Exam 6 (STDs and UTIs) Flashcards
39 yo male presents to hospital with tender penile ulcer on foreskin present for 2 weeks accompanied by swollen tender right sided inguinal lymph nodes. Treated for presumed syphilis with high dose penicillin. 1 week later, ulcer was unchanged, but developed inguinal lymphadenopathy on left side. Serologic tests for syphilis were negative as were direct fluorescent antibody tests. HSV tests were negative. What is most likely diagnosis? Treatment?
- Chancroid (causative agent = H. ducreyi). Treatment = macrolide
HPV. Describe diagnosis
5.) Diagnosis: - Clinical appearance sufficient for diagnosis. Hyperkeratosis and koilocytes (halo surrounding hyperchromatic nuclei) seen in histology from tissue sample. - PCR to identify HPV serotypes
Types of UTIs
- Upper/ascending UTI: nephritis/pylenonephritis = kidney +/- ureter infection - Lower UTI: a.) Cystitis: bladder infection b.) Urethritis: urethra infection c.) Prostatitis: prostate infection
What is the typical treatment of pyelonephritis?
- Fluoroqunionoles for gram negs - Amoxicillin for gram positives
HIV. Describe virion structure/virus types/tropism
1.) Virion structure/virus types - Retroviridae virus, +ssRNA (carries polymerase with it), enveloped - HIV-1: most common worldwide, including US - HIV-2: primary in W. Africa – longer asymptomatic period with lower mortality and more gradual decline in CD4 count - Tropism: a.) R5-tropic: uses CCR5 coreceptor, predominant early in disease b.) X4-tropic: uses CXCR4 coreceptor, associated often with rapid progression to AIDS - Structure: a.) p24 nucleocapsid protein encasing diploid genome b.) p17 matrix protein c.) envelope d.) gp120 attachment protein embedded into envelope e.) gp41 fusion protein embedded into envelope
HPV. Describe diseases caused/clinical presentation
2.) Diseases caused/clinical presentation: a.) Genital/cervical warts (aka condyloma acuminatum): 1mm-2cm hyperkeratotic firm exophilic papules: itching, pain, burning b.) Respiratory papillomatosis/laryngeal papillomas: nodules in larynx. Typical in babies. Symptoms = altered cry, hoarseness, stridor, resp distress c.) Cervical cancer
Most common bacterial sexually transmitted disease
- Chlamydia trachomatis
What causes alterations in normal vaginal microbiota?
- Age - Menstruation - Hysterectomy or cervicectomy increase in bacterioides, E. coli and/or Enterococcus
Symptoms of pylenonephritis
- Flank pain - Fever - Frequency, urgency, hematuria, dysuria - Severe cases: diarrhea, vomiting, tachycardia
24 yo female presents to clinic with painless, wart-like vaginal lesions. Recently arrived in US from brazil. Exudate from warts were stained with Giemsa and intracellular bodies were apparent. What is most likely diagnosis? Treatment?
- Donovanosis aka granuloma inguinale (causative agent = K. granulomatis). Treatment = tetracycline, sulfamethoxazole, gent, cipro, erythro
Test to distinguish non-enterobacteriaceae family of enteric bacteria from enterobacteriaceae enteric bacteria
- Oxidase pos = non-enterobacteriaceae enteric bacteria (campylobacter, fusobacterium, helicobacter, pseudomonas, vibrio) - Oxidase neg = Enterobacteriaceae = enterobacter, Escherichia, klebsiella, proteus, salmonella, shigella, Yersinia
27 yo woman presents with a vaginal itching, odor, and discharge for 1 week. She has one partner who is asymptomatic. Speculum exam shows a strawberry cervix. There is scant white discharge with a fishy odor. Strawberry pattern is caused by inflammation and punctate hemorrhages on the cervix. What is likely diagnosis?
- Trichomoniasis (causative agent = T. Vaginalis)
Enterobacteriaceae are family of enteric bacteria that are causative agents of UTIs. How are these diagnosed in lab – what are the characteristics of these organism and what tests are they positive/negative for? What are common virulence factors associated with them?
