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Infectious disease Archer USMLE Step3 Review Lectures


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Infectious Diseases HighYield and Frequently tested concepts on USMLE Step 3. These slides are samples from Archer USMLE Step 3 Review Lectures. Couple it with Archer Step 3 Question bank and Step 3 CCS to easily pass your final part of USMLE licensing exams

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Infectious disease Archer USMLE Step3 Review Lectures

  1. 1. Infectious Diseases Archer online USMLE reviews All Rights reserved Archer Slides are intended for use with Archer USMLE step 3 video lectures. Hence, most slides are very brief summaries of the concepts which will be addressed in a detailed way with focus on High-yield concepts in the Video lectures.
  2. 2. Antibiotics An Overview
  3. 3.  Penicillins  Monobactams – Aztreonam  Carbapenems – primaxin, ertapenem  Cephalosporins  Macrolides  Quinolones  Aminoglycosides  Tetracyclines  Glycoproteins – vancomycin  Linezolid
  4. 4. Anti-Pseudomonal Antibiotics GOOD ACTIVITY :  Piperacillin/ tazobactam  Cefepime  Ceftazidime  Imipenem/ cilastatin (Primaxin) Fair Activity  Aminoglycosides  Quinolones
  5. 5. Skin and Soft Tissue Infections Impetigo Cellulitis Necrotizing Fasciitis
  6. 6. Impetigo  Infection of superficial layers of epidermis  Nonbullous impetigo starts as a single erythematous macule that rapidly evolves into a vesicle or pustule, and ruptures leaving a crusted yellow exudate over the erosion.  Bullous impetigo begins as a rapid onset of blisters that enlarge and rupture. ( cause mostly s.aureus, also MRSA)  Common bugs : gram +ves - S.aureus and GABHS ( S.pyogenes)  Rx – Topical mupirocin for mild cases, Cephalexin p.o for severe cases
  7. 7. Cellultis  Inflammation of skin and underlying subcutaneous tissues – can be infectious or non infectious.  Commonest causes – group A streptococci (S.pyogenes) and S.aureus  Rx – usually a cephalosporin such a cephalexin can be used. If allergic to penicillin, use clindamycin  If MRSA is suspected, use oral drugs for mild/ moderate cellulitis such as Bactrim, Doxycycline, Clindamycin or quinolone. For severe MRSA cellulitis, use Vancomycin or Tigecycline IV. If resistant to Vanco, use Linezolid
  8. 8. MRSA – Risk factors Emperically, treat patients with moderate to severe cellulitis with risk factors for MRSA infection:  Recent antibiotic use  Recent hospitalization  Hemodialysis  IV drug use  Diabetes  Previous MRSA infection or colonization
  9. 9. Recurrent MRSA  In patients with recurrent MRSA soft tissue infections, consider NASAL CARRIAGE  Culture the nares of patients with recurrent infection who are suspected of carrying MRSA.  Treat nasal carriers with mupirocin to the nares twice a day for 7 days
  10. 10. Cellultis from Bites  Pasteurella multocida – etiology in cat bites and rarely, dog bites. Rx – Amoxicillin/clavulanate. Tmp/smx in penicillin allergic patient.  Eikenella cordans – human bites. Rx – Amoxicllin/ clavulanate or Ampicillin/sulbactam. TMP/SMX plus clindamycin in penicillin-allergic patient  Capnocytophaga tonsurans – cellulitis, disseminated infection seen in asplenic patients after Dog bites ( meningitis, endocarditis, renal failure).
  11. 11. Bites  Risk of wound infection:  2-30% in dog bites  15-50% in cat bites ( since cat bites are more likely to be puncture wounds, risk of infection is high)  9-50% of human bites  Risk of infection is particularly high in ( high grade wounds):  puncture wounds  hand injuries  full-thickness wounds  wounds involving joints, tendons, ligaments, or fractures.
  12. 12. Bites – Antibiotic Prophylaxis  In case of cat and dog bites, there is no necessity for giving prophylactic antibiotics if it is a low grade non-infected bite. Cleansing with sterile/ tap water and debridement are sufficient.  However, remember that cat bite that is a true puncture wound will need antibiotic prophylaxis as even when they are small they can cause a deep puncture and carry 50% risk of infection. So, if it is a minor scrape or nip , there is no necessity for antibiotics but if there is a puncture, antibiotic should be given. ( Dog bites have less risk of infection)  If it is a high grade non infected wound, antibiotic prophylaxis should be given to prevent cellulitis ( i.e; if the wound involves the hands, feet, cartilaginous structures, or is deeper than the epidermal layer(puncture).)  Human bites have the highest risk of getting infected. However, antibiotic prophylaxis is recommended only in high grade wounds.
  13. 13. Bites – Wound Closure  Primary closure with sutures  not recommended for non-facial bite wounds, deep punctures, bites to the hand, clinically infected wounds and wounds greater than 6 hours old 9 due to high risk of infection) . Delayed closure is appropriate in this conditions.  Facial wounds may need sutures to prevent scarring and improve cosmetic outcome. owever, the risk of such closure is uncertain, but in most cases this is safe if the person has presented early and the wound has been thoroughly cleaned.  Delayed primary closure (after 3-5 days)  Recommended for bites to the hand, bites with extensive crush injury, wounds needing a considerable amount of debridement, and wounds more than 6 hours old.
  14. 14. Human Bites – HIV Transmission  HIV transmission has been reported only very rarely after a human bite.  Exposure to saliva alone is not regarded as a risk factor for transmission of HIV (or hepatitis). So, CDC does not recommend routine prophylaxis in human bites.  Transmission risk in human bites is significant when :  If the biter has HIV, his saliva is mixed with his blood and the bite caused a breach in the skin of the victim.  If the Victim has HIV, the blood drawn from him should come in to contact with mucous membranes of the biter ( Victim to biter transmission) .  CDC (2005) recommends postexposure prophylaxis with active antiretroviral therapy (HAART) ( 28 day course) ONLY in either of the above two scenarios
  15. 15. Human Bites – Closed Fist Injury Closed-fist injuries:  Consult a hand surgeon  Requires exploration under anesthesia for joint space violation or tendon injury.  Patients with tendon injury or joint space violation or underlying fractures should be admitted for inpatient treatment.  Management :  Thorough cleansing and antibiotics. This is a high grade wound. Antibiotic should be started even when there is no evidence of infection.  If discharged, close follow up is needed as outpatient.  In a infected closed fist injury, patients should be admitted for IV antibiotic therapy ( ampicillin/ sulbactam). Surgical debridement is needed. ( Remember that these infected close fist wounds need aggressive care because of poor vascular supply to the tendons and because of the deep nature of this infection.)
  16. 16. Tetanus Prophylaxis Tetanus prone wounds:  Age > 6 hours  Configuration : avulsion, stellate  Depth > 1cm ( puncture wounds)  If devitalized tissue is present  If contaminants ( dirt, saliva i.e; bites) are present.
