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Infectious Disease

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Infectious Disease

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Infectious Disease

  1. 1. Review on Infectious Diseases http://crisbertcualteros.page.tl
  2. 2. Fever and Skin Lesions
  3. 3. S. pneumoniae , H. influenzae , N. meningitidis     Purpura fulminans Rickettsia rickettsii      Rocky Mountain spotted fever N. meningitidis      Meningococcemia     Petechiae: Sepsis with skin findings   Erythroderma: toxic shock syndrome Group A Streptococcus , Staphylococcus aureus  
  4. 4. Lesion, Clinical Syndrome Infectious Agent Vesicles     Smallpox Variola virus   Chickenpox Varicella-zoster virus   Shingles (herpes zoster) Varicella-zoster virus   Cold sores, herpetic whitlow, herpes gladiatorum Herpes simplex virus   Hand-foot-and-mouth disease Coxsackievirus A16   Orf Parapoxvirus   Molluscum contagiosum Pox-like virus   Rickettsialpox Rickettsia akari     Blistering distal dactylitis Staphylococcus aureus or Streptococcus pyogenes   Bullae     Staphylococcal scalded-skin syndrome S. aureus     Necrotizing fasciitis S. pyogenes , Clostridium spp., mixed aerobes and anaerobes    Gas gangrene Clostridium spp.    Halophilic vibrio Vibrio vulnificus  
  5. 5. Crusted lesions     Bullous impetigo/ecthyma S. aureus     Impetigo contagiosa S. pyogenes     Ringworm Superficial dermatophyte fungi   Sporotrichosis Sporothrix schenckii     Histoplasmosis Histoplasma capsulatum     Coccidioidomycosis Coccidioides immitis     Blastomycosis Blastomyces dermatitidis     Cutaneous leishmaniasis Leishmania spp.    Cutaneous tuberculosis Mycobacterium tuberculosis     Nocardiosis Nocardia asteroides   Folliculitis     Furunculosis S. aureus     Hot-tub folliculitis Pseudomonas aeruginosa     Swimmer's itch Schistosoma spp.    Acne vulgaris Propionibacterium acnes  
  6. 6. Papular and nodular lesions     Fish-tank or swimming-pool granuloma Mycobacterium marinum     Creeping eruption (cutaneous larva migrans) Ancylostoma braziliense     Dracunculiasis Dracunculus medinensis     Cercarial dermatitis Schistosoma mansoni     Verruca vulgaris Human papillomaviruses 1, 2, 4   Condylomata acuminata (anogenital warts) Human papillomaviruses 6, 11, 16, 18   Onchocerciasis nodule Onchocerca volvulus     Cutaneous myiasis Dermatobia hominis     Verruca peruana Bartonella bacilliformis     Cat-scratch disease Bartonella henselae     Lepromatous leprosy Mycobacterium leprae     Secondary syphilis (papulosquamous, nodular, and condylomata lata lesions) Treponema pallidum     Tertiary syphilis (nodular gummatous lesions) T. pallidum  
  7. 7. Ulcers with or without eschars     Anthrax Bacillus anthracis     Ulceroglandular tularemia Francisella tularensis     Bubonic plague Yersinia pestis     Buruli ulcer Mycobacterium ulcerans     Leprosy M. leprae     Cutaneous tuberculosis M. tuberculosis     Chancroid Haemophilus ducreyi     Primary syphilis T. pallidum   Erysipelas S. pyogenes   Cellulitis Staphylococcus spp., Streptococcus spp., various other bacteria 
  8. 8. Necrotizing fasciitis     Streptococcal gangrene S. pyogenes     Fournier's gangrene Mixed aerobic and anaerobic bacteria Myositis and myonecrosis     Pyomyositis S. aureus     Streptococcal necrotizing myositis S. pyogenes     Gas gangrene Clostridium spp.  Nonclostridial (crepitant) myositis Mixed aerobic and anaerobic bacteria   Synergistic nonclostridial anaerobic myonecrosis Mixed aerobic and anaerobic bacteria
  9. 9. Dengue