1.) Characteristics - Gram neg rods - Ferment glucose, reduce nitrate, catalase pos, oxidase neg 2.) Virulence factors - LPS, capsule (K), flagella (H), T3SS, sequester growth factors, antimicrobial resistance is high
HSV. Describe diagnosis
5.) Diagnosis: - Typical clinical diagnosis: 1-2 mm groups of vesicles-pustules-ulcers - Tzanck smear – presence of syncytia (multi-nucleated) - PCR, IHC – to distinguish HSV-1/2
31 yo feamle with malodorous discharge for 3 weeks. No associated vaginal itching or pain. Married and monogamous. Admits to douching about once per month to prevent odor but it is not working this time. On exam, her discharge is visible. Wet prep more than 50% of epithelial cells are clue cells. The pt most likely has an overgrowth of _______ and a reduction in ______ A. Yeast, lactobacillus B. Lactobacillus, small gram variable rods C. Small gram rods, lacto D. T.vaginalis, small gram variable rods E. G.vaginalis, T. vaginalis
Answer = C
Name that ulcer! How would you confirm diagnosis? A.) Painful, non-indurated, recent travel B.) Painless, indurated, no travel C.) Painless, wart-like, indurated, bleeds easily, travel
- A.) Chancroid (H. ducreyi): rule out syphilis, HSV, pt presents with inguinal lymphadenopathy. If positive send for culture with chocolate agar (with X and V factors) - B.) Syphilis (T. pallidum): serology (non-treponemal and treponemal), darkfield microscopy for visualization of spirochetes - C.) Donovanosis (K. granulomatis): rule of syphilis, HSV, look for Donovan bodies under microscope (intracellular bacteria)
HSV. Describe diseases caused/clinical presentation
2.) Diseases caused/clinical presentation a.) Genital herpes: - Lesion on vulva, cervix, peritoneum, penis, thighs, buttocks. Progression from macules – papules – vesicles – pustules – ulcers. Lesions are painful +/- pruritus, fever, inguinal lymphadenopathy, malaise. Primary infection lasts 3 weeks. Recurrent lesions less severe than initial, multiple times per year with prodrome (tingling/pain), heal within 7-10 days. b.) Neonatal herpes infection i.) skin, eyes, mouth ii.) encephalitis iii.) disseminated infection c.) Herpetic whitlow d.) Herpes labialis e.) Herpes simplex keratitis f.) Herpes simplex encephalitis
How to distinguish in a micro lab between staph and strep?
- Catalase pos = staph - Catalase neg = strep
HIV. Describe life cycle/pathogenesis
2.) Life cycle/pathogenesis a.) Attachment: gp120 binds CD4 (on T, mono and MO cells) leading to conformational change and binding to chemokine co-receptors (CCR5 or CXCR4) b.) Fusion: gp41 brings virion closer to host cell and mediates fusion c.) Reverse transcription: reverse transcriptase (pol) produces linear dsDNA of genome, it is highly error prone d.) Integration: viral integrase integrates viral dsDNA into host – genome now = provirus e.) Genome replication/transcription: provirus is transcribed and replicated f.) Budding: buds through PM at lipid rafts and leaves host g.) Protein cleavage/maturation: viral protease cleaves gag and gag-pol polyproteins leading to virion maturation – essential step
How to diagnose a UTI?
- Symptoms - UA: a.) Pyuria = leukocyte esterase pos b.) Typically greater than 100,000 CFU/ml of bacteria (can have UTI with less) c.) E.coli = nitrite pos
Leading cause of preventable blindness in the world?
- C. Trachomatis that causes trachoma
Name that discharge! What is the disease, causative agent? A. Thick white cottage-cheese like odorless B. Frothy, yellow-green, foul smelling C. Mucopurulent D. Thin white grey fish odor
- A. Vulvovaginal candidiasis = C. albicans - B. Trichomoniasis = T. vaginalis - C. Gonorrhea or chlamydia - D. Bacterial vaginosis = reduction in lactobacillus in normal flora
HPV. Describe characteristics of virus/serotypes
1.) Characteristics of virus/serotypes:hpv - Papovaviridae, dsDNA, non-enveloped Serotypes: - Laryngeal papillomas: HPV 6, 11 - Anogenital warts: HPV 6, 11 + high risk = HPV 16, 18, 31, 33. HPV 16 associated with ~50% of cervical cancers
Causes of genital ulcers. Describe ulcers in each
1.) Syphilis (Treponema pallidum): painless ulcerated, indurated lesion 2.) Genital herpes (HSV): see viral STD lecture 3.) Chancroid (Haemophilus ducreyi): painful, non-indurated, soft ulcer with erythematous base 4.) Donovanosis/Granuloma inguinal: wart-like, non painful lesions that bleed easily and can cause significant damage
True/false. Lactobacillus is a cause of UTI
- False
HPV. Describe transmission
4.) Transmission: - Sexual transmission of genital warts
Which of the following is not a complication/symptom of infection with N. Gonorrhoeae? A.) ectopic pregnancy B.) pustular rash C.) enteritis D.) conjunctivitis E.) pharyngitis
- Enteritis
Reasons HIV is thought to escape immune system destruction
1.) Antigenic drift of gp120 2.) Destruction of CD4 T-cells, macrophages and monocytes 3.) Causes cell-cell fusion
How to distinguish between lesions seen from syphilis vs chancroid?