  17. 17. Tetanus Prophylaxis  If hx of tetanus immunization is unknown or < 3 doses  give Td+TIG for a dirty tetanus prone wound. Td alone for a clean, non tetanus prone wound.  If hx of Tetanus immunization is present and if the patient has already received 3 or more doses  no TIG needed. In case of dirty wound, Give Td only if it is greater than 24 hour old or if greater than 5 years since last booster ( bites are dirty). In case of clean wound, give Td booster if greater than 10 years since last booster.
  18. 18. Rabies Post-Exposure Prophylaxis  All wounds must be thoroughly cleansed with soap and water.  In case of Dogs and cats  if the animal is healthy and available for 10 day observation, do not start prophylaxis until animal develops symptoms. If animal develops symps, start HRIG+HDCV ( if patient is not previously vaccinated). If pt is previously vaccinated, give HDCV alone ( don’t give HRIG)  If animal is known rabid or suspected rabid, immediate vaccination.  If animal is a skunk, bat or a fox  considered as rabid always!  Immediate vaccination eg: even if the bat was found flying in the room
  19. 19. Necrotizing Fascitis - Infection of the fascial planes resulting in the death of the affected tissues. - Skin color – blue-black (Black necrotic eschar may be seen at the borders of the affected areas). Crepitance at the site, Fever, malaise and leukocytosis can be seen - Common bugs – Group A strep, S.aureus, C.Perfringens Rx – Aggressive debridement + Clindamycin. - Rare causes – Vibrio vulnificus ( clue : necrotizing fasciitis after immersion in warm salt water) Rx - Tetracycline - Diagnosis – mainly clinical, however in early cases CT may be obtained. Finding of gas or inflammatory stranding on CT is very suspicious of necrotizing fasciitis. Differentiate simple cellulitis from skin changes associated with a deeper infection, such as necrotizing fasciitis or gas gangrene, in patients with:  A rapid increase in lesion size  Evolution of bullous lesions  Reddish-purple coloring of the skin  Systemic toxicity (Hypotension, altered mental status)  Pain out of proportion to the clinical findings (extreme local tenderness)
  20. 20. Toxic Shock Syndrome  Caused by an exotoxin that acts as a superantigen  Fever, Nausea, vomiting, diarrhea, Shock and Skin rash characterized by exfoliation.  The initial lesion might be cellulitis or necrotizing fasciitis  Causes : S.aureus, Group A Streptococci  Rx – shock appropriately  Drug of choice : clindamycin as it blocks toxin production.
  21. 21. Ecthyma Gangrenosum  Caused by P.aeruginosa/ can be associated with pseudomonas septicemia ( obtain blood cultures and local cultures).  Usually affects critically ill and immunocompromised hosts – AIDS, Steroid use, Cancer, Chemotherapy.  Characteristic lesions  hemorrhagic pustules or infracted-appearing areas with surrounding erythema that evolve into necrotic ulcers surrounded by erythema  Rx with antipseudomonal antibiotic
  22. 22. Ecthyma Gangrenosum
  23. 23. Sexually Transmitted Diseases
  24. 24. Syphilis Approach
  25. 25. Clinical Stages  Primary Syphilis : a solitary, painless chancre that develops at the site of infection three weeks after exposure  Screen with Dark Field microscopy of skin lesion.  Secondary Syphilis: Without treatment, blood-borne spread of T. pallidum over the next several weeks to months results in secondary syphilis  c/f are fever, lymphadenopathy, diffuse rash ( including palms and soles) , and genital or perineal condyloma latum  If lesions present  Screen with dark filed microscopy. If no lesion, screen with Non Treponemal tests and confirm with Treponemal Specific tests  Latent syphilis : Skin lesions resolve, and patients are asymptomatic. However, serologic tests are positive for T. pallidum. Diagnosis – Screen with Non Treponemal and confirm with Treponemal Specific tests  Tertiary or late syphilis: develops years after the initial infection and can involve any organ system. Complications are neurosyphilis and Aortic Aneurysms).  Diagnosis – Screen with Treponemal Specific tests.  Neurosyphilis: A type of late syphilis. ( TABES DORSALIS)  Seizures, ataxia, aphasia, paresis, hyperreflexia, personality changes, cognitive disturbance, visual changes, hearing loss, neuropathy ( Vibration/ Position lost) , loss of bowel or bladder function.  Dx is by CSF examination.
  26. 26. Secondary Syphilis  Maculopapular rash in secondary syphilis  Note involvement of palms and soles  Pruritic
  27. 27. Diagnosis  Dark Field Microscopy  Non-treponemal tests  Treponemal Specific Tests
  28. 28. What is the next step in diagnosis ?  A. VDRL  B. RPR  C. FTABS  D. Cultures  E. Dark field microscopy of the scraping ANS. ???
  29. 29. Dark Field microscopy  Most specific technique for diagnosing syphilis when an active chancre or condyloma latum is present ( Lesion must be present – so usually good for primary/ secondary syphilis if lesion is present)  T. pallidum is identified by its characteristic corkscrew appearance  its accuracy depends on operator experience, number of treponemes in the lesion and the presence of non- pathological treponemes in oral/ anal lesions.  Given the difficulties of dark-field microscopy, negative examinations on three different days are necessary before a lesion is considered negative for T. pallidum.
  30. 30. Non Treponemal Tests VDRL, RPR  Principle: Syphilitic infection leads to the production of nonspecific antibodies that react to cardiolipin  the basis of traditional non- treponemal tests such as the VDRL test and rapid plasma reagin test.  Mainly used as screening tests  Sensitivity, however, is very low in Early Primary syphilis and during late syphilis  during these periods, 1/3 of pts may be non reactive. So, if suspicion is very high despite a negative screening test, go ahead with treponemal specific test ( FTA-Abs)  False Positives are common in pregnancy, autoimmune diseases and infections  False negative reactions can occur too : large amounts of antibody block the antibody-antigen reaction, causing a false-negative test in the undiluted sample ( Prozone phenomenon – similar to hook effect)  Use in Monitoring treatment adequacy : In many cases nontreponemal tests become nonreactive after adequate syphilis treatment – so, use VDRL/ RPR for follow-up after treatment. However, remember that even with sufficient treatment, patients sometimes have a persistent low-level positive nontreponemal test (referred to as a serofast reaction). However, this drop in titers can help in follow up  Remember  Titers are not interchangeable between different test types. Hence, the same nontreponemal test should be used for follow-up evaluations.( If used RPR for screening, use the same for follow up)
  31. 31. Treponemal Tests  Treponemal-specific tests detect antibodies to antigenic components of T. pallidum.  Used primarily to confirm the diagnosis of syphilis in patients with a reactive nontreponemal test. ( So, if you have a positive RPR, the next step is FTA-Abs or TPHA)  Treponemal-specific tests : EIA for anti-treponemal IgG, the T. pallidum hemagglutination (TPHA) test, the microhemagglutination test with T. pallidum antigen, the fluorescent treponemal antibody- absorption test (FTA-abs), and the enzyme-linked immunosorbent assay.  Treponemal tests have sensitivities and specificities equal to or higher than those for nontreponemal tests. However, treponemal- specific tests are more difficult and expensive to perform, which limits their usefulness as screening tests.  False-positive results can occur, especially when the FTA-abs test is used in patients with systemic lupus erythematosus or Lyme disease.