  10. 10. <ul><li>Dengue Virus </li></ul><ul><ul><li>~Causes dengue and dengue hemorrhagic fever </li></ul></ul><ul><ul><li>~Is an arbovirus </li></ul></ul><ul><ul><li>~Is a flavivirus in the same family as the viruses that causes yellow fever, St.Louise encephalitis,West Nile fever </li></ul></ul><ul><ul><li>~Transmitted by mosquitoes </li></ul></ul><ul><ul><li>~Composed of single-stranded RNA </li></ul></ul><ul><ul><li>~Has 4 serotypes (DEN-1, 2, 3, 4) </li></ul></ul><ul><li>Aedes aegypti </li></ul><ul><ul><li>~Dengue transmitted by infected female mosquito </li></ul></ul><ul><ul><li>~Primarily a daytime feeder </li></ul></ul><ul><ul><li>~Lives around human habitation </li></ul></ul><ul><ul><li>~Lays eggs and produces larvae preferentially in artificial containers </li></ul></ul>
  11. 11. Dengue Clinical Syndromes <ul><li>Four dengue clinical syndromes: </li></ul><ul><li>Undifferentiated fever; </li></ul><ul><li>Classic dengue fever; </li></ul><ul><li>Dengue hemorrhagic fever, or DHF; and </li></ul><ul><li>Dengue shock syndrome, or DSS. </li></ul><ul><li>Dengue shock syndrome is actually a severe form of DHF. </li></ul>
  12. 12. <ul><li>Clinical Characteristics of Dengue Fever </li></ul><ul><ul><li>~Fever </li></ul></ul><ul><ul><li>~Headache </li></ul></ul><ul><ul><li>~Muscle and joint pain </li></ul></ul><ul><ul><li>~Nausea/vomiting </li></ul></ul><ul><ul><li>~Rash - may present at different stages of the illness, and whose appearance can be variable—it may be maculopapular, petechial, or erythematous. </li></ul></ul><ul><ul><li>~Hemorrhagic manifestations </li></ul></ul>
  13. 13. <ul><li>Some cases may present with or develop encephalitic or encephalopathic signs and symptoms, such as: </li></ul><ul><li>~Decreased level of consciousness—including lethargy, confusion, and coma; </li></ul><ul><li>~Seizures; </li></ul><ul><li>~Nuchal rigidity; and Paresis </li></ul>
  14. 14. <ul><li>Hemorrhagic Manifestations of Dengue </li></ul><ul><li>~Skin hemorrhages: petechiae, purpura, ecchymoses </li></ul><ul><li>~Gingival bleeding </li></ul><ul><li>~Nasal bleeding </li></ul><ul><li>~Gastrointestinal bleeding: hematemesis, melena, hematochezia </li></ul><ul><li>~Hematuria </li></ul><ul><li>~Increased menstrual flow </li></ul><ul><li>DHF 4 Criteria: </li></ul><ul><li>~Fever, or recent history of acute fever </li></ul><ul><li>~Hemorrhagic manifestations </li></ul><ul><li>~Low platelet count (100,000/mm3 or less) </li></ul><ul><li>~Objective evidence of “leaky capillaries:” </li></ul><ul><ul><li>* elevated hematocrit (20% or more over baseline) </li></ul></ul><ul><ul><li>* low albumin </li></ul></ul><ul><ul><li>* pleural or other effusions </li></ul></ul>
  15. 15. <ul><li>Dengue Shock Syndrome </li></ul><ul><li>4 criteria for DSS </li></ul><ul><li>~Evidence of circulatory failure manifested indirectly by all of the following: </li></ul><ul><ul><li>* Rapid and weak pulse </li></ul></ul><ul><ul><li>* Narrow pulse pressure ( < 20 mm Hg) OR hypotension for age </li></ul></ul><ul><ul><li>* Cold, clammy skin and altered mental status </li></ul></ul><ul><li>~Frank shock is direct evidence of circulatory failure </li></ul>
  16. 16. <ul><li>Four Grades of DHF </li></ul><ul><li>~Grade 1 </li></ul><ul><ul><li>* Fever and nonspecific constitutional symptoms </li></ul></ul><ul><ul><li>* Positive tourniquet test is only hemorrhagic manifestation </li></ul></ul><ul><li>~Grade 2 </li></ul><ul><ul><li>* Grade 1 manifestations + spontaneous bleeding </li></ul></ul><ul><li>~Grade 3 </li></ul><ul><ul><li>* Signs of circulatory failure (rapid/weak pulse, narrow pulse pressure, hypotension, cold/clammy skin) </li></ul></ul><ul><li>~Grade 4 </li></ul><ul><ul><li>* Profound shock (undetectable pulse and BP) </li></ul></ul>