- Syphilis chancres are painless, ulcerated and indurated - Chancroid lesions are painful, ulcerated with erythematous base Mnemonic: “You do cry with ducreyi” – H. ducreyi = causative agent of chancroid
Three weeks after a normal birth, infant presents with rhinitis and a widespread desquamating maculopapular rash. No other reports of rashes/illness in household; however, mother experienced flu-like symptoms and disseminated rash during second month of pregnancy. What is the most likely diagnosis? Treatment?
- Congenital syphilis (causative agent = T. pallidum) . Penicillin, or if allergic, azithromycin or doxy
What is asymptomatic bacteriuria? Are these treated? If so, with what
- Asymptomatic UTIs from two successive urine cultures with greater than 100,000 CFU/mL - Treated in: pregnant women, if pt is receiving urologic surgery, after renal transplant - Treatment = amoxicillin, cephalexin or nitrofurantoin
Mycoplasma genitalium. Characteristics, disease caused, treatment
- Characteristics: small free-living bacteria, no cell wall, not stained by gram or acid-fast or other typical methods, fried-egg appearance, plasma membrane has sterols (stolen from host), extracellular, part of normal GU tract flora - Diseases: NGU in males, cervicitis/PID in females - Treatment: nothing that targets cell wall (they don’t have cell wall), treat with azithromycin, resistant to doxycycline
24 yo sexually active male presents to clinic c/o 48 hour history of dysuria and penile discharge. Partner recently informed him she was diagnosed with chlamydia. Specimen collected and gram stain and urine samples for NAAT (nucleic acid tests). Pt sent home with rx for doxycycline given suspicion for chlamydia. Pt returns 10 days later c/o persistent symptoms as previously seen. Has been compliant with doxy. Gram stain reviewed with no organisms detected. NAAT negative for G/C. What is most likely cause of pts urethritis? What should happen next? A. N. gonorrhoeae B. C. trachomatis C. T. pallidum D. M. genitalium E. Ureaplasma F. H. ducreyi G. K. granulomatis
- Answer = M. genitalium. This is resistant to doxycycline, must be given rx for azithromycin
Populations at risk for STDs
- Fetuses - Adolescents - Rape victims - CSW: commercial sex workers - MSM (highest rates of STIs traditionally) - WSW (lowest rates of STIs traditionally) - Drug and IV drug users
Enterococcus (E. faecalis, faecium). Diseases caused, Characteristics/diagnosis, risk factors
- Diseases: UTI (hospital associated), peritonitis, endocarditis - Gram pos cocci, catalase neg, group D strep, resistant to optochin, tolerates high salt and bile - Risks: prolonged hospitalization, including tx with broad spectrum abx
Disease caused by mycoplasma hominis. What is the treatment?
- Postpartum or portabortal fever and PID - Treatment is doxycycline (which M. genitalium is resistant to). Resistant to erythromycin.
Vulvovaginal candidiasis. Cause, symptoms, risk factors, complications, diagnosis, treatment
1.) Cause: fungal infection, typically from Candida species (mostly C. albicans) 2.) Symptoms: itching, discharge - Discharge = thick, white, odorless, cottage-cheese/curd-like 3.) Risk factors: abx use, immunocompromised (can get esophagitis, disseminated infection), oral contraceptive use, diabetics 4.) Complications: recurrent infections, esophagitis and dissemination in immunocompromised 5.) Diagnosis - Gram pos stain or KOH prep shows budding yeast with hyphae and pseudohyphae if C. albicans, it also forms germ tubes at 37 degrees 6.) Treatment: 1-3 day topical azole for uncomplicated, 7-14 day topical or two doses or oral fluconazole for complicated
Treponema pallidum. Describe diagnosis, special risk factors, treatment, prevention
3.) Diagnosis: - No growth in free culture, difficult in cell culture, no gram stain - Detection via dark-field microscopy or direct fluorescence with antibody - Serology = most common a.) Non-treponemal tests = antibody directed to cardiolipin (RPR, VDRL tests) b.) Treponemal tests = antibody directed to T.pallidum 4.) Special risk factors: higher incidence in MSM population 5.) Treatment: penicillin, if allergic, treat with doxy or azithro 6.) Prevention: no vaccine, safe sex
Haemophilus ducreyi. Characteristics, epidemiology, diseases/clinical presentation, diagnosis, treatment, prevention
1.) Characteristics: gram-neg pleomorphic facultative anaerobe, small 2.) Epidemiology: rare in US, associated with travel to Africa, SE Asia, Caribbean 3.) Disease: - Chancroid: non-indurated and soft, tender/painful papule with erythematous base develops on genitalia/perianal area, can have multiple, presents with inguinal lymphadenopathy often 4.) Diagnosis: - Culture: requires factors X (hemin) and V (NAD) in “chocolate”/heated blood agar, catalase pos - Typically diagnosis via ruling out of syphilis (lack of pain at ulcer, no inguinal lymphadenopathy) and HSV testing 5.) Treatment: macrolide (azithro or erythro) 6.) Prevention: condoms
When a pt presents to clinic with genital ulcers, what should you be most suspicious of?
