Micro Flashcards
Cryptococci
Can resolve on own in normal pts, PROBLEMATIC in immunocomp
Cryptococci reservoir
Soil, bird poop
Not communicable person to person
Cryptococci
Skin or pulm –> CNS Meningoencephalitis (fatal)
Inhalation of desiccated yeast cells
Cryptococci
India ink on direct exam(yeast)
Sabaroud’s & Potato dextrose agar (SDA or PDA culture)
Growth on CGB medium
Crypto most likely pathogen
Cryptococcus Neoformans
Cryptococcus neoformans: Virulence Factors
Diphenol oxidase forms melanin from phenol containing subst
Ability to grow at 37C
Capsule evades phago
Crypto clinical sx
Pulmonary: No sx, OR flu-like
Disseminated: Meningitis, Crypto skin lesions
(C. Gattii: more extensive infections)
Toxoplasmosis Gondii
Foodborne illness
Toxoplasmosis Gondii
Usually not a problem in normal pts, PROBLEMATIC in Immunocomp and Pregnant
Triad of sx in Congenital Toxoplasmosis
Chorioretinitis (eye)
Hydrocephalus
Intracranial calcifications
Toxoplasmosis has 2 forms
Trophozoite (Tachyzoite and Bradyzoite)
Cyst (INFECTIOUS)
Toxoplasmosis subtypes of Trophozoites: Tachyzoite and Bradyzoite
Tachyzoite: acute dz, actively proliferating
Bradyzoite: chronic dz, slowly replicating
Toxoplasmosis subtypes of Cysts: Zoitocyts and Oocyst
Zoitocyst: tissue type that contains bradyzoites
Oocyts: sexual stage in Cats
How does Toxoplasmosis generally spread through Foodborne illness?
Via Zoitocyst (the tissue type containing bradyzoites)
Toxoplasmosis Gondii dx
Difficult to get samples
ELISA: IgG, IgM in pregnant mother
PCR: detect parasite DNA in amniotic fluid
Prevent Toxoplasmosis
Cook meat thoroughly
Wear gloves/ wash hands after gardening
Keep sandbox covered
Do not allow pregnant mothers to clean litter box- stay away from cats bc they are evil
Naegleria Fowleri
Soil and Fresh water
Lake Havasu- rare brain infection
Amoeboid is the DANGEROUS form
N. Fowleri
Cyst and
Trophozoite (flagellate and amoeboid*)
N. Fowleri
Can cause PAM in HEALTHY pts
Travels olfactory nerves –> brain, eats RBC, WBC, olfactory bulbs, and brain tissue
N. Fowleri
PAM!
1-14 d post exposure
Often death within 2 wks of sx onset
N. Fowleri dx
Clearing zone on E.Coli agar (takes long)- Flagellated form is confirmation
Wet mount for motile Amoeba
CSF findings
PCR test in the making
N. Fowleri, Trophozoite subtypes
- Flagellate
- Amoeboid
Flagellate: INFECTIOUS, enters nasal passage then transforms into–>
Amoeboid: DANGEROUS, DESTRUCTIVE, travels along olfactory bulb to brain
Acanthamoeba spp
Enter through break in skin OR Lower respiratory tract
Acanthamoeba spp
Soil and Contact lens
Acanthamoeba spp
Trophozoite (INFECTIVE, spiked pseudopodia) and
Cyst (3 layered wall, resistant to environment)
3 clinical syndromes of Acanthamoeba spp
- GAM/GAE- Granulomatous Amoebic Meningoencephalitis (100% mortality)
- Ocular Acanth/ Keratitis and Uveitis
- Disseminated dz
- GAM/GAE of Acanthamoeba
Frm break in skin or inhaling cyst
Sx: CNS, flu-like, Parenchymal (lung) edema, DEATH
- Ocular Acanthamoebiasis
After trauma to eye
Ulcer and pain (might look like Herpes)
Blurred vision, FB sensation
Acanthamoebiasis
Most ppl are resistant
Mostly PROBLEMATIC for Immunocompromised
Acanthamoeba dx
Both forms (Tropho and cytst) can be seen in tissue sections
Corneal scrapings
