on Sabouraud culture and characteristic TONGUE ULCERS
Schistosoma haematobium
where? how? what it do?
Africa and Middle East - URINARY schistosomiasis
freshwater snails release larvae > penetrate skin > migrate to + mature in liver > travel to bladder venous plexus
terminal hematuria, dysuria + frequent pissing
hydronephrosis, pyelonephritis and bladder SCC
Schistosoma mansoni / japonicum
where? how? what it do?
Mansoni - Africa, Middle East, S. America + Carribean
Japonicum - Asia, Philippines, Japan
same pathogenesis as haemotobium, but travels thru portal veins to GI
intestinal schisto - D and pain, ulceration with IDA
hepatic schisto - HSmegaly, periportal fibrosis + portal htn
all 3 spp. have Th2 granulomatous response with eosinophils and M2 macrophages
Echinococcus granulosus
transmission + disease
DOG TAPEWORM - dog host (sheep intermediate)
food contaminated with dog poop > hydatid cysts
Diphyllobothrium latum
transmission + disease
FISH TAPEWORM - raw freshwater fish
vitamin B12 deficiency and megaloblastic anemia
Taenia solium
transmission + 2 diseases
PIG TAPEWORM - undercooked pork (worm infection) or eggs in carrier feces (cysticercosis)
Parvovirus B19
type of virus? transmission?
naked ssDNA
respiratory, hematogenous or congenital transmission
Parvovirus B19
prodrome and 2 clinical manifestations in normal patients
Prodrome - HA, coryza, GI sx (heavy viremia + shedding)
Erythema Infectiosum - in KIDS; bright red cheek rash, circumoral pallor, fever +/- reticular rash on arms, legs, trunk
Acute arthropathy - in ADULTS; polyarthritis that is SYMMETRIC on PIP, knee and ankle joints; self-limited + non-destructive
(both have immune complexes + low shedding)
Parvovirus B19
2 clinical manifestations in unique types of patients
Aplastic crisis - “reticulocytopenia” in pts with pre-existing RBC issues such as sickle cell or spherocytosis
Hydrops fetalis - pregnant woman infected > hydrops in baby is common; direct hemolysis + precursor interruption
Asplenic patient
more susceptible to infection with which bacteria? (general type + species examples)
encapsulated bacteria
group B strep (agalactiae) H. flu Strep pneumo Meningococcus Salmonella typhi
Malarial life cycle
this card is a nightmare, just for review
Anopheles bite > SPOROZOITEs infect hepatocytes
in liver - dormant infection with HYPNOZOITEs or a SCHIZONT of many MEROZOITES forms in liver cell > schizont rupture releases merozoites to blood
in blood - merozoites infect RBCs and form TROPHOZOITES > asexual formation of more schizonts in RBCS with further merozoite release or…
gametocyte formation > picked back up by mosquitos
Toxocara canis
manifestations? dx?
DOG ROUNDWORM - incidental infection in humans
eosinophilic GRANULOMATOUS inflammation
visceral LARVA MIGRANS
ocular larva migrans
dx by serology
Oncogenesis by HBV vs. HCV
1 mechanism for both, 2 mechanisms unique to only 1 of them
- Increased Hepatocyte Turnover - with local inflammation > incr. mutation risk (both HBV + HCV)
- Genome Integration - only HBV! partial dsDNA integration into host genome via topoisomerase I can cause insertional mutagenesis
- Oncogenic Viral Proteins - viral protein “HBx” activates cell growth genes + interferes with p53 (HBV only!)
MCC of sepsis in asplenic pt?
MCC of osteomyelitis in asplenic pt?
prevention?
Sepsis - S. PNEUMO > H. flu > (E. coli, pseudomonas, staph, other strep)
Osteomyelitis (in sickle cell) - SALMONELLA > (S. aureus, E. coli)
penicillin prophylaxis and pneumococcal vaccination
Mefloquine
active against what phase of malarial life cycle? clinical consequence?
a SCHIZONTICIDE that kills replicating parasites IN RBCS
does NOT kill hepatic schizonts (is inactivated in liver)
must take for 4 WEEKS after return (liver schizonts rupture after 8-30 days)
Plasmodium in Africa is often which species?
Resistant to what?
Treated with what?
Falciparum
chloroquine-resistant
mefloquine, doxycycline or atovaquone-proguanil
Zika virus
pathogenesis? clinical? dx?
ssRNA Flavivirus; TRANSPLACENTAL transmission; targets NEURAL PROGENITORS
microcephaly, craniofacial disproportion; SPASTICITY + SEIZURE; ocular issues
imaging - calcifications, ventriculomegaly, cortical thinning
RNA detection by PCR of urine, serum or CSF
Shigellosis
infects which type of cells? then what?