- Genital herpes - Syphilis - Less commonly: chancroid or donovanosis (Granuloma inguinal) as these are rare in US, associated with travel
Symptoms typical of urethritis and cystitis
a.) dysuria (painful urination) b.) frequency (multiple episodes of urination) c.) urgency (must urinate soon) d.) hematuria (blood in urine) e.) positive UA culture • no discharge typically seen
E. coli (incl. UPEC). Characteristics, virulence factors, diagnosis,
- Characteristics: Gram neg rod - Virulence factors a.) Adhesins b.) Hemolysin: lyses RBCs and other cells = inflammation c.) LPS/endotoxin: inflammation d.) Type I pili: binds to mannose residues on epithelial surfaces e.) P pili (on some E. coli, for example UPEC): binds sugar residue on uroepithelial cells - Diagnosis: gram neg, glucose fermenter, lactose fermenter (pos on MacConkey’s agar = red), reduces nitrates, catalase pos, oxidase neg
Predominant normal vaginal microbe. Describe
- Lactobacillus: gram pos, microaerophilic or anaerobic rod. Metabolizes glycogen to lactic acid causing pH of 4-5 - C. albicans
Most frequent bacterial causative agents of community acquired UTIs
- # 1 = E.coli (UPEC) – up to 95% - #2 = Staph. Saprophyticus
How many people are infection with syphilis in the US every year?
- 50,000
HIV. Describe disease progression (including viremic load, CD4 levels, antibody production)/associated symptomatology
4.) Disease progress/symptomatology a.) Acute infection (3-6 weeks post infection) - Symptoms: fever, malaise, arthralgia, lymphadenopathy, sore throat, perhaps faint rash – similar to mono. - Viremia spikes during this period, CD4 relatively stable, antibody level rising (may not be detectable) b.) Chronic/latent (post acute infection, median time frame for untreated = 10 years) - Symptoms: mostly asymptomatic - Low viremia during this time, CD4 levels declining, antibody levels are still rising c.) AIDS - CD4 T-cells severely reduced to below 200/ul, although antibody levels are high initially they drop, viremic load begins increasing - Sympatomatology is d/t associated / opportunistic infections – signature infections: 1.) Oral hairy leukoplakia: EBV 2.) Pneumonia: pneumocystis carinii (previously jiroveci), MB tuberculosis 3.) Thrush: C. albicans 4.) CMV retinitis: CMV 5.) Neoplasms: Kaposi’s sarcoma (HHV-8), B-cell lymphoma 6.) Diarrhea: cryptosporidium, isospora belli
Chalmydia trachomatis. Describe characteristics
1.) Characteristics: - obligate intracellular bacteria, lack peptidoglycan, gram neg like but cannot gram stain, exclusively human host, not spread on fomites - Biovars: a.) trachoma and b.) LGV - Serovars: based on MOMP (major outer membrane protein)
Pseudomonas aeruginosa. Characteristics, diagnosis, pathogenesis, risks, treatment
- Characteristics: gram neg motile rod, minimalist - Diagnosis: oxidase pos, non-fermenter - Pathogenesis: a.) Toxin A: halts protein synthesis via ADP ribosylation of EF-2 b.) Leukocidin: pore forming toxin targeting leukocytes c.) PLC: membrane disruption d.) Capsule: anti-phagocytic e.) Pyocyanin: blue compound toxic to host f.) Pyoverdin: fluorescent green iron uptake protein - Risks: primarily nosocomial infection – UTI from pts with indwelling catheters and exposure to other hospital instrumentation, multiple antibioitics - Treatment: Antipseudomonal penicillins (Ticarcillin / piperacillin) + aminoglycoside (amikacin, gentamycin or tobramycin)
HIV. Describe transmission
3.) Transmission: - sexual: most common route worldwide = heterosexual transmission, risk of transmission increased with other STDs esp those that breakdown mucosa - perinatal: risk = ¼ overall, highest risk at birth, can cross placenta, carried in breast milk - exposure to blood/body fluids: 0.3% skin puncture via needles, 0.09% mucosal membrane exposure
35 yo woman presents with severe vaginal and vulvar itching. She also complains of a thick white non-odorous discharge. What is the most likely diagnosis?