  32. 32. Treponemal Tests  Can they be used for follow-up?  Unlike nontreponemal tests, which show a decline in titers or become nonreactive with effective treatment, treponemal-specific tests usually remain reactive for life  Therefore, treponemal-specific test titers are not useful for assessing treatment efficacy.
  33. 33. Genital Lesions – Differential Diagnosis Disorder or disease Characteristics of genital lesion Etiology Primary syphilis: chancre Solitary, painless ulcer with indurated border Treponema pallidum Secondary syphilis: condyloma latum Slightly raised or flat, round or oval papules covered by gray exudate T. pallidum Genital herpes Cluster of shallow, small, painful ulcers on a red base Herpes simplex virus Chancroid Painful ulcers with sharp, undermined borders + tender lymphadenopathy Haemophilu s ducreyi Venereal warts Soft, usually painless skin-colored or red papules Human papillom avirus Lymphogranuloma venereum: primary stage Painless papule, shallow erosion, or ulcer; may be multiple or single ( Bubos or unilateral massive inguinal nodes will be helpful in differentiating it from syphilitic Chlamydia trachom atis
  34. 34. Treatment  Primary Syphilis : Diagnosed by dark-field microscopy of a suspected lesion or by serologic testing. Either technique can have a false-negative result early in the course of the disease. Thus, if clinical suspicion is high, treatment for syphilis should be initiated.  Clinical Manifestation : Chancre  Treatment: -Penicillin G benzathine, 2.4 million units IM (single dose)  Alternatives in nonpregnant patients with penicillin allergy: doxycycline (Vibramycin), 100 mg orally twice daily for 2 weeks or tetracycline, 500 mg orally four times daily for 2 weeks. ceftriaxone (Rocephin), 1 g once daily IM/IV for 10 days; or azithromycin (Zithromax), 2 g orally (single dose)  Follow-up : At six and 12 months after treatment, reexamine and repeat serologic testing. Treatment failure is defined as recurrent or persistent symptoms or a sustained fourfold increase in nontreponemal test titers despite appropriate treatment.  Patients with treatment failure should be tested for HIV infection and evaluated for neurosyphilis with a cerebrospinal fluid (CSF) examination.
  35. 35. Treatment  Secondary Syphilis : The diagnosis of secondary syphilis is confirmed by nontreponemal and treponemal-specific tests.  Treatment employs the same antibiotic regimens used for primary syphilis. Follow- up is the same as that for primary syphilis. Definition of treatment failure is the same.
  36. 36. Treatment  Latent Syphilis : early/ late Latent  CNS involvement may be asymptomatic. Therefore, the possibility of neurosyphilis should be considered in patients with early or late latent syphilis.  Early latent syphilis Rx the same way as primary and secondary syphilis.  Late latent syphilis  RX with 2.4 million units of penicillin G benzathine IM once a week for three weeks. Alternative regimens in nonpregnant patients with penicillin allergy include doxycycline 100 mg po twice daily for four weeks, or tetracycline 500 mg po four times daily for four weeks.  Follow- up: After treatment of early or late latent syphilis, quantitative nontreponemal titers should be measured at six, 12, and 24 months.  Neurosyphilis should be strongly considered in patients who show a fourfold increase in titers, patients who have an initially high titer (1:32 or greater) that fails to decline at least fourfold, patients who have HIV infection, and patients who develop signs or symptoms of neurosyphilis.
  37. 37. NeuroSyphilis  Occurs in up to 10% of patients with untreated syphilis.  Neurosyphilis  consider in patients with signs or symptoms of neurologic involvement at any stage of T. pallidum infection and in all patients with late latent or tertiary syphilis, although asymptomatic neurosyphilis is the most common presentation.  Neurologic involvement  strongly suspect and evaluate in patients who previously have been treated for neurosyphilis, patients who have not responded to treatment for primary, secondary, or latent syphilis, and patients who have HIV infection/ other immunocompromised states.  in pts with HIV, newly diagnosed of Syphilis, next step is always LUMBAR PUNCTURE TO R/O NEUROSYPHILIS  Diagnosis : Lumbar puncture. CSF should be tested for white blood cell count and protein level, and for reactivity on a VDRL test  Although a positive CSF VDRL test result is specific for neurosyphilis, a negative result does not exclude the possibility of this infection, because sensitivity is less than 100 percent. A CSF white blood cell count greater than 10 per mm3 (10 3 106 per L) or a CSF protein level greater than 50 mg per dL (0.50 g per L) indicates possible neurosyphilis.  Treponemal-specific testing (e.g., TPHA) has high negative-predictive value  is helpful only when the result is negative (i.e., it rules out neurosyphilis). Because IgG can cross the blood-brain barrier, a positive test may falsely imply CNS involvement. ( so not used for diagnosis)
  38. 38. Neurosyphilis  C/F : seizures, ataxia, aphasia, paresis, hyperreflexia, personality and cognitive changes, visual changes, hearing loss, neuropathy, and loss of bowel and bladder functions.  Penicillin is the only drug that has proved effective in the treatment of neurosyphilis. If pen-allergic , desensitize and treat.  Follow-up : following treatment, follow-up depends on the initial CSF findings. If pleocytosis was present, the CSF should be reexamined every six months until the white blood cell count is normal. Retreatment should be considered if the CSF white blood cell count does not decline after six months or completely normalize after two years.  The CSF also can be reexamined to look for serial decreases in antibodies on the VDRL test or serial decreases in protein levels. It is expected that CSF parameters will normalize within two years. Failure to normalize may warrant retreatment. Most treatment failures occur in immunocompromised patients
  39. 39. Genital Herpes A recurrent, lifelong disease with no cure  Two types of HSV (i.e., HSV-1 and HSV-2) are distinguished by antigenic differences in their envelope proteins  HSV-1 normally is associated with oral infections and HSV-2 with genital infections, but either type can infect a person anywhere on the skin.