  17. 17. <ul><li>Danger Signs in Dengue Hemorrhagic Fever </li></ul><ul><ul><li>~Abdominal pain - intense and sustained </li></ul></ul><ul><ul><li>~Persistent vomiting </li></ul></ul><ul><ul><li>~Abrupt change from fever to hypothermia, with sweating and prostration </li></ul></ul><ul><ul><li>~Restlessness or somnolence </li></ul></ul>
  18. 18. Warning Signs for Dengue Shock
  19. 19. Unusual Presentations of Severe Dengue Fever ~Encephalopathy ~Hepatic damage ~Cardiomyopathy ~Severe gastrointestinal hemorrhage
  20. 20. <ul><li>PATHOGENESIS: </li></ul><ul><li>Risk Factors Reported for DHF </li></ul><ul><li>~Virus strain </li></ul><ul><li>~Pre-existing anti-dengue antibody </li></ul><ul><ul><li>* previous infection </li></ul></ul><ul><ul><li>* maternal antibodies in infants </li></ul></ul><ul><li>~Host genetics </li></ul><ul><li>~Age </li></ul><ul><li>~Higher risk in secondary infections </li></ul><ul><li>~Higher risk in locations with two or more serotypes circulating simultaneously at high levels (hyperendemic transmission) </li></ul>
  21. 21. Tourniquet Test ~Inflate blood pressure cuff to a point midway between systolic and diastolic pressure for 5 minutes ~Positive test: 20 or more petechiae per 1 inch² (6.25 cm²)
  22. 22. <ul><li>Laboratory Tests in Dengue Fever </li></ul><ul><li>~Clinical laboratory tests </li></ul><ul><ul><li>~CBC-WBC, platelets, hematocrit </li></ul></ul><ul><ul><li>~Albumin </li></ul></ul><ul><ul><li>~Liver function tests </li></ul></ul><ul><ul><li>~Urine-check for microscopic hematuria </li></ul></ul><ul><li>~Dengue-specific tests </li></ul><ul><ul><li>~Virus isolation </li></ul></ul><ul><ul><li>~Serology </li></ul></ul>
  23. 23. TREATMENT: Outpatient Triage ~No hemorrhagic manifestations and patient is well-hydrated: home treatment ~Hemorrhagic manifestations or hydration borderline: outpatient observation center or hospitalization ~Warning signs (even without profound shock) or DSS: hospitalize
  24. 24. Treatment of Dengue Fever ~Fluids ~Rest ~Antipyretics (avoid aspirin and non-steroidal anti- inflammatory drugs) ~Monitor blood pressure, hematocrit, platelet count, level of consciousness ~Continue monitoring after defervescence ~If any doubt, provide intravenous fluids, guided by serial hematocrits, blood pressure, and urine output ~The volume of fluid needed is similar to the treatment of diarrhea with mild to moderate isotonic dehydration (5%-8% deficit)
  25. 25. Acquired Immune Deficiency Syndrome (AIDS)
  26. 26. Acquired Immune Deficiency Syndrome (AIDS) ~1st recognized in the U.S. in 1981 when Center for Disease Control (CDC) reported the unexplained occurrence of Pneumocystis carinii pneumonia in 5 previously healthy homosexual men in Los Angeles ~Kaposi’s sarcoma (KS) was also noted in 26 previously healthy homosexual men in New York and L.A. ~1983 – HIV was isolated from pxs with lymphadenopathy ~1984 – clearly demonstrated as causative agent of AIDS ~1985 – ELISA was developed leading to appreciation of the scope and evolution of HIV epidemic in the U.S. and other nations
  27. 27. Definition ~currently, CDC classification system for HIV-infected adolescents and adults categorizes persons on the basis of clinical conditions associated with HIV infections and CD4+ T lymphocyte count ~the system is based on 3 ranges of CD4+ T lymphocyte counts and 3 clinical categories and is represented by a matrix of nine mutually exclusive categories
