microbiology Flashcards
Genital herpes is characterized by what type of lesion and what type of inguinal adenopathy?
Lesion-multiple grouped vesicles to coalesced ulcers that are painful.
Inguinal lymphadenopathy-tender, nonsupprative (pus producing)
What are the characteristic features of herpesviridae?
Icosahedral, dsDNA, enveloped, replicates in the nucleus, multiplies in mucosal epithelial cells
How are herpes acquired and how easy is it to catch? What are the complications for neonates?
Risk of infection with contact of a symptomatic person is 75%, most acquire it via non-symptomatic persons.
Neonates have a 50% chance of infection and usually develop a disseminated disease involving the CNS; 60-70% mortality rate of these patients with survivors having permanent neurological defects.
How do herpes evade the immune system and become recurrent?
HSV-2 invades local nerve endings and travels up the axons to the sacral ganglia where it replicates. Travels back down to same general area and is usually less severe the second time, but can shed even in the absence of a lesion.
How do you diagnose HSV-2? What are you looking for?
Tzank test of lesions to look for MNGC
Tissue culture is gold standard.
What bacteria leads to the development of chancroid/soft chancre?
Haemophilus ducreyi
What are the characteristics of haemophilus decreyi?
G- coccobacillus, anaerobic, facultative, fastidious:CO2, chocolate agar, humidity, very infectious
Whats a bubo?
swollen painful LN which can rupture and discharge pus. 50% have an acute painful lymphadenopathy.
How do you dx and tx a chancroid?
Gram stain the ulcer exudate looking for G- coccobacilli “school of fish”. Culture is the gold standard (hard)
Tx drain the lymphadenitis with needle and give antibiotics.
Syphilis comes from what bacteria, describe it?
Treponema pallidum
G- spirochete which is too hard to see without using dark field microscopy or immunofluorescence.
Very motile with axial filaments. Not very antigenic but can illicit an inflammatory response that destroys tissue.
How can you get syphilis?
sex, kissing, touching, congenital
What’s the pathogenesis of syphilis?
No symptoms for 3 wks, then a hard painless chancre (primary) heals spontaneously.
During this phase spirochetes can enter the bloodstream, lymphatics (regional lymph adenoma)
Secondary (highly infectious): generalized lymphadenoma skin infection, joints, mucous membranes (mouth/genitals), painless warty condyloma late, and a moth-eaten alopecia.
Then it goes latent for years and can relapse into secondary symptoms or progress to tertiary
Tertiary is rare, noncontagious and highly destructive
Tertiary syphilis has what three forms?
gummatous-hypersensitivity reaction
cardiovascular- aortic valve dilation/regurg
neurosyphilis- most common. Meningitis to dementia
Dx syphilis: what are the strengths and weaknesses of the two tests used?
Treponemal test-anti-treponemal Abs, weakness is that its positive after treatment so it can’t be used for monitoring therapy
Nontreponemal test (VDRL, RPR): Tests for normal components of mammalian membranes that cross react with the treponema surface molecules. This leads to more false positive results (though you can confirm using the first test) but is better for monitoring; neg after 1 yr.
VDRL venereal disease research lab
RPR rapid plasma reagin
Your attending has you inspect a patient with urethral discharge that is serous and clear and asks you the question: Is his urethritis from Gonorrhea or not?
NO, Gonorrhea would produce copious amounts of purulent discharge making this a NGU non gonorrheal urethritis; possibly chlamydia
What are the two most common causes of cervicitis?
Chlamydia and N. Gonorrhea.
Descrive phase and antigenic variation in N. Gonorrhea?
Phase variation is the turning ON/OFF of opa surface proteins and pili.
Antigentic variation is the changing of these as an immune evasion strategy.
What is another name for a Gonorrheal patient with neonatal conjunctivitis?
Opthalmia neonatorum
N. Gonorrhea infection spread from a woman cervix into the blood stream. What are the symptoms of this disseminated spread? Who’s at highest risk for complications from this type of spread?
DGI disseminated gonococcal infection
migratory polyarthritis
septic arthritis (pain and swelling)
tenosynovitis
High risk individuals include-SLE, HIV, C6-9 deficiencies.
Men usually have urethra infections of N. Gonorrhea only but what about women? What are the associated symptoms with the areas of spread?
Urethra- bartholin cysts, dysuria, purulent
Rectum- purulent, bleeding, pain
PID leading to chronic endometritis
acute Endometritis
Anorectal proctitis is characterized by what symptoms and caused most commonly by what pathogen?
Puritus, discharge, painful defication
N. Gonorrhea
How do you diagnose N. Gonorrhea in men and women?
Men gram stain of pus smear looking for G- diplococci
Women additional PCR and clinical symptoms
On a trip to Ecuador you see a 30 y/o patient that is having trouble seeing. You notice conjunctival bumps and inflammation during the eye exam. What do you call this?
A) neonatal conjunctivitis
B) trachoma
C) adult endogenous conjunctivitis
D) inclusion conjunctivitis
B) Trachoma THIS IS NOT INCLUSION CONJUNCTIVITIS
(which can be acquired via the birth canal or endogenously) and is NOT an STI.
Caused by Chlamydia trachoma’s which also causes inclusion conjunctivitis. This is really just a different serotype based on outer membrane proteins.
lymphogranuloma venereum is caused how and by what?
Describe the lesion and adenopathy
Chlamydia infects the epithelial cells of the mucus membrane in the vagina, cervix etc. It then infects the lymphatics and LN and multiplies within phagocytes. This causes LN swelling or tropical bubos.
Lesion-painless, small ulcer
Adenopathy-discrete, suppurative, or draining fistula
Pathognomonic groove sign
Long term-LN obstruction and deforming edema of genitalia or anus.
Usually homosexual male in south american africa or asia