  40. 40. Risk Factors for Genital HSV  Advent of sexual activity at or before 17 years of age  History of sexually transmitted diseases  History of undiagnosed genital lesions or discharge  Human immunodeficiency virus infection  Multiple sex partners  Multiple lifetime sex partners  strongest predictor for genital Herpes  Partner diagnosed with genital HSV infection
  41. 41. Clinical Features  Prodrome: lasts 2-24 hrs  characterized by localized or regional pain, tingling, and burning  may have constitutional symptoms such as headache, fever, inguinal lymphadenopathy, anorexia, and malaise.  As the disease progresses, papules, vesicles on an erythematous base, and erosions appear over hours to days.  Patterns of HSV-1 and HSV-2 infection appear identical: vesicles usually are uniform in size, and the tense center umbilicates to form a depressed center. These lesions usually crust and then re-epithelialize and heal without scarring.  In women, ulcers can occur on the introitus, urethral meatus, labia, and perineum. In men, ulcers often appear on the shaft or glans of the penis. In both men and women, lesions may appear on the perianal area, thighs, or buttocks.  Recurrent HSV outbreaks usually are milder than the initial episode: there typically are fewer grouped lesions and viral shedding occurs at a lower concentration and for a shorter duration (i.e. about 3 days).  Recurrence rates for HSV-2 vary greatly, but the median is four recurrences per year.  Patients who experience more severe primary infections (i.e., lasting 35 days or more) have recurrent episodes twice as often.  Recurrences are spontaneous, but various factors such as fever; nerve or tissue damage; physical or emotional stress; exposure to heat, cold, and ultraviolet light; immunosuppression; menses; concurrent infection; fatigue; and sexual intercourse have been associated with recurrences
  42. 42. Prevention  Most genital herpes is spread asymptomatically  In the U.S., 22% of persons age 14 years or older are infected with HSV-2, and almost 90% do not know they are infected  Most transmission occurs from persons who have no recognized lesions and who do not know they are infected  As many as one third of new genital herpes cases may be caused by HSV-1, which is usually transmitted by oral sex; however, only 5% to 10% of recurrent genital herpes is due to HSV-1 infection  The use of condoms has been shown to reduce transmission rates of HSV-2 significantly in susceptible women but not in men.  Using condoms during 25 percent or more instances of sexual intercourse was associated with reduced rates of HSV transmission, which suggests that even occasional condom use can protect women from acquisition of HSV-2.  To be effective, the condom must completely cover lesions on an infected man.  Inform patients that asymptomatic shedding is common and that condoms should be used routinely, even when no lesions are recognized
  43. 43. Diagnosis  Clinical exam/ high risk history  Swab test : swab from HSV lesions taken for culture or PCR 1. Viral Culture : Not very sensitive but it is the preferred method for identifying HSV infection, when pts present with lesions. Also, very helpful in differentiating HSV-1 from HSV-2 2.POLYMERASE CHAIN REACTION TESTING for HSV DNA : greater sensitivity than the traditional viral culture (sensitivity > 95%, compared with 75% for culture) High cost is its limitation  hence, used only for the diagnosis of HSV encephalitis because the results are more rapid than viral culture 3. SEROLOGIC TESTING  HSV antibodies form during the first several weeks after infection and remain indefinitely.  Fifty to 90 percent of adults have antibodies to HSV, but only about 30 percent have antibodies specific to HSV-2.  Type-specific serologic assays can be used to confirm HSV infection in persons with a questionable history or in those who have unrecognized or subclinical infections.  Serologic testing also is helpful in the presence of a false-negative culture, which is common in patients with recurrent infection or healing lesions. Because HSV-2 infection is almost exclusively sexually acquired, HSV-2 antibodies are consistent with an anogenital infection. However, HSV-1 antibodies may be present in anogenital and orolabial infections; they cannot be used to differentiate between infections.  If HSV antibodies are present, testing for other causes of genital ulcers (e.g., syphilis, chancroid) should be considered, especially in high-risk populations..
  44. 44. Screening  Consider offering type-specific serologic testing for HSV- 2 to:  Persons with undiagnosed past or present genital symptoms or lesions, especially if recurrent  Patients who have a current or past partner with genital herpes  Patients who have been diagnosed by clinical exam only and want confirmation of their diagnosis or typing of their infection  Patients requesting a full STD screen  Persons who are HIV positive  Be aware that the false-positive rate can be high in populations with a low prevalence of infection; confirmation of the initial serology with another assay can be used to increase the specificity.  Universal screening for HSV antibodies is not recommended
  45. 45. Management Hospitalization is indicated for patients with genital Herpes if they also have  Symptoms of meningitis: Severe headache, Stiff neck, Photophobia  Symptoms of autonomic nervous system dysfunction: Urinary retention, Constipation , Dysesthesias of the perineal, sacral, or lower back regions  Symptoms of transverse myelitis: Leg weakness , Decreased deep tendon reflexes , Autonomic nervous system dysfunction  If meningitis is suspected, send CSF for PCR to detect HSV DNA.  Next step: Begin therapy with intravenous acyclovir, 5 to 10 mg/kg every 8 hours. ( do not wait for PCR results to come back if pt has genital lesions suspicious of HSV and has above indications for aggressive therapy)  When symptoms improve, switch to oral therapy for a total of 10 to 14 days of treatment
  46. 46. Treatment  FIRST CLINICAL EPISODE  must be treated with anti HSV agents ( Acyclovir/ Famciclovir/ valacyclovir) as soon as possible. Studies have shown prompt Rx for initial episode reduced constitutional symptoms by three days, local pain by two days, viral shedding by seven days, time until all lesions were crusted by three days, and time until all lesions were healed by six days.  Counsel patients about the high frequency of recurrences, the inevitability of asymptomatic shedding, and the risk of transmission even after initial therapy.
  47. 47. Rx – Recurrent herpes  Recurrences :  For mild, infrequent recurrences  Episodic therapy is the best. To be efective, it is very important that treatment is started early during prodromal phase or within 1 day of lesion onset. So, counsel pts to recognize the recurrences early and self-initiate the treatment ASAP. Provide prescriptions in advance.  The goal of episodic therapy is to reduce symptoms and to reduce infectivity during the episodes. This therapy does not prevent future recurrences or asymptomatic shedding between the episodes.  Topical Acyclovir is not effective.  For Frequent recurrences  six or more episodes per year  START LONG TERM SUPPRESSIVE THERAPY ( ACYCLOVIR/ FAMACYCLOVIR/ VALACYCLOVIR)  Inform patients that continuous suppressive therapy decreases, but does not eliminate, transmission:  Instruct patients taking suppressive therapy to continue to use condoms, although they are only 50% effective in reducing transmission  Explain to patients that treatment is not curative and will not affect the severity or frequency of recurrences when stopped  Inform patients that long-term, continuous treatment is safe and does not require laboratory-test monitoring
  48. 48. Treatment  Immunocompromised pts : Genital herpes Rx in HIV pts is similar to that without HIV  But recognize that immunosuppressed patients often develop extensive genital lesions that may not respond to routine courses of antiviral therapy  So, be sure to treat aggressively and early.  Treat early lesions that are not extensive with usual doses of oral medications  If no improvement occurs, or if initial involvement is extensive, try higher doses of oral medications.  If still not responding  Treat with high-dose intravenous acyclovir or foscarnet, or topical trifluridine, foscarnet, or cidofovir; note that prolonged treatment may be required.