- vulvovaginal candidiasis, likely d/t C. albicans
Are enteric bacteria gram neg or positive?
- Neg, contain LPS
Bacterial vaginosis. Cause, symptoms, risk factors, diagnosis, complications, treatment
1.) Cause: dysbiosis, overgrowth of anaerobes, reduction in lactobacillus *not considered STD 2.) Symptoms: vaginal pain, itching, burning, discharge - Discharge = thin, white/grey/milky, foul, fishy 3.) Risks: oral sex, douching, smoking, sex during menses, IUD, early age sex, new/multiple partners, WSW 4.) Diagnosis: - Amsel criteria: must meet three out of 4 a.) Discharge (see above) b.) Clue cells from wet prep c.) KOH whiff test – fishy odor d.) pH>4.5 - Nugent score: scoring from 0 to 10 looking on slides for lactobacillus dominance or absence and other cell types. 0 = lactobacillus dominant, 7-10 = lactobacillus absent, other bacteria present 5.) Complications: susceptibility to HIV and other STDs, preterm delivery, miscarriage, post delivery infection 6.) Treatment: a.) Anaerobes/parasites: oral metronidazole (inhibits NA synthesis) b.) Gram pos cocci and anaerobes: clindamycin
15 yo hetero male to ED with 24 hour history of dysuria with pus-like drainage in his underwear and the tip of penis. Urine appeared clear and culture was negative. UA was positive for leukocyte esterase and multiple WBCS. Had 5 / 6 sexual partners in past 6 months with history of STDs. PEX indicated yellow urethral discharge with tenderness to tip of penis. Based on knowledge of symptoms and gram stain indicating gram neg intracellular diplococci, what is the likely diagnosis? What is the result of the maltose fermentation test? What is the treatment?
- Gonorrhea - Negative for maltose fermentation - Tx: ceftriaxone plus doxy/macrolide (for presumed chlamydia)
Treponema pallidum. Describe characteristics
1.) Characteristics: spirochete, microaerophilic, has gram-neg cytology, but doesn’t gram stain, axial fibrils/endoflagella for motility, human reservoir
HPV. Describe prevention
7.) Prevention: - Pap smears - Reduce high risk behavior - Vaccines (L1 capsid protein) a.) Quadrivalent = Gardasil b.) Bivalent = cervarix *only high risk 16/18 strains
HSV. Describe transmission
4.) Transmission: - Direct contact with lesions, saliva, sexual transmission of genital herpes
Neisseria gonorrhoeae (aka the clap, the drip). Describe diseases caused/complications
2.) Diseases caused - Gonorrhea: mucopurulent discharge (from urethra, cervix, epididymis, prostate or anus) and dysuria. Complications: PID in women leading to infertility and ectopic pregnancy. Can be asymptomatic in women, most male infections are symptomatic. - Gonococcemia = disseminated infection = septicemia, infection of skin and joints – associated with fever, migratory athralgias, suppurative arthritis, postural rash - Gonococcal opthalmia neonatorum = purulent conjunctivitis: mainly in newborn d/t exposure during vaginal delivery - Pharyngitis: mild to asymptomatic, typically accompanies genital infection - Anorectal gonorrhea
Treponema pallidum. Describe disease caused/clinical presentation
2.) Disease/clinical presentation a.) Syphilis (transmission sexual or congenital) - Primary: characterized by chancre, which is painless ulcerated indurated papule at site of spirochete penetration lasting weeks to months. Pts typically don’t present at this phase d/t no pain. - Secondary: flu-like syndrome (ST, HA, fever, myalgias, anorexia, lymphadenopathy) with disseminated prominent skin lesions called condyloma lata (soft, flat, moist, pink-tan papules and nodules over body including palms, soles and skin folds). This occurs 2-8 weeks after chancre. Resolves over weeks to months. - Latent: asymptomatic lasting years to decades, transmission to others possible - Tertiary (late): diffuse chronic inflammation of virtually all organs. Gummas (granulomatous lesions) found in bone, skin and other tissues. Pts can present with blindness, dementia, arteritis – worst impacts in neurological and cardio systems. 1/3rd of pts proceed to this stage. - Congenital: infected mothers transmit to fetus, which if it doesn’t kill the fetus will cause them to have this. Symptoms included chronic rhinitis leading to destruction of nose = Saddle nose. Desquamating maculopapular rash. Condyloma lata also seen. Typically have Hutchinson’s triad: Hutchinson’s teeth, blindness and deafness.