(most common species? other species)
infects “MICROFOLD (M) CELLS” of GI mucosa (at base of villi in Peyer’s patch in ileum)
is endocytosed, lyses the endosome, multiplies and spreads laterally to other cells > denuding + ulceration of mucosa > bloody D
HIV biding, fusion + entry process
gp120 binds CD4 plus CCR5 or CXCR4 co-receptors
gp120 undergoes conformational change to expose gp41 which mediates fusion
(Maraviroc blocks CCR5; enfuvirtide blocks gp41)
Two HIV regulatory genes
not gag, pol, env
Nef - regulates MHC-I expression on infected cells
Tat - transcriptional activator, promotes viral gene expression
MCC viral meningitis in children
what else can it cause, more rarely?
Enterovirus, specifically Coxsackie B
more rarely, encephalitis with flaccid paralysis
What kind of organisms are CGD patients susceptible to?
CGD = NADPH oxidase inactivation > no ROS formation
CATALASE-POSITIVE MICROBES - without catalase, microbes can’t prevent H2O2 accumulation from THEIR OWN metabolism in phagosomes > hypochlorite is formed + damages microbe; with catalase, H2O2 is broken down
What are the 5 most common organisms that infect CGD patients?
CATALASE-POSITIVES:
S. aureus Burkholderia cepacia Serratia marcescens Nocardia Aspergillus
Molecule linked to PG wall in Gram-positive microbes only
Teichoic acid
Ag determinant for microbe ID and Ag target for immune system
Which bacteria produce IgA protease? (4)
what does it do?
Neisseria (both), S. pneumo, H. flu
Cleaves IgA at its hinge region > Fab and Fc fragment
facilitates bacterial mucosa adherence
Bacillus anthracis
antiphagocytic feature
D-glutamic acid capsule
B. anthracis
toxins
edema factor - adenylate cyclase
lethal factor - hydrolyzes MAPK kinases
B anthracis
culture + micro characteristics
large, nonmotile, spore-former
nonhemolytic, gram-positive rod
cultures grow curled edges with “MEDUSA HEAD” shape
B anthracis
severe form of disease + its signs
Hemorrhagic Mediastinitis in “Pulmonary Anthrax”
prodrome > widened mediastinum on x-ray
can cause shock, brain edema/hemorrhage + death
seen in woolsorters and mail sorters
“Genetic Reassortment” in viruses
what happens? what kind of viruses / example?
another name for the result
2 strains infect same cell > SEGMENTS reassort > progeny with reassorted genomes (since genome is changed, progeny of the progeny will retain same changes)
SEGMENTED viruses only
in cause of INFLUENZA viruses, NA and HA are on different segments > novel strain created by reassortment = ANTIGENIC SHIFT
(drift is just point mutations)
segmented viruses
4
all are RNA viruses
Orthomyxo - INFLUENZA
Arena - LASSA FEVER virus
Bunya - HANTA virus
Reo - ROTAvirus
typical HEP B histo picture
“GROUND GLASS” hepatocytes have finely GRANULAR, diffusely homogeneous PALE PINK cytoplasm
due to accumulation of HBsAg in cells
typical Hep C histo picture
less specific picture than Hep B (no ground glass)
LYMPHOID AGGREGATES in portal tracts and MACROVESICULAR STEATOSIS
Strongyloides stercoralis infection
two larvae types? special infectious mechanism?
roundworm
infection - infectious FILARIFORM larvae in feces soil > penetrate skin > lungs > swallowed > adults lay eggs in GI mucosa > non-infectious RHABDITIFORM larvae release in poo
AUTOINFECTION - some rhabdi larvae molt into filari larvae and auto-infect host > widespread dissemination = HYPERINFECTION
Strongyloides stercoralis
hyperinfection in which patients (general answer is obvious but be more specific)
immunocompromised
specif. on drugs or HTLV-1 infection > impaired Th2
Strongyloides
s/s? specific findings? tx?
asymptomatic, or…
chronic GI and pulmonary sx
“LARVA CURRENS” - red itchy linear streaks on thigh/butt via subcutaneous larval migration away from butt
Dx - RHABDITIFORM larvae in stool; O+P on GI biopsy
Tx - IVERMECTIN
polysaccharide component of Hib capsule
polyribosylribitol phosphate
how does PRP capsule of Hib prevent phagocytosis?
binds “FACTOR H” in host circulation
factor H normally degrades C3b deposited on host cells > prevention of C3b deposition on Hib > no opsonization / complement mediated lysis
M protein
which microbe? function?
in cell wall of Strep pyogenes
binds factor H > prevents opsonization / complement mediated lysis
Protein A
which microbe? function?
