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UGS Microbiology
Microbiology of the Urogenital System Final Material
| Question | Answer |
|---|---|
| What is characteristic about Parvovirus B19? | ONLY Single stranded linear DNA virus Smallest icosahedral virus Replicates in the nucleus |
| What disease does parvovirus cause? | A childhood disease called Erythema or fetiosum(fifth disease) |
| How does the erythema manifest clinically? | By a fever and slapped face rash on the cheeks Malaise, headache, myalgia, itching, and enlarged liver and spleen |
| What percentage of women of child-bearing age are immune to congenital parvovirus? | 50% |
| If congenital parvovirus is acquired by a non-immune pregnant women what is the transmission rate? | 33% |
| What effects can congenital parvovirus have on a non-immune pregnant woman? | Fetal loss through hydrops fetalis, severe anemia, congestive heart failure, and edema |
| Risk of fetal death to congenital parvovirus is highest in: | The second trimester |
| How is congenital parvovirus diagnosed? | IgM-sepcific Ab |
| How is congenital parvovirus treated? | Intrauterine infusions in case of hydrops fetalis and administration of digoxin to the fetus |
| What are the characteristics of Herpesviruses? | Double stranded linear DNA Enveloped and Icosahedral |
| What are the three subfamilies of Herpesviruses? | Alpha, beta and gamma viruses Alpha --> HSV1,2, and VZV Beta --> CMV, HHV-6, and 7 Gamma --> EBV, and HHV8 |
| What are the clinical manifestations of a herpes infection? | Ulcers, chickenpox, encephalitis |
| What is the herpes virus capable of? | Latency and reactivation |
| What are the types of proteins in Herpesviruses? | IE --> transcription E --> non-structual proteins L--> Major structural proteins |
| How is the neonate infected with herpes? | During passage through the birth canal, especially in case of premature membrane rupturing May also be infected transplacental or oral |
| What makes it difficult to diagnose herpes prenatally? | It may be confined to the cervix |
| How long does it take for Herpes to manifest in the neonate and how does it manifest? | 1-2 weeks --> 4 weeks max Skin vesicles in 55% or localized CNS disease (encephalitis, pleocytosis) Disseminated disease --> hepatitis, pneumonoa, DIC |
| How is Herpes in the neonate diagnoses? | Samples from skin vesciles tested with culture, PCR, IF, or Electron microscope Tzanck test may show multinucleated giant cells and intranuclear inclusions |
| How is herpes treated? | Acyclovir/Zovirax or supportice therapy Herpetic keratoconjunctivitis requires topical trifluridine or vidarabine |
| What is the mortality rate of untreated disseminated disease and encephaltis? | 85% 50% Brain involvement --> Almost 100% mortality |
| How can herpes transmission to the child be prevented? | C-section |
| What are the characteristics of the VZV? | Alpha herpes virus |
| How is VZV transmitted? | Respiratory or contact with lesion |
| How does VZV manifest? | URTI, Lymph node enlargement, respiratory disease, viremia, skin lesions Scarring, limb hypolasia, CNS defects, death in infancy |
| What percentage of pregnant women are immune to VZV? | 90% |
| How can VZV spread to the fetus? | It can cross the placenta in late stages of the virus |
| Which form of hepatitis is a major cause of neonatal hepatitis? | HBV |
| What is the mode and risk of transmission from the mother tot he fetus? | During delivery and the risk is from 70-90% Postpartum transmission and transplacental transmission is RARE |
| What are the clinical manifestations of neonatal hepatitis? | Mostly asymptomatic Can have low birth weight, jaundice, failure to thrive, abdominal distension, red-ish stool, heptamegaly, ascites, and hyperbilirubinemia |
| How is HBV diagnosed? | Measure HBsAg, HBeAg, anti-HBe, and HBV DNA in blood |
| Which markers are positive in acute HBV infection? | HBsAg, IgM anti-HBc, HBeAg, and HBV-DNA |
| What markers are positive in chronic HBV infection? | HbSAg, IgG, HBeAg, Anti-HBe, and HBV-DNA |
| What markers are positive in prior HBV infection? | Anti-HBs, IgG, and Anti-HBe |
| What is the treatment for HBV infection? | Symptomatic care and nutrition Immunization for other forms of Hepatitis Antiviral infection like IF-alpha |