GAE-post mortem brain biopsy
NO POINT to examine CSF
Balamuthia Mandrillaris
Baboon dz
AGGRESSIVE, both forms (Tropho and Cyst) are INFECTIOUS
Balamuthia Mandrillaris
Can infect healthy person
Enters via Skin break or Respiratory
Balamuthia Mandrillaris infections
Healthy person: PAM
Immunocompromised: GAE
Balamuthia Mandrillaris sx
Face paralysis, difficulty swallowing
Seizures
Double vision
Balamuthia Mandrillaris feeds on other Amoeba… co-infection
With Legionella, you are screwed
Allows Legionella to txr to be 1000x more virulens–> CNS and Respiratory complications
Forms of Balamuthia Mandrillaris (Both are infectious)
Trophozoite: flat pseudopodia for locomotion
Cyst: 3 layered wall
Balamuthia Mandrillaris
Soil organism
Southern states and Latin america
Balamuthia Mandrillaris dz
Cyst and Tropho can be seen in tissue sections
Culture only works as Co-culture with Primate liver cells or Human brain cells
Tetanus
“Lowjaw” and “Trismus”
Death usually d/t Respiratory or Cardiac failure
Tetanus vaccine
Routine DTap and Td
Tetanus tx
Human tetanus immunoglobulin (HTIG) will neutralize toxin
Clostridial infections (2 subtypes)
C. Tetani-Tetanus
C. Botulinum- Botulism
Both are Neurotoxins and ANAEROBES
Clostridial infections: Tetanus and Botulinism
Gram (+) Bacilli
Environmentally resistant spores
Exotoxins: imp in dz progression
Tetanus spores
“tennis racket” appearance
Tetanus dz can arise from
Contaminated soil or Human/animal feces
Ppl at risk for Tetanus
Newborns, IVDU
Tetanus pathogenesis
Trauma to skin allows entry of spore
Extent of dz depends on site of infection and infectious dose
Tetanus
Bacteria remains local but if multiplies and releases Tetanospasmin (potent exotoxin), this can be absorbed by local nerve endings and transported thru neurons, blood, and lymph
Clinical forms of Tetanus (3 subtypes)
Generalized (most common)
-includes neonatal infection of umbilical stump
-broken skin
Localized (uncommon)
-muscle spasm confined close to injured area, immunocompromised
Cephalic (rarest)
-assoc w/lesions to head/face/ear. only affects face, but can progress
Tetanus clinical sx
Severe dz, toxin –> cramping, twitching, spasm of muscles
Tetanus clinical sx
HA, trouble swallowing, fever, sweating, Clenched jaw: “Risus Sardonicus”, arched back
Tetanus extremity sx
Flexed arms
Extended legs
Dx of Tetanus (early is vital!)
Clinical findings more reliable than labs
Botulism
Bacillus has distended shape
Great heat resistance
Spores in soil, GI tract of birds, fish, mammals
Food poisoning assoc w/contaminated foods
Botulinim toxin (A-H)
A and B: Human dz
Botulinum toxin is Neurotoxic on chromosome
Prevents ACh from being released –> Flaccid paralysis
Botulinum toxin type H
Considered the most deadly substance ever
Inhaling only 13 ng or injecting ONLY 2 ng will kill adult
NO standard anti-toxin
(found in a strain that also produces type B)
3 Clinical forms of Botulism
Infant: ingest spores, 70% cases, colonize in intestine that has no established gut flora yet
Foodborne: ingested toxin, canned foods
Wound: spores reproduce in Anaerobic environment, IVDU
Botulism sx
NO FEVER
Infant: lethal (sudden infant death)
Foodborne: Gi disturbance, Toxemia, Eventual neuroparalysis
Wound: Neuroparalysis
Do you have a fever with Botulism?