  49. 49. Preventing Mother-Infant Transmission  Advise pregnant women to avoid acquiring genital herpes infection, especially late in pregnancy, in order to prevent exposing the infant to herpetic lesions during birth:  In general, recommend abstinence or only protected coital activity in late pregnancy (week 34 onward)  Advise patients that both HSV-1 and HSV-2 can cause neonatal herpes  Inform women that if they acquire HSV 1 or 2 during the third trimester, there is a 30% to 50% chance of transmitting HSV to their neonate  Ask pregnant women regarding h/o genita or orolabial herpes. However, remember 90% of those infected with HSV would deny a history of genital herpes, making history taking of limited value  Advise pregnant women with no history of orolabial herpes or genital HSV-1 infection to avoid vaginal intercourse with a partner who has or may have genital HSV-1 infection and to avoid cunnilingus in the third trimester with partners who may have orolabial herpes, even if no lesions are present at the time of sexual contact  Inform women who do experience their first episode of genital herpes late in pregnancy that:  They are at high risk of perinatal transmission  Mother and child should be managed by a specialist  Cesarean section is generally recommended  Acyclovir treatment should usually be given  Exposed infants often are monitored with surveillance cultures and treated with acyclovir
  50. 50. Preventing Mother-Infant Transmission  Identify women who are at risk for reactivation of HSV-2 at time of delivery:  Consider type-specific antibody testing for some pregnant women (or women who plan to become pregnant) and their partners to determine the risk of acquiring HSV-1 or HSV-2, but do not obtain periodic viral cultures from pregnant patients with a history of recurrent genital herpes if no lesions are present  Inform women with a history of recurrent genital herpes that they have a low risk (<1%) for perinatal transmission:  If during labor they have no symptoms of genital herpes or its prodrome and if a careful clinical examination shows no genital lesions in the entire area innervated by the sacral ganglia, they may deliver vaginally  If herpetic lesions are present, cesarean section is usually recommended  Culture lesions during pregnancy, especially those present during labor, to determine whether they contain herpes virus  Administer intravenous acyclovir to all pregnant women with severe HSV infection or disseminated infection, pneumonitis, hepatitis, or CNS infection. Give oral acyclovir to pregnant women with an uncomplicated first episode of genital herpes or severe recurrences of genital herpes.  Consider suppressive antiviral therapy (acyclovir, 400 mg tid or valacyclovir, 500 mg bid) beginning at 36 weeks' gestation for women with first-episode genital herpes during pregnancy and for pregnant women with frequent recurrent episodes.
  51. 51. Genital warts
  52. 52. Prevention Most commonly acquired STD, affecting 50% to 75% of sexually active men and women.  Abstinence is the most effective strategy to prevent HPV infection. Maintain monogamy. Condoms do not efficiently protect against HPV.  HPV can spread by skin-skin contact without exchange of body fluids.  Treating HPV-related genital warts MAY reduce infectivity but will not eliminate it.  Counsel pregnant women with HPV infection about the risk of peripartum transmission of HPV infection, pointing out that:  Infection with HPV types 6 and 11 can result in respiratory papillomatosis in infants and children  The role of cesarean section in reducing peripartum transmission of HPV is unknown  SO, NOT RECOMMENDED
  53. 53. Screening  Screening modalities  Papanicolaou test (Pap)  Liquid-based cytology  For women > 30 years of age, combined cytology (either Pap or liquid-based) and HPV DNA testing.  Start to Screen ( pap smear) for HPV-related cervical lesions (e.g., cervical cancer, LSIL, HSIL) in sexually active women 3 years after onset of sexual intercourse or at the age of 21, whichever is earlier.  HIV associated with increased risk of cervical cancer/ dysplasia  Perform cervical cytology screening in HIV-seropositive women twice in the first year after HIV diagnosis, then annually if the results are normal.  Perform cervical cytology screening in women under age 30 on an annual basis.  If three consecutive cytologies are normal , consider increasing the interval between cervical cytology screening in women > 30 years of age without a history of either CIN-2 or CIN-3, immune compromise, HIV infection, or in utero exposure to diethylstilbestrol to every 2 to 3 years.  Consider HPV DNA testing in addition to cervical cytology screening in women < 30 years of age.  Do not screen women who are negative by both HPV DNA testing and cytology before 3 years.  Repeat HPV DNA testing and cervical cytology testing at 6 to 12 months in women whose results are negative by cytology but who are high-risk HPV DNA positive.
  54. 54. Stop Screening!  Discontinue routine cervical cytology screening (pap) in women who have had a hysterectomy for benign disease.  Consider discontinuing routine cervical cytology screening in women at age 65 or 70 who have had adequate recent cervical cytology screening and have no other risk factors for cervical cancer.
  55. 55. Diagnosis  History, physical exam  the morphologic characteristics of cutaneous or genital warts.  Hx of smoking – increases risk of cervcal ca  Symptoms – Pruritis, burning, vaginal bleeding/ post coital bleeding.  Consider differential diagnosis:  Benign lesions mimicking warts : Pearly penile papules ( surrounding corona) , Achrocordon ( skin tag), Vulvar lymphangiomata, Vestibular papillae in females and sebaceous glands  Other infectious etiologies : molluscum contagiosum ( immunocompromised pts), HSV, condyloma lata.  Malignancies : Squamous cell ca, Bowens disease, malignant melanoma
  56. 56. What are these?
  57. 57. Ans. Vestibular Papillae •For more pictures on benign lesions mimicking warts, please refer Dermatology Slides. • Vestibular Papillae are common benign lesions that are often mistaken as genital warts and cause unnecessary concern to the patients. So, questions like these are often high yield on the USMLE. • Vestibular papillae are flesh-colored, soft pearly papules found on the inner aspects of labia minora. They are usually symmetrically distributed on either side of the vulva and can be easily separated from each other on examination. •On the other hand, genital warts are not confined to the vestibule. The cauliflower or filiform projections of genital warts tend to fuse at the base and cannot be seperated easily. • Acetic acid test : When 5% acetic acid is applied to condyloma acuminatum, a whitening occurs. There is usually no whitening with Vestibular papillae. •Vestibular papillomatosis is a normal vulvar anatomical condition. It is a female counterpart of male pearly penile papules. A correct diagnosis is important and prevents unnecessary stress to the patient.