| How can we prevent HBV? | Testing pregnant women Treating pregnant women with lamivudine or Telbivudine Immunize children with HBIG IM after birth |
| What is the prognosis of HBV infection in neonates? | Carrier state after vertical transmission --> 20x liver disease 86x hepatoma |
| What is the chance of spontaneous transmission in case of HCV infection? | 25-50% |
| What are the clinical manifestations of HCV infection? | Commonly asymptomatic Cirrhosis with liver failure and hepatocellular carcinoma may occur in childhood |
| How id HCV treated? | Interferon, ribavirin, and Sofosbuvir |
| What are the risk factors of children being affected with HIV? | High viremia in the mother Low maternal CD4 count Primary HIV infection during pregnancy Other STDs Rupture of membranes more than 4 hours before delivery Vaginal delivery, older age, and preterm births |
| How often is HIV vertically transmitted? | 15-25% |
| How can transmission of HIV be drastically reduced? | By administration of retroviral to the mother IV in labor and to the infant during the first 4 weeks of life This can decrease risk by 66% or more |
| How can HIV be identified? | By antenatal testing in 25-50% of cases (MANDATORY) |
| How many cases of pediatric HIV are due to vertical transmission? | More than 90% of cases |
| How can congenital and perinatal infection be reduced? | Serological screening of rubella, syphilis, HBV, and HIV in pregnancy By washing hands: prevent CMV and toxoplasmosis Modify behavior: to prevent STDs and blood borne viruses Avoid undercooked food Avoid vaginal delivery in active herpes |
| Which organisms are retroviruses found in? | All vertebrae |
| Which classes are included in the retroviridae? | HIV, FIV, and FeLV |
| What is a characteristic feature of Retroviruses? | Their nucleic acids are RNA in the virus, and DNA in infected cells |
| How are retroviruses transmitted? | Either by exogenous viruses of vertically by endogenous viruses |
| What are the general characteristics of retroviruses? | Enveloped with a lipid bilayer and viral spike glycoproteins Outer matrix and inner capsid Single stranded positive RNA |
| How are retroviruses classified? | Alpha, beta, and gamma --> simple genome Delta, epsilon, lenti, spuma, meta, and errant --> Complex genome |
| What are the proteins of the HIV? | gag core proteins--> p17 (Matrix) and p24 (Capsid) pol --> p16 (protease), p31 (integrase/endonuclease), RT, and RNaseH env--> gp160 (gp:120 outer membrane part, and gp41: transmembrane part) |
| How does the HIV replicate? | 1) Viruses attaches to CD4 2) binding of gp120 to CD4 3) Penetration and uncoating 4) RNA reverse transcribed into a DNA provirus 5) Latency or active transcription --> synthesis and maturation of virus progeny |
| Which type of HIV is the main cause of infection? | HIV1 |
| How many people are living with HIV in the world and how many new cases are there each year? | 34 million 2.5 million |
| What are the modes of transmission and risk factors of HIV infection? | 1) Sexual transmission 2) Blood products 3) Vertical transmission 4)Other: Contact with non-intact skin and accidental needle sticks |
| How is HIV staged? | 1) Stage 1--> HIV+ blood with no other HIV symptoms 2) Stage 2 --> CD4 count between 200-499 cells/microL 3) Stage 3 --> AIDS, most severe stage CD4 <200 |
| What conditions are AIDS defining? | Candidiasis of the bronchi, trachea, lungs, or esophagus Cervical cancer Disseminated coccidiomycosis/Cryptococcus CMV disease in unusual sites Herpes does not heal Kaposis sarcoma Burkitt's lymphoma Mycobacterium infections Recc pneumonia |
| What are the clinical manifestations of the acute HIV infection? | 2-4 weeks up to 3 months after infection comes a SEVERE flu with fatigue, sore throat, enlarged lymph nodes, loss of apetite, mouth sores, neck stiffness, headache, and rash |
| What are the clinical manifestations of HIV when it is latent? | Patients are contagious but others no specific symptoms |
| Which oppurtunistic infections occur with AIDS? | Pneuocystis jirovecii Toxoplasmosis, cyrptospoidosis Candidiasis, crytococcosis, histoplasmosis Mycobacterim avium, salmonella septicaemia, reccurent pyogenic infection CMV, HSV, VZV, JCV |
| What is the most common neurological disorder observed in AIDS patients? | Encephalopathy in almost 2/3rds of patients |