cell wall of S. aureus
prevents opsonization by binding Fc region of Igs
Aeromonas hydrophila
micro characteristics?
disease?
risks?
oxidase-positive
non-lactose-fermenting
Gram-negative rod
gastroenteritis, wound infection, bacteremia
exposure to contaminated water
Pyrrolidonyl arylamidase test (PYR)
S. pyogenes?
S. aureus?
S. pyogenes is PYR POSITIVE
S. aureus is PYR NEGATIVE
Best method for confirmatory dx of Trichomonas
Saline microscopy for MOTILE TRICHOMONADS
Diff. dx of vaginal infections by vaginal pH
3 infections
Bacterial vaginosis and trichomonas show HIGH pH (>4.5)
Candidiasis shows NORMAL pH (3.8-4.5)
How to diff btwn two types of gram positive cocci?
Catalase
Staph - cat pos
Strep - cat neg
How to differentiate Strep by hemolysis?
alpha hemolytic - slight zone, greenish > S. pneumo + viridans
beta hemolytic - S. agalactiae or S. pyogenes
Which 2 types of cat-neg Gram+ cocci are gamma-hemolytic (no hemolysis)?
Enterococci
Strep gallolyticus (bacteremia/infective endocarditis assoc. with colon cancer)
How to diff btwn alpha hemolytic strep?
bile and optochin sensitive - S pneumo
bile and optochin resistant - S. viridans
How to diff btwn beta hemolytic strep?
S pyo - bacitracin-sensitive and PYR positive
S agalact - bacitracin resistant, PYR negative, and CAMP positive
How to diff btwn gamma hemolytic gram+ cocci?
Enterococcus - grow in 6.5% NaCl and bile, PYR positive
S. galloyl - grow in BILE BUT NOT SALT and are PYR negative
which two bacteria are PYR positive?
S. pyogenes
Enterococci spp.
Campylobacter jejuni
source other than contaminated food?
domesticated animals
especially puppies from kennels
1 cause viral gastroenteritis
transmission? presentation?
Norovirus
feces-contaminated food/water
vomit-predominant illness with pain and moderate amt diarrhea (non-inflammatory, no blood/WBCs in stool)
Vibrio parahaemolyticus
where + from what? presentation? worse in whom?
marine environments; contaminated shellfish
diarrhea-predominant gastroenteritis
sepsis in liver disease / HEMOCHROMATOSIS
dx for Giardia
3 things, first 2 most important
- Stool O + P
- Fecal immunoassay for antigens
(3. SI biopsy - villus atrophy + crypt hyperplasia dependent on disease severity)
main mechanism for Giardia immunity
considering this, who gets Giardia more?
CD4 function and SECRETORY IgA (binds trophozoites > impaired adherence to upper small bowel wall)
Kids with IgA deficiency, X-linked agammaglobulinemia or COMMON VARIABLE IMMUNODEFICIENCY get giardia more
M protein
which microbe? structural homology with what?
S pyogenes
homologous to human tropomyosin and myosin (both have many alpha helices + coiled coils)
cross-rxn with heart myosin > rheumatic carditis
prophylaxis for Strep agalactiae
universal screening by maternal vaginal + rectal culture at 35-37 weeks
any woman who is CULTURE POSITIVE or has PAST CHILD AFFECTED should take…
INTRA-PARTUM PENICILLIN (or ampicillin alternative) will prevent sepsis, pneumonia + meningitis in baby
(prepartum penicillin has a risk of re-colonization before birth)
Primaquine
unique use in malaria?
kills HYPNOZOITES dormant in liver > prevents disease relapse
what 2 plasmodium spp. tend to create hypnozoites?
consequence? tx?
P. vivax and ovale
can cause disease recurrence after hypnozoite rupture from liver; tx with primaquine
how can LACTOSE-FERMENTING GRAM-NEGATIVE RODS be differentiated in UTIs in women?
differentiates what species?
Indole test - conversion of Trp to indole
E. Coli - indole-positive
Enterobacter cloacae - indole-negative
What is FIRST used to differentiate gram-negative rods biochemically?
MacConkey agar
Lactose fermenters form PINK colonies (Klebs, E coli, Enterobacter, Citrobacter, Serratia)
Non-fermenters form WHITE colonies (Pseudomonas, Shigella, Salmonella, Proteus)
Among lactose fermenting gram negative rods, how are they differentiated by fermentation speed?
Fast fermenters - Klebs, E. coli, Enterobacter
Slow fermenters - Citrobacter, Serratia
Among non-lactose fermenting gram-neg rods, what is the FIRST step in differentiation?
oxidase test
oxidase positive - Pseudomonas
oxidase negative - Shigella, Salmonella, Proteus