  58. 58. Diagnosis  Biopsy not routinely done. Consider it for excluding intraepithelial lesions/ cancer/ dysplasia in:  Atypical appearing lesions  Vaginal/ Cervical warts  Uncertain diagnosis  Progression of disease during treatment  Frequent recurrence  Warts that are pigmented, indurated, ulcerated, or fixed to underlying tissue  Warts >1 cm  Suspected neoplasia (e.g., blue or black discoloration)  Occurrence in immunocompromised patients
  59. 59. Treatment Options – Drug therapy Mechanisms of action – drug therapy  Patient-applied therapies include podophyllotoxin and imiquimod  Provider-applied therapies include podophyllin resin and TCA  Imiquimod (Aldara) : Cell-mediated immune response modifier; induces interferon production  Interferon: Antiviral, antiproliferative, and immunomodulatory activity  Podofilox (Condylox)solution or gel : Cytotoxic, antimitotic; major biologically active component of podophyllin resin  Podophyllin resin: Cytotoxic, antimitotic (causes tissue necrosis)  Trichloroacetic acid : Protein coagulation of wart tissue Surgical therapy  Cryotherapy: Destruction by thermal-induced cytolysis  Excision  Electrosurgery  Laser surgery RECURRENCES ARE COMMON EVEN AFTER SURGERY OR DRUG THERAPY
  60. 60. Treatment  The choice of therapy is based on the number, size, site, and morphology of lesions, as well as patient preference, treatment cost, convenience, adverse effects, and provider experience.  Consider gynecology consult in pts with cervical/ vaginal warts – r/o CIN/ cancer
  61. 61. Treatment Approach
  62. 62. Treatment in Pregnancy  TCA has been used in pregnant patients without adverse effects.  Podophyllin, podofilox, and fluorouracil should not be used in pregnant patients because of possible teratogenicity.  Imiquimod is not approved for use in pregnant women, although treatment with this agent can be considered after informed consent has been obtained.  Surgical excision, cryotherapy, and electrocautery are appropriate treatment options during pregnancy if treatment is necessary.  The goal of treatment in pregnant women primarily is to minimize neonatal exposure to the virus by reducing the number of lesions present during delivery.  Anogenital warts and laryngeal papillomatosis are potential complications in infected children. ( children born to mother with anogenital warts)
  63. 63. Molluscum Contagiosum -Umbilicated pearly papules -Look for clues – “Central depression” -May be filled with pus like material -Rx is Liquid Nitrogen
  64. 64. Gonorrhea
  65. 65. Screening  Test all pregnant women for gonorrhea at the first prenatal visit if they are at risk for acquisition (defined as report of new or multiple sex partners) or if they live in an area with high prevalence.  Screen for gonorrhea and chlamydia in all patients by the third trimester  Screen young women (under age 25) at risk for STD acquisition if they are seeking care in a clinic with high gonorrhea prevalence  Screen men who have sex with men on an annual basis or more frequently depending on risk behavior.  Use any approved test, including culture, nucleic acid probe ( cervical probe for N.gonorrheae) , and nucleic acid amplification methods, for screening
  66. 66. Clinical Features - Men  Suspect gonorrhea as a likely cause of urethritis in a man with purulent or mucopurulent urethral discharge.  Could be a possible infectious cause of epididymitis, particularly in sexually active men under age 35. ( In older men, likely cause is E.coli)  A possible cause of proctitis (esply among men who have sex with men).  Recognize that pharyngeal infection with N. gonorrhoeae is usually asymptomatic but occasionally causes mild sore or “scratchy” throat.  Consider gonorrhea in the differential diagnosis of conjunctivitis, especially if it is associated with copious, purulent conjunctival discharge.  Disseminated Gonococcal infection can occur in men and, if considered, should prompt examination of mid- to large-sized joints and major tendon sheaths and their insertions for tenderness and inflammation.  Be aware that N. gonorrhoeae is an unusual cause of endocarditis and meningitis
  67. 67. Clinical Features - Women  Consider gonorrhea as a cause of mucopurulent cervicitis (defined by the presence of mucopurulent discharge or easily induced endocervical bleeding) or PID.  Be aware that while N. gonorrhoeae is a major cause of mucopurulent cervicitis (along with C. trachomatis), infection of the cervix most frequently causes neither signs nor symptoms.  Evaluate sexually active women with mucopurulent cervicitis or a laboratory-confirmed diagnosis of gonorrhea for the presence of PID. ( pelvic exam  discharge, cervical motion tenderness, adnexal tenderness; fever; elevated ESR/ CRP – aid in diagnosis  maintain high index of suspicion for PID and treat in view of high incidence of infertility and morbidity)  Consider gonorrhea as a possible cause of proctitis in women who have been exposed through receptive anal sex.  Recognize that pharyngeal infection with N. gonorrhoeae is usually asymptomatic but occasionally causes mild sore or “scratchy” throat.  DGI occurs more commonly in women than in men
  68. 68. Diagnosis – Best tests  In men with urethral discharge  perform a Gram stain smear of urethral secretions.  In women with mucopurulent cervicitis or PID  obtain DNA Probe or nucleic acid amplification of discharge and urine ( not gram stain)  Obtain urine for nucleic acid amplification tests at least 1 hour after last void, and be sure that it contains the initial 15 to 20 mL of the urine stream (“first catch”).  Proctitis or Pharyngitis  get cultures ( not gram stain)  If DGI (rash, arthritis) is suspected, obtain blood cultures and also cultures from mucosal sites exposed during sex (e.g., cervix, urethra, oropharynx, and rectum), even if no signs or symptoms are evident at these sites.
  69. 69. Diagnosis  In sexually active patients with acute, monoarticular, nontraumatic arthritis, perform bacterial culture and Gram stain of aspirate from affected joints.  N. gonorrhoeae is a rare cause of bacterial meningitis; the overwhelming majority of meningitis cases presenting with gram-negative intracellular diplococci in the cerebrospinal fluid are due to N. meningitidis.
  70. 70. Diagnosis  Test for other common STDs  Chlamydia  HIV  Syphilis  When gonorrhea is suspected in the setting of urethritis, cervicitis, or proctitis, also consider infection with C. trachomatis, which can cause presentations identical to gonorrhea.  In men whose urethritis does not respond to antibiotic treatment for gonorrhea and chlamydia, consider less common causes of urethritis, including T. vaginalis.  Among women with pelvic pain, also consider noninfectious etiologies, including ovarian cyst, ectopic pregnancy, endometriosis, ovulation, and gastrointestinal causes  In case of DGI, D/D includes other causes of acute, nontraumatic, oligoarticular arthritis in young adults, including Reiter's syndrome, Lyme disease, and various viral infections.
  71. 71. Hospitalization Indicated only if  Patients with DGI if they are moderately severely or severely ill (including temperature >38.0°C [100.4°F] or inability to take oral antibiotics).  All patients with documented or suspected gonococcal endocarditis or meningitis  Hospitalize women with PID in any of the following circumstances:  If surgical emergencies, such as appendicitis, cannot be excluded  Pregnancy  Failure to respond to previously administered oral or outpatient parenteral antibiotics  Inability to take oral therapy ( VOMITING/ NAUSEA)  Severe illness (nausea and vomiting, high fever, hemodynamic instability)  Presence of tubo-ovarian abscess  IMMUNOCOMPROMISED STATES
  72. 72. Treatment  Quinolones are no longer recommended for Rx of gonorrhea in the USA due to increasing resistance.  Treat patients with gonococcal cervicitis for chlamydial infection as well, even if laboratory confirmation of the latter is not obtained ( vice versa is not needed)  In sexually active men under age 35, treat epididymitis empirically with an antibiotic regimen active against both N. gonorrhoeae and C. trachomatis  Ceftriaxone + doxycycline  Always treat sexual partners.