| How is HIV diagnosed? | Serology-Most likely ELISA or Western blot Viral detection is done by testing for p24 antigens ELISA can detect it 4-6 weeks after exposure Western blot detects gp120, gp160, and gp41 Clearview/ Rapid tests are also available |
| How can we decide what the prognosis of a patient with HIV is? | By measuring the HIV viral load with antiviral therapy By measuring HIV Antigens |
| How do we treat HIV? | HAART Nucleoside analogue RTI --> Lamivudine, Zidovudine Non-nucleoside RTI --> Nevirapine Protease I -->Indinavir, Ritonavir Fusion I--> Fuzeon (IM) |
| What does HAART consist of? | 2 nucleoside reverse TI and a protease inhibitor |
| What is the general prognosis of HIV? | Progression to AIDS within 10 years, death within 3 years of AIDS onset With tx --> Almost normal life span |
| How can you prevent HIV infection? | Use of condoms and less sexual partners Blood donor screening AZT in HIV+ mother and child Inoculate health care workers (controversial) Do not share razors or toothbrushes |
| What are the 4 types of Schistosomas likely to infect humans? | 1) S. Mansoni 2) S. Haematobium 3) S. Japonicum 4) S. Mekongi |
| After mating in the portal vein, adult Schistosomas ascend which vessels? | The mesenteric vessels Japonicum and Mekongi enter the superior mesenteric Mansoni and Haematobium enter the inferior mesenteric |
| Which Schistosoma reaches the venous plexus of the bladder and other pelvic organs? | Haematobium |
| Once reaching the submucosal venules, what do the worms perform? | Oviposition--> deposition of 300 eggs per day for 4-35 ears |
| Where do the ova laid by the schistosomas rupture? | Into the lumen of the bladder and are passed into the urine |
| What are the sizes of the eggs laid by schistosomas? | 60-140 microns |
| What is characteristics of the eggs laid by the schistosomas? | They have a terminal spine |
| What are the hosts of the schistosomas? | 1) First intermediate host -Snail host after the hatch in the water (Miracidia) 2) Infectious stage (Cercariae) 3) Come in contact with human skin (Second intermediate host) |
| What are the methods of prevention of schistosomiasis? | Modern waste disposal Water purification Den snail access to newly irrigated lands |
| What severe outcome can result from developing heavy loads? | Possible live cirrhosis, cancer, and subsequent death |
| What are the clinical stages of Schistosomiasis? | 1) Penetration and migration of the schistosomula 2) Oviposition and clinical manifestation 3) Chronic stage --> granuloma formation and scarring around eggs |
| What are the characteristics of the 2nd/intermediate stage? | 1-2 months after exposure Acute febrile illness like serum sickness Formation of immune complexes Fever, chills, cough, urticaria, athralgia, lymphadenopathy, splenomegaly, abdominal pain, and diarrhea |
| What are the clinical symptoms of a chronic S. Haematobium infection? | Bladder mucosa becomes thickened, papillated, and ulcerated Hematuria, dysuria, anemia due to hemorrhage, and severe muscular bladder infection Possible renal failure, uremia, and bladder carcinoma |
| How is schistosomiasis diagnosed? | Recovery of eggs in urine and biopsy Painless hematuria Cytoscopy with biopsy of the bladder Conventional serology --> Antibodies over 90$ |
| How is schistosomiasis treated? | Antihistamine and corticosteroids for dermatitis Praziquantel --> Effective against all times |
| Candida albicans is able to form hyphae in changes in: | pH, temperature, and available nutrients |
| What are the types of Candidiasis? | Localized and Disseminated |
| What are the clinical manifestations of Localized Candidiasis? | Erythema, white plaques (diaper rash), oral thrush in the immunocompromised Itching and thick white discharge of vulvovaginits |
| What are the clinical manifestations of disseminated Candidiasis? | Limited almost exclusively to the immunocompromised Diffuse pneumonia and urinary tract involvement (Ascending or hematogenous cystitis. pyelonephritis, renal pelvis infections or abscesses) Endophthalmitis |
| Candida albicans is a member of which flora? | Oropharyngeal, GI, and female genital flora |
| What are the causes of Candida infection? | Infections are usually endogenous except in directmucosal contact with lesions (sexual contact) Nosocomial infections |