Examples of CoNS (coagulase neg staph). Characteristics?
- Examples = Staph saprophyticus and epidermidis - Characteristics = Gram pos, cocci clusters, catalase pos, coagulase neg, non-spore forming, non-motile, form biofilms - Saprophyticus = novobiocin resistant
HPV. Describe treatments
6.) Treatments: a.) Laryngeal papillomas: surgical removal b.) Genital warts: cryotherapy, CO2 laser c.) Cervical neoplasias: low grade vs high grade - low grade = cauterization, cryo, CO2 laser, loop excision - high grade = hysterectomy, radiation, chemo
What is the typical treatment of uncomplicated cystitis?
- TMP-SMX
Which immunodeficiency below would result in increased susceptibility to gonococcal infection? A.) C8 deficiency B.) IgA C.) C4 D.) IgG E.) IgM
- C8 defiency. Any deficiency in C5b through C9
Chlamydia trachomatis. Describe disease(s) caused and presentations/complications
2.) Diseases/presentation: a.) Trachoma (serovars A-C): chronic conjunctivitis that can progress to blindness - Transmitted by eye-to-eye droplets, fomites endemic in poorest countries. b.) Inclusion conjunctivitis - Acute conjunctivitis: mucopurulent discharge in sexually active adults - Neonatal conjunctivitis: infants exposed at birth, develops 1-2 weeks after birth c.) STI/urogenital infections (serovars D-K): - Men: dysuria, thin (yellow) mucopurulent urethral discharge. Complications = epididymitis, prostatis and can progress to Reiter syndrome (triad = urethritis, conjunctivitis and polyarthritis). Infection is symptomatic in men mostly - Women: (yellow) mucopurulent discharged, PID, can lead to sterility or ectopic pregnancy. Majority of infections are asymptomatic in women. d.) Lymphomagranuloma venereum/LGV (L serovars): genital infection, pt presents with painless lesion at infection site, inguinal lymphadenopathy, lymph nodes become supurative (buboes) and can rupture forming fistula. Proctitis (rectal inflammation) is commonly seen. Sporadic in US, prevalent in Africa, Asia and S. America. e.) Infant pneumonia
HSV. Describe characteristics of virus/types
1.) Characteristics of virus/types: - Herpesviridae virus, enveloped, dsDNA, contains HSV polymerase - *HSV-1: oral lesions - *HSV-2: genital lesions - * not always true
HSV. Describe treatment
6.) Treatment (target lytic infection, notso latent) Antiviral = a.) Acyclovir = nucleoside analogue – converted into active form via viral kinase and blocks polymerase b.) Foscarnet = non-nucleoside inhibitor – used in acyclovir-resistant infections, blocks polymerase - Oral lesions: not treated typically - Genital: primary = oral antiviral tx, recurrent = long term oral antiviral tx - Neonatal: IV antiviral tx - Ocular: topical antiviral tx
Rank top three most prevalent STIs in the US
1.) Chlamydia trachomatis 2.) Neisseria gonorrhoeae 3.) Treponema pallidum
Chlamydia trachomatis. Describe lifecycle/pathogenesis
3.) Lifecycle/pathogenesis: - Exists in two forms: EB (infectious) and RB (non-infectious). - Tropism for nonciliated, columnar, cuboidal and transitional epithelium - EB phagocytosed– progresses to RB (inclusion bodies in cell) – undergoes binary fission – converts back into EB form – cell is lysed and EB continues infecting other cells. Destroys epithelium and leads to inflammation through activation of cytokine response. LPS present with weak endotoxin activity. - Prolonged inflammation = fibrosis
What are the most common causes of Non-gonococcal urethritis
- Chlamydia - Secondly: mycoplasma genitalium and ureaplasma urealyticum
Neisseria gonorrhoeae (aka the clap, the drip). Describe diagnosis, special risk factors, treatment, prevention
4.) Diagnosis: - Culture from scrapings: gram neg aerobe diplococci in neutrophils, oxidase pos, catalase pos, non-spore forming and non-motile. Non-maltose fermenting. Requires chocolate agar/Thayer-Martin media. - Nucleic acid 5.) Special risk factors: - Deficiencies in late complement (C5b – 9 = MAC) 6.) Treatment: ceftriaxone plus doxy/macrolide to treat chlamydia, which is presumed with this infection. Neonates get prophylactic erythromycin ophthalmic ointment. 7.) Prevention: - No immunity to reinfection, patient education on safe sex practices
S. saprophyticus. Characteristics, disease, pathogenesis, diagnosis
- Characteristics: gram pos, cocci clusters, non-spore forming, non-motile, forms biofilm - Disease: 2nd most common cause of community acquired UTIs - Pathogenesis: enhanced capacity to adhere to uroepithelial cells possible d/t hemagglutinin/adhesion - Diagnosis: a.) Gram pos b.) Catalase pos c.) Coagulase neg d.) Novobiocin resistant
Symptoms of prostatitis
- LBP - Perirectal/testicular pain - Fever, chills and symptoms of cystitis (dysuria, frequency, urgency, possibly hematuria) - Positive UA culture
Pt presents with symptoms similar to chlamydia and is given doxycycline. Returns 2 weeks later with worsening symptoms. What do you suspect?