  73. 73. Treatment – uncomplicated gonorrhea  For uncomplicated cervicitis due to gonorrhea : Ceftriaxone 125 mg IM. Also effective for rectal gonorrhea.(proctitis)  For endometritis/ uncomplicated PID  Ceftriaxone 250 mg IM.  Cefixime  Oral single dose Rx for uncomplicated gonorrhea ( 400mg single dose)  For gonococcal pharyngitis  use 1gm single dose ceftriaxone  cure rates for pharyngeal gonorrhea lesser when compared to other sites  Provide concomitant Rx to chlamydia  Doxycycline 100mg po bid x 7 days is first line Rx in non pregnant pts or alternative is Azythromycin 1gm single dose ( also preferred in pregnant pts). Also, Amoxicillin 500 po tid x 7 days alternative Rx for Chlamydia in Pregnancy
  74. 74. Treatment – Uncomplicated Gonorrhea  Penicillin Allergic Patients : due to cross reactivity with cephalosporins, use spectinomycin therapy as a choice.  Alternatively, use Azithromycin 2gm po dose in penicillin allergy pts ( double the dose required for chlamydia)  Neonates : Treat all newborns prophylactically for gonococcal conjunctivitis with topical silver nitrate solution, tetracycline ointment, or erythromycin ointment.
  75. 75. Treatment - DGI  For Disseminated Gonococcal infection   Hospitalize the patient  Obtain blood, cervical and pharyngeal cultures  Start IV therapy with Ceftriaxone 1gm/d until clinical improvement occurs and then switch to oral antibiotics to complete total 7 days of Therapy  Oral choices : Cefixime 400/d, cefpodoxime 400 bid
  76. 76. COUNSEL  Counsel persons with gonorrhea to abstain from sexual contact for at least 1 week after treatment and until all sex partners have been treated  OTHERWISE, RE-INFECTION CAN OCCUR!
  77. 77. HIV infection High-yield topics
  78. 78. Acute Retroviral Syndrome  Occurs within 4 to 28 days after infection corresponding to exponential increase in HIV viral load. Occurs in 50- 90% of patients  Diagnosis often missed due to confusion with other illnesses  Most common complaints : low grade fever, headache and malaise. Symptoms last 1-4 weeks and involves lymphadenopathy, anorexia, weightloss and a maculopapular rash that may extend to palms and soles. Pharyngeal erythema, oral ulcerations and oro- pharyngeal candidiasis are common.  Severe cases include meningo-encephalitis, neuropathy, radiculopathy and Guillianne-barre syndrome  A similar type illness can occur in 5% pts who discontinued HAART owing to exponential increase in HIV viral load
  79. 79. Acute Retroviral Syndrome  D/D :  Infectious mononucleosis ( EBV/ CMV)  Secondary syphilis  Acute early hepatitis B or A  Influenza  Acute Toxoplasmosis  Roseola  Acute HSV infection  Still disease  Diagnosis : one of the two criteria sets below 1. symptoms consistent with Acute retroviral syndrome + Negative HIV ELISA in past 6 months + Positive HIV ELISA at current testing (or) 2. symptoms consistent with Acute retroviral syndrome + Negative HIV ELISA at current testing + High HIV RNA titer at current testing ( usually > 100,000 copies/ ml)  Once Acute Retroviral syndrome is diagnosed  screen pt for Syphilis, chlamydia, gonorrhea, HSV and HPV.  Baseline Genotype testing recommended to r/o resistant mutations, regardless of whether or not you are starting PT on HAART  As per current guidelines, HAART is optional in Rx of Acute retroviral illness
  80. 80. When to start HAART?  When to start depends on symptoms, CD4 counts, and to a lesser extent, viral load. Current (March 2004) North American guidelines state that treatment should be:  Considered at CD4 counts below 350 cells/mm3,  Definitely started before CD4 counts fall below 200, and  definitely started if there are serious symptoms or AIDS-related illnesses irrespective of CD4 count  Also consider HAART if viral load > 50,000 by RT PCR
  81. 81. Question  A 27-year-old man with HIV presents to your clinic to establish care. He believes he acquired his infection from a blood transfusion he received in sub-Saharan Africa while serving in the Peace Corps 3 years ago. He is currently asymptomatic and has a strong social support network. His examination is unremarkable. During the clinic visit, he asks about starting medical therapy for his HIV. His CD4+ T cell count is 450/mm3, and his HIV RNA level is 20,000 copies/ml.  Which of the following is an indication to initiate HAART?  1. CD4+ T cell count of less than 500/mm3 2. HIV RNA level of 50,000 copies/ml and a normal CD4+ T cell count 3. Oral thrush 4. HIV RNA level of 75,000 copies/ml and CD4+ T cell percentage of 28%
  82. 82. Preventing Mother-Child Transmission  Use of Cesarean section  Use of HAART therapy during pregnancy and labor  No breast feeding ( formula feeding only)
  83. 83. Prophylaxis in HIV  Prophylaxis against Pneumocystis jiroveci (PCP) when CD4 count is <200 cells/µL with trimethoprim/sulfamethoxazole, one double- strength tablet daily or every other day. In pts allergic to Bactrim, atovaquone.  If CD4 count < 100, do IgG serology for Toxoplasmosis. If +ve serology, give trimethoprim/sulfamethoxazole.  In patients with positive PPD skin tests (>5 mm induration in an HIV- infected patient), evaluate and treat for either active or latent tuberculosis.  When CD4 count is <50 cells/µL, begin prophylaxis against Mycobacterium avium complex with azithromycin, 1200 mg/week  Recognize that patients with refractory, frequent, or severe mucosal candidiasis may require long-term systemic antifungal therapy ( oral diflucan).
  84. 84. Vaccinations in HIV  Administer annual influenza vaccination to all HIV-infected patients.  Administer pneumococcal vaccine to all HIV-infected patients (and strongly consider repeating at intervals of 5 to 10 years).  Administer vaccination to patients who are at risk for hepatitis A and B.