  28. 28. 1993 Revised classification System for HIV Infection and Expanded AIDS Surveillance Case Definition for Adolescents and Adults Clinical Categories CD4+ T Cell categories A Asymptomatic, Acute(Primary) HIV or PGL B Symptomatic, Not A or C Conditions C AIDS-Indicator Conditions >500/µL A1 B1 C1 200-499/µL A2 B2 C2 <200/µL A3 B3 C3
  29. 29. <ul><li>Etiologic Agent </li></ul><ul><li>~HIV belongs to the family of human retroviruses and the subfamily of lentiviruses </li></ul><ul><li>~4 Human Retroviruses: </li></ul><ul><ul><li>* HTLV I, II – transforming retroviruses </li></ul></ul><ul><ul><li>* HIV 1,2 – cytopathic viruses </li></ul></ul><ul><ul><ul><li>** HIV 1 – most common cause of HIV disease throughout the world </li></ul></ul></ul><ul><ul><ul><li>** HIV2 – 1st identified in 1986 in West African </li></ul></ul></ul><ul><ul><ul><li>**closely related to SIV (Simian Immunodeficiency Virus) than HIV1 </li></ul></ul></ul><ul><ul><ul><li>** both are zoonotic infections </li></ul></ul></ul>
  30. 30. <ul><li>Transmission </li></ul><ul><li>1.homosexual and heterosexual contact </li></ul><ul><ul><li>* in U. S. 42% of HIV infections are among men who have sex with men </li></ul></ul><ul><ul><li>* 33% - by heterosexual transmission </li></ul></ul><ul><ul><ul><li>** most common mode of infection </li></ul></ul></ul><ul><ul><ul><li> worldwide especially in developing countries </li></ul></ul></ul><ul><ul><li>* HIV has been demonstrated in seminal fluid, cervical smears and vaginal fluid particularly in conditions where there is increased monocytes and lymphocytes e.g. urethritis and epididymitis </li></ul></ul>
  31. 31. <ul><ul><li>* Risks for HIV transmission </li></ul></ul><ul><ul><ul><li>** Receptive Anal intercourse – </li></ul></ul></ul><ul><ul><ul><ul><li>** HIV transmitted bec. of the thin, fragile rectal mucosa </li></ul></ul></ul></ul><ul><ul><ul><ul><li>** Trauma assocd. with anal intercourse </li></ul></ul></ul></ul><ul><ul><ul><ul><li>** Male to female transm. - 8x more efficient than female to male due to prolonged exposure to infected seminal fluid of the </li></ul></ul></ul></ul><ul><ul><ul><ul><li>vaginal and cervical mucosa </li></ul></ul></ul></ul>
  32. 32. <ul><ul><ul><li>Risks of HIV Transmission…… </li></ul></ul></ul><ul><ul><ul><li>* History of STD’s </li></ul></ul></ul><ul><ul><ul><li>* Presence of genital ulcerations (T. pallidum, H. ducreyi, </li></ul></ul></ul><ul><ul><ul><li>HSV) </li></ul></ul></ul><ul><ul><ul><li>* Lack of circumcision due to </li></ul></ul></ul><ul><ul><ul><ul><li>- Inc. susceptibility of uncircumsized men to ulcerative STD’s and microtrauma </li></ul></ul></ul></ul><ul><ul><ul><ul><li> - inner foreskin contains high density of Langerhans cells & lymphocytes, macrophages </li></ul></ul></ul></ul><ul><ul><ul><ul><li>- Moist environment </li></ul></ul></ul></ul><ul><ul><ul><li>* Use of oral contraceptives </li></ul></ul></ul><ul><ul><ul><li>* Oral sex= less efficient mode of transmission </li></ul></ul></ul><ul><ul><ul><li>* alcohol consumption and illicit drug use with unsafe sexual behavior </li></ul></ul></ul>
  33. 33. <ul><li>2. by blood and blood products </li></ul><ul><ul><li>a. individuals who received HIV infected blood transfusions, blood products or transplanted </li></ul></ul><ul><ul><li>tissue, IV drug users exposed to HIV while sharing injection paraphernalia </li></ul></ul><ul><ul><li>b. parenteral transm. of HIV in IV drug users </li></ul></ul><ul><ul><li>does not require IV punctures, subcutaneous(“skin </li></ul></ul><ul><ul><li>popping”) or IM (“muscling”) injections can </li></ul></ul><ul><ul><li>transmit HIV </li></ul></ul>