- Suspicious of M. genitalium infection, which are resistant to doxycycline. Effective treatment against M. genitalium is azithromycin.
Ureaplasma. Characteristics, disease caused, treatment
- Characteristics: small free-living bacteria, no cell wall, not stained by gram or acid-fast or other typical methods, plasma membrane has sterols (stolen from host), extracellular, part of normal GU tract flora in sexually active individuals - Disease: common cause of NGU in males - Treatment: Doxycycline. For recurrent infections, tx with azithromycin or quinolones
How to tell Neisseria meningitidis and N. gonorrhoeae apart in culture?
- Both gram neg aerobe diplococci, oxidase pos, catalase pos, non-spore forming, non-motile - N. meningitidis ferments maltose (mnemonic: M = meningitidis, M=maltose), while N. gonorrhoeae doesn’t
Menstrual toxic shock syndrome. Clinical presentation/symptomatology, cause and pathogenesis, diagnosis, treatment
1.) Presentation: diarrhea, general ill-feeling, high fever +/- chills, nausea, vomiting, sunburn rash with peeling of hands, feet, low BP, myalgias, HA, confusion, redness of eyes, mouth, throat, seizures 2.) Cause/pathogenesis: S. Aureus - Toxin mediated: TSST-1 exotoxin - TSST-1 penetrates mucosal barrier, is superantigen and activates high number of T cells leading to cytokine storm. - TNF-alpha (and beta) is primarily what leads to sepsis and shock 3.) Diagnosis: - Culture: gram-pos, catalase/coagulase pos, cocci clusters - Major criteria (all for diagnosis): hypotension, orthostatic syncope, less 90 SBP, macular erythroderma (sunburn-like rash), fever, skin desquamation (hands, palms, soles). Minor criteria (three): GI (diarrhea, vomiting), mucous membrane (oral, pharyngeal, conjunctiva, vagina), muscular (myalgia) 4.) Treatment: remove tampons (avoid in future), supportive measures, beta-lactamase resistant penicillin or vancomycin
Bacterial cause of kidney stones?
- Proteus mirabilis via urease
Klebsiella granulomatis. Characteristics, epidemiology, diseases/clinical presentation, diagnosis, treatment
1.) Characteristics: gram-neg intracellular rod, encapsulated 2.) Epidemiology: endemic in subtropics, rare in US, associated with travel 3.) Disease/clinical presentation - Donovanosis (aka Granuloma inguinale): wart-like lesions that are painless, but bleed easily, can rupture causing severe damage if untreated 4.) Diagnosis: slide shows Donovan bodies (which are bacteria inside of cells infected) via Giemsa staining 5.) Treatment: tetracycline, sulfamethoxazole, gent, cipro or erythro
Proteus (proteus mirabilis). Characteristics, disease caused, pathogenesis, treatment
- Characteristics: gram neg, facultative anaerobe - Disease caused: UTI, kidney stones - Pathogenesis: a.) urease converts urea to Co2 and ammonia leading to alkalization of urine b.) alkalization = precipitation of mag and calcium = production of renal calculi (kidney stones) c.) produces biofilm - Treatment: TMP-SMX (trimethoprim-sulfamethoxazole)
What is the CD4 T-cell count that is indicative of AIDS?