  85. 85. Progressive Multifocal Leucoencephalopathy Cause : Papova virus JC c/f : Dementia a common presenting symptom. Other c/f - hemiparesis, aphasia, dysarthria Dx : MRI/ CT. If +ve for white matter lesions, next step is CSF analysis for JC virus by PCR Rx – HAART
  86. 86. Toxoplasmosis Screen all patients with HIV with CD4 less than 100. screening test toxoplasma IgG Screen all patients undergoing organ transplantation C/F – encephalitis, pneumonitis, myocarditis in immunocompromised. Mononucleosis like syndrome and chorioretinitis in immunocempetant If Suspected Toxoplasmosis  get IgM and IgG serologies. If neurological symptoms  get CT/MRI. If patients are seronegative for Toxoplasma or if lesions don’t respond to toxoplasma Rx in 2 weeks  r/o Lymphoma. Get a stereotactic brain biopsy Rx  Sufladiazine + pyremethamine + folate ( Start emperic Rx in patients with ring enhancing lesions in brain and +ve IgG serology for toxoplasma and CD4 less than 200). If CD4 goes higher than 200, may d/c therapy
  87. 87. Cryptococcal Meningitis AIDS with CD4 less than 50 Headache, fever, delirium are present Diagnosis : LP, India ink and Cryptococcal antigen in serum and CSF Rx: Amphotericin + Fluconozole Increased CSF pressure is associated with increased mortality  do a daily therapeutic lumbar punctures to keep CSF pressures < 20
  88. 88. Lyme disease
  89. 89. Prevention Advise Patients to avoid exposure to vector ticks in endemic areas and to promptly remove attached ticks.  Wear protective clothing  Use insect repellant containing diethyltoluamide (DEET) or a tick-killing spray containing permethrin, the latter to be applied to clothing, not skin
  90. 90. Lymes  Acute, localized Lyme disease:  Erythema migrans and other symptoms (e.g., fever, fatigue, headache, arthralgias, myalgias) occuring within 30 days of possible tick exposure ( this is sufficient to diagnose Lyme disease)  Acute, disseminated Lyme disease :  Multiple, secondary erythema migrans lesions, Acute carditis (heart block) , CNS Disease (e.g., cranial neuropathy, radiculoneuropathy, lymphocytic meningitis) and brief episodes of monoarticular or oligoarticular inflammatory arthritis occuring within weeks to months after tick exposure  Late Lyme disease:  Occuring within months to years after possible tick exposure  Chronic (>1 year) inflammatory monoarthritis or oligoarthritis  Nervous system complications : peripheral neuropathy or encephalomyelitis
  91. 91. Diagnosis and Rx  Erythema migrans in an endemic area is sufficient for diagnosis  do not get serology ( can be negative in acute disease - ). Start therapy as next step – oral doxycycline or amoxicillin or cefuroxime.  Disseminated Lymes  Get serologic testing. Use 2 step approach – first ELISA. If ELISA indeterminate, get western blot.  Arthritis, Carditis ( except third degree block, cranial nerve palsy without meningitis  Rx similar to erythema migrans  Third degree block or Meningitis/ neuroborreliosis  Rx with ceftriaxone IV
  92. 92. Q  A 30 y/o pregnant woman has a one week history of a slowly enlarging red lesion on her right thigh. She reports having gone on a camping trip about 3 weeks ago and now recalls that she removed a tick from the site of the lesion. An ELISA test is negative for Lymes. What is the next step? A. Re-assurance B. Ampicillin C. Doxycycline D. Western blot testing E. Medical termination of pregnancy
  93. 93. Ans. B  Acute lymes – serology is often –ve. No need to do western blot – give rx wioth ampicillin  Doxycycline is contraindicated in pregnancy.
  94. 94. Other  RMSF  Rash starting on ankles and wrists few days after fever.  Doxycycline. If pregnant, cholramphenicol  Ehrilichiosis  central distribution of rash, no involvement of periphery. Dx  inclusions in leucocytes
  95. 95. Meningitis Refer Neurology Lecture
  96. 96. Meningitis  Symptoms : Fever, Photophobia, Headache, Neck stiffness, vomiting, seizures  Use physical exam findings to confirm a diagnosis of meningitis.  Look for:  Fever  Nuchal rigidity  Brudzinski's sign  Kernig's sign  Signs of encephalitis, such as weakness and change in mental status
  97. 97. Meningitis  Do lumbar puncture to obtain CSF for:  Protein, glucose, and cell count determinations  Gram stain and bacterial culture  PCR testing for enterovirus and HSV if bacterial Gram stain and culture results are negative and cell counts suggest viral meningitis  Obtain CT scan before lumbar puncture in patients with: ( HIPFAN)  Immunucompromised state (I)  History of CNS disease (H)  New onset seizures (N)  Papilledema (P)  Altered level of consciousness ( suggests encephalitis)(A)  Focal neurologic signs (F) Be aware that delay in initiating appropriate antibiotics while awaiting results of CT scan in patients with bacterial meningitis may result in an adverse clinical outcome.
  98. 98. Meningitis
  99. 99. Meningitis – Empiric Rx  Base empiric antibiotic therapy on:  Patient's age  CSF gram-stain result  Potential bacterial pathogens  Knowledge of local resistance patterns for those pathogens Thereafter, base targeted antibiotic therapy on culture results and susceptibility data. Administer dexamethasone 15 to 20 minutes before the first antimicrobial dose in adult patients with suspected meningitis.
  100. 100. Meningitis – Emperical therapy Predisposing Factor AGE Common Bacterial Pathogens Antimicrobial Rx <1 month Streptococcus agalactiae, Escherichia coli, Listeria monocytogenes, Klebsiella species Ampicillin plus cefotaxime or ampicillin plus an aminoglycoside 1 - 23 months Streptococcus pneumoniae, Neisseria meningitidis, S. agalactiae, Haemophilus influenzae, E. coli Vancomycin plus a third- generation cephalosporin 2- 50 years N . meningitidis, S. pneumoniae Vancomycin plus a third- generation cephalosporin >50 years S. pneumoniae, N. meningitidis, L. monocytogenes, aerobic gram-negative bacilli Vancomycin plus ampicillin plus a third- generation cephalosporin
  101. 101. Meningitis – Emperical therapy Predisposing Factor HEAD TRAUMA Common Bacterial Pathogens Antimicrobial Rx Basilar skull fracture S. pneumoniae, H. influenzae, group A - hemolytic streptococci Vancomycin plus a third- generation cephalosporin Penetrating trauma Staphylococcus aureus, coagulase-negative staphylococci (especially Staphylococcus epidermidis), aerobic gram-negative bacilli (including Pseudomonas aeruginosa) Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem  YOU ARE Adding an antipseudomonal antibiotic. Postneurosurgery Aerobic gram-negative bacilli (including P. aeruginosa), S . aureus, coagulase-negative staphylococci (especially S. epidermidis) Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem CSF shunt Coagulase-negative staphylococci (especially S. epidermidis), S. aureus, aerobic gram-negative bacilli (including P. aeruginosa), Propionibacterium acnes Vancomycin plus cefepime,c vancomycin plus ceftazidime,c or vancomycin plus meropenem
  102. 102. Pneumonias Pulmonology
  103. 103. UTIs Nephrology
  104. 104. Catheter Related Infections Indwelling catheters  suspect candida. R/o endophthalmitis in candida sepsis, get Ophthal consult If catheter site looks infected  remove catheter. Do not use same site.
  105. 105. Febrile Neutropenia  Absolute neutropenia - < 500  Consider Neupogen  Start Gram - ve emperic therapy with cefepime or imipenem.  If very critically ill or MRSA risk, add vancomycin  If no response in 48 hours, add antifungals
  106. 106. Neutropenic Precautions  Remove any offending drugs or agents.  Use careful oral hygiene to prevent infections of the mucosa and teeth.  Avoid rectal temperature measurements and rectal examinations.  Use good skin care for wounds and abrasions
  107. 107. Influenza  Vaccination  Drugs used in Influenza
  108. 108. Anti-flu drugs  ZANAMAVIR  OSTELTAMAVIR ( Tamiflu)   These drugs are effective only if given in 48hrs of onset of flu symptoms.   Zanamavir can cause bronchoconstriction  caution in asthmatics ( keep a bronchodilator inhaler handy)   Osteltamavir causes nausea and vomiting.
  109. 109. Immune Reconstitution Syndrome