NO
Dx of Botulism
diff bc similar presentation to many other dz
Confirmation related to toxin presence- stool sample
Tx: Antitoxin to neutralize
Dx of UTI
Microscopy: 2-5 WBC or 15 bacteria per high power
Dipstick test
E. Coli
Most common cause of UTI
Caused by UPEC: Uropathogenic E. Coli strains
E. Coli
Gram (-) bacillus, flagellated
UPEC E. Coli virulence factors
P. Fimbrae (pili) and Dr adhesins bind to uroepithelial cells and RBC
Produce a and b-hemolysins which lyse both types of cells
UPEC E.Coli
can produce K (capsular) antigen- typically in upper UTI and Chronic UTI d/t increased biofilms
Proteus spp (UTI)
Proteus vulgaris most common for UTI
Proteus Vulgaris cause of UTI
Nursing home/hospitals
(nare of hospital staff)
Can be part of normal flora
Proteus Vulgaris
UTI
“Swarming” on culture agar
Proteus causing UTI
Organism spread –> Sepsis
Produces UREASE and makes urine more Alkaline
Proteus causing UTI
Urease makes urine more alkaline –> Struvite Stones
Proteus UTI
Struvite stones
S. Saprophyticus causing UTI
Gram (+)
coag negative
Sexually active females
“Honeymoon cystitis”
S. Saphrophyticus causing UTI
2nd leading cause of UTI
sexually active Females
(normal flora of female genital tract)
S. Saphro causing UTI
Organism not very virulent
Has ADHESINS (lactosamine)
No exotoxins
Difficult to dx bc little number of bacteria present
How to differentiate S. Saphro causing UTI from other Coag negative organisms
Novobiocin resistance
S. Agalactae causing UTI
AKA Group B strep (GBS)
S. Agalactae (Group B Strep) causing UTI
Gram (+) coccus
S. Agalac (GBS) causing UTI
Gray-white colony w narrow zone of Beta-hemolysis
S. Agalac (GBS) causing UTI
infections in adults mostly only affects IMMUNODEFICIENT
S. Agalac (GBS) virulence factors
Capsular polysacch
Hyaluronidase
Collagenase
Hemolysin
Dx of S. Agalac (GBS)
Detection of CAMP factor
Definitive: isolation from blood, urine, CSF
Ulcerative STDs
Syphilis
Chancroid
Herpes
Non-ulcerative STDs
Gonorrhea
Trich
Chlamydia
Trepenoma pallidum causes:
Syphillis
Haemophilus Ducreyi causes:
Chancroid
Syphillis
Requires mammal host
Spirochete with slow rotational motility
Syphillis virulence factors
Fibronectin coat
Lesions are result of Inflammatory Respone
Syphilis
Only a HUMAN pathogen
Spread: usually STD, also needle sharing, lesion near mouth, MOTHER TO BABY
Clinical stages of syphillis
Primary: Chancre, if untreated heals in 3-8 wks w/ Fibrosis
Secondary: Maculopapular rash, Condyloma lata (warts)
LATENCY?? Or–>
Tertiary: NEURO, CARDIO, and Skin GUMMAS
Chancre (Primary Syphillis)
Thin, gray exudate
Base smooth
Border raised, firm, and indurated
Tertiary Syphillis
Neurosyph: cortical degeneration
Cardiovasc syph: aneurysm of ascending aorta
Gumma: skin, bones, joints
Congenital syphilis
Maculopap rash
Nasal obstruction w/mucoid discharge (infectious)
Osteitis of nasal bone
Neurosyphilis
+HUTCHINSONs TRIAD
Congenital syphilis
“Hutchinson’s Triad”:
Notched incisors, interstitial keratitis, 8th nerve deafness
Hutchinsons triad of Congenital Syphilis
Simple version
Incisors, Keratitis, Deaf
Dx of Syphillis
Darkfield microscopy
Most diagnosed w Serology: Trepenomal test- specific antibodies are confirmatory
Dx of Syphillis
Non-trep: used as screening. If (+), then move on to Trepenomal test… FTA-ABS, MHA-TP
N. Gonorrhea
Gram (-) diplococcus w kidney bean shaped cell
PICKY (fastidious) growing requirements
N. Gonorrhea virulence factor
Plasmid and Chromosome mediated RESISTANCE to PCN, Tetracycline, Specto, and Fluoroq
More N. Gonorrhea virulence factors
Attachment via Pili
Surface proteins can dodge phagocytic activity
Bacteria alter surface property
Antigenic variation of pili
Gonorrhea epidemiology
Presence of b-lactamase positive strains (increasing #s of cases)
Major reservoir is Asymptomatic pt
Gonorrhea
Injury to cells d/t released Lipooligosacch and Peptidoglycan
Spread to other tissues via PILAR ATTACHMENT
Gonorrhea clinical spectrum
Can enter/exit any mucosal service
Female: endocervix, urethra
Male: anterior urethra with THICK mucopurulent d/c
Complications of Gonorrhea
Acute salpingitis
PID