- Less than 200 cells/uL
Neisseria gonorrhoeae (aka the clap, the drip). Describe pathogenesis/virulence factors
3.) Pathogenesis/virulence factors: - *Pilin: attachment, antiphagocytic - *Por protein/porin: promotes intracellular survival - *Opa (opacity) protein: attaches to eukaryotic cells - *LOS (lipooligosaccharide): endotoxin (lacks O-antigen), inflammatory stimulates TNFalpha - Outer blebs: absorb antibodies and enhance toxicity - IgA protease: destroys IgA in mucosa where it infects - Beta-lactamase * Exhibit antigenic variation to avoid immune system
Trichomonas vaginalis. Characteristics, disease caused/presentation, pathogenesis, diagnosis, treatment
1.) Characteristics: pear-shaped protozoa with flagella and undulating membrane for motility, anaerobe, exists only in trophozoite (ie. Non-cyst) form therefore obligate parasite, reservoir is human UG tract 2.) Disease caused/presentation: - Trichomoniasis: majority of infected women are asymptomatic. Symptoms range from discharge to vaginitis with itching, burning and dysuria. Petechial hemorrhages on cervix, characteristic “strawberry cervix” - Discharge = yellow-green, frothy, foul smelling - Men are asymptomatic carriers, can sometimes have urethritis, prostatitis or UTI 3.) Pathogenesis: contact with squamous epithelium of GU tract results in destruction, neutrophil influx 4.) Diagnosis: - T. vaginalis swimming in exudate via Pap 5.) Treatment: metronidazole
HIV. Describe treatments including MOAs
6.) Treatments and MOAs (intervening during virus life cycle) – Goal = reduce viral load as low as possible for as long as possible a.) Attachment/fusion - Chemokine coreceptor antagonists: prevents co-receptor interaction with gp120 - Fusion inhibitors (FIs): binds to gp41 preventing fusion b.) Reverse transcription - Nucleoside inhibitors (NRTIs): incorporates into DNA chain during provirus synthesis causing termination - Non-nucleoside inhibitors (NNRTIs): inhibits reverse transcriptase c.) Integration - Integrase inhibitors (IIs): blocks integration d.) Protein cleavage/maturation - Protease inhibitors (PIs): inibitors of viral protease leading to production of immature defective HIV virions - Combination therapies are used in standard of care (at least three ARV drugs usually from two different classes) – always 2NRTIs plus: a.) 1 NNRTI b.) 1 PI c.) 1 II
HIV. Describe serological markers with acute to chronic infection and the diagnostic measures / testing schemes
5.) Serological markers, Testing/diagnosis Serology - HIV RNA = 1st marker present in plasma (as early as 10 days) - HIV-1 p24 antigen = 2nd marker present (as early as 15 days) - HIV antibody = 3rd marker Testing/diagnosis - #1: HIV1/2 antigen/antibody combo immunoassay – antigen = p24 specifically - #2: Differentiation HIV1/2 antibody immunoassays – if indeterminant, do nucleic acid testing
HSV. Describe pathogenesis
3.) Pathogenesis: - Entry and replication in peripheral epithelium - Retrograde transport of HSV into sensory neurons - Latency established in ganglia - Spontaneous reactivation (d/t stress, UV, trauma, hormonal etc.) and virion production resumes - Anterograde transport to epithelium - Replication in epithelium and HSV shedding
Predisposing factors to UTIs
- Obstruction of UT (d/t prostate hyperplasia for example) - Kidney surgery - Catheterization - GU malformation - Diabetes - Pregnancy - Female
Chlamydia trachomatis. Describe diagnosis, treatment, prevention
4.) Diagnosis: - Cannot culture by themselves, must be with cells. Use scrapings - Iodine identifies RBs, immunofluorescence of EBs - Choice test = nucleic acid from urine or discharge 5.) Treatment: Doxycycline or macrolide, both inhibit protein synthesis. No beta-lactam as no peptidoglycan. 6.) Prevention: education about safe sex practices, no immunity conferred with previous infection, no vaccine
Neisseria gonorrhoeae (aka the clap, the drip). Describe characteristics
1.) Characteristics - Gram neg aerobe diplococci, exclusively human host
HPV. Describe pathogenesis
3.) Pathogenesis: - Target for primary infection = basal surface of epithelium - Migrates towards suprabasal level and undergoes replication/differentiation along this path – key to have the levels in epidermis - In CA: genome integration is the only component that occurs – no replication. Increases in E6/E7 expression seen in virus during this time. E2 (negative regulator) is decoupled from E6/7 in genome and leads to increases in their respective levels. E6 represses p53, E7 represses Rb – both push cells into S phase and proliferative replication.
What is the best method for diagnosis of infection with chlamydia? A. culture of urethral discharge in liquid broth followed by staining B. culture of urethral scraping in liquid broth followed by staining C. culture of urethral discharge with cells followed by staining D. culture of urethral scraping with cells followed by staining
- D. Obligate intracellular bacterium
Most frequent bacterial causative agents of nosocomial acquired UTIs
- Klebsiella, enterobacter, serratia, p. aeruginosa, enterococcus - Proteus