| What determines the severity of infection? | Neutrophil function and count |
| How can we diagnose Candida? | Potassium hydroxide Gram smears of superficial lesions ==> yeat/hyphae Direct aspirate, biopsy, or lavage in lung involvement |
| How is Candida treated? | Nystatin, Amphociterin B, Flucytosine, and Azoles Superficial lesions --> Topical Nystatin and Azoles |
| What are the general characteristics of Chlamydia trachomatis? | Round cells between 0.3-1 microns in diameter Enveloped with a trilaminar outer membrane which contains LPS and proteins similiar to gram -ve bacteria but without peptidoglycan |
| What are the two forms of Chlamydia in the replicative cycle? | 1) Elementary body -small and infectious 2) Reticulate body - larger and IC replicative |
| What happens as the reticulate bodies increase in number? | The membrane expands by fusing with the golgi apparatus forming the inclusion body After 24-72 hours, the process reverses and multiple EBs are formed and released from the disintegrated host cell membrane |
| What characteristic does C. trachomatis have which enables it to complete its replication? | It inhibits apoptosis of epithelial cells |
| Where does C. trachomatis cause disease? | Conjunctiva and genital tract (MOST COMMON STD) Tropism for epithelium of the endocervix, upper genital tract, urethra, rectum, and conjunctiva |
| What is the sole reservoir of Chlamydia? | Humans |
| Non-gonococcal urethritis is most commonly caused by : | C. trachomatis |
| Where does LymphoGranuloma Venereum enter through | Skin or mucosa that is not intact |
| What are the characteristics of the early stage of C. Trachomatis? | Release of proinflammatory cytokines such as interleukin-8 |
| What are the characteristics of the late stage of C. Trachomatis? | Aggregates of lymphocytes and macrophages may form in the submucosa; can progress to necrosis, fibrosis and scarring. |
| What diseases can C. Trachomatis cause? | Urethritis, epididymitis in men Cervicitis, salpingitis, and a urethral syndrome in women |
| What are the clinical manifestation of C. trachomatis infection? | Urethritis --> Dysuria and urethral discharge Uterine cervix -->Asymptomatic vaginal discharge |
| The scarring produced by chronic or repeated infection is an important cause of | Sterility and ectopic pregnancy |
| More than 50% of infants born to mothers with C.trachomatis show: | Infection during first year Inclusion conjunctivits Infant pneumoni syndrome |
| What is LymphoGranuloma Venereum characterized by? | Primary genital lesion, painless and heals Abscess and fistulas--> chronic Suppurative involvement of the inguinal lymph nodes |
| How is Chlamydia diagnosed? | Epithelial cells from the site of infection Cervical or urethral speciments Acheieved in cell culture of McCoy cells Ligase chain reaction or PCR--> most sensitive |
| How is Chlamydia treated? | Tetracycline, macrolides, and floroquiolones Azithromycin --> Single dose Erythromycin --> Pregnancy Doxycycline --> DOC for LGV |
| What are the characteristics of Ureaplasma urealyticum? | Diameter of 0.2-0.3 mm Highly pleomorphic May appear coccoid, filamentous or multinucleoid No cell wall but membrane containing STEROLS |
| What diseases does it cause? | One half of cases of nongonococcal, nonchlamydial urethritis Chorioamnionitis and postpartum fever (10%) |
| How is Ureaplasma infection treated? | Tetracycline Spectinomycin or quinolone |
| What are the characteristics of Gardnerella vaginalis? | Facultative anaerobe |
| Gardnerella vaginalis most commonly cause: | Bacterial vaginosis |
| Gardnerella vaginalis grows on what media? | Small, circular, convex, gray colonies on Chocolate agar |
| What areas can Gardnerella vaginalis be isolated from? | Genitalia, blood, urine, and pharynx |
| Gardnerella vaginalis is associated microscopically with: | Clue cells |
| What are the clinication manifestations of infection with Gardnerella vaginalis? | Gray, thin, and homogenous vaginal discharge Musty odor |
| How is Gardnerella vaginalis diagnosed? | A wet mount of saline with vaginal secretions examined under microscope WBCs, lactobacilli, and clue cells |
| How is Gardnerella vaginalis treated? | Oral metronidazole --> contraindicated in pregnancy and lactation Cephradine |
Created by:
Ulaisl
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