  34. 34. <ul><ul><li>c. risk of HIV infection increases with </li></ul></ul><ul><ul><ul><li>~ duration of injected drug use </li></ul></ul></ul><ul><ul><ul><li>~ the frequency of needle sharing </li></ul></ul></ul><ul><ul><ul><li>~ number of partners with whom paraphernalia are shared (“shooting galleries”) </li></ul></ul></ul><ul><ul><ul><li>~ comorbid psychiatric conditions </li></ul></ul></ul><ul><ul><ul><li>~ use of cocaine in injectable form or smoked as “crack” </li></ul></ul></ul><ul><ul><ul><li>~ use of injection drugs in a geographic location with a high prevalence of HIV </li></ul></ul></ul>
  35. 35. <ul><ul><li>d. risk of infection via transfused screened blood is 1 in 725,000 </li></ul></ul><ul><ul><li>e. chance of infec. of a hemophiliac via clotting factor conc. - eliminated due to heat treatment </li></ul></ul>
  36. 36. <ul><li>3. occupational transmission </li></ul><ul><ul><li>a. 0.3% risk of HIV transm. ffg. skin puncture from a needle or a sharp object contaminated with blood from a person w/ documented HIV infec. </li></ul></ul><ul><ul><li>b. 0.09% risk of HIV infec. after a mucous membrane exposure </li></ul></ul>
  37. 37. <ul><li>4. infected mothers to infants either intrapartum, perinatally or via breast milk </li></ul><ul><ul><li>a. occurs as early as 1st and 2nd trimesters of pregnancy </li></ul></ul><ul><ul><li>b. most common in the perinatal period </li></ul></ul><ul><ul><li>c. relative proportion of mother to child transm. </li></ul></ul><ul><ul><ul><li>~ 23-30% before birth </li></ul></ul></ul><ul><ul><ul><li>~ 50-65% during birth </li></ul></ul></ul><ul><ul><ul><li>~ 12-20% via breast feeding </li></ul></ul></ul><ul><ul><li>d. 15-25% probability of transm. from mother to fetus in industrialized countries, 25-35% in developing countries </li></ul></ul>
  38. 38. <ul><ul><li>e. factors assoc. with high risk of transm. </li></ul></ul><ul><ul><ul><li>~ high maternal levels of plasma viremia </li></ul></ul></ul><ul><ul><ul><li>~ low maternal CD4+ T cell counts </li></ul></ul></ul><ul><ul><ul><li>~ prolonged interval bet. membrane rupture and delivery </li></ul></ul></ul><ul><ul><ul><li>~ chorioamnionitis </li></ul></ul></ul><ul><ul><ul><li>~ STD’S during pregnancy </li></ul></ul></ul><ul><ul><ul><li>~ Hard drinks drug use during pregnancy </li></ul></ul></ul><ul><ul><ul><li>~ Cigarette smoking </li></ul></ul></ul><ul><ul><ul><li>~ Preterm delivery </li></ul></ul></ul><ul><ul><ul><li>~ Obstetric procedures (amniocentesis, amnioscopy, episiotomy) </li></ul></ul></ul>
  39. 39. 5. breast feeding <ul><ul><li>= risk factors for transm. </li></ul></ul><ul><ul><ul><li>~ detectable levels of HIV in breast </li></ul></ul></ul><ul><ul><ul><li>milk </li></ul></ul></ul><ul><ul><ul><li>~ presence of mastitis </li></ul></ul></ul><ul><ul><ul><li>~ Low maternal CD4+ T cell counts </li></ul></ul></ul><ul><ul><ul><li>~ maternal vit A deficiency </li></ul></ul></ul><ul><ul><li>= lower risk of HIV transm. from exclusive breastfeeding than mixed feeding </li></ul></ul>
  40. 40. 6. human bite = rare 7. no evidence that HIV transm. can occur as a result of exposure to tears, sweat, and urine <ul><li>Epidemiology </li></ul><ul><li>35 M cases of HIV infection worldwide </li></ul><ul><ul><li>2/3 found in subSaharan Africa </li></ul></ul><ul><li>50% cases in women </li></ul><ul><li>2.5M children <15 yrs old are living w/ HIV/AIDS </li></ul><ul><li>4th leading cause of mortality worldwide with about 3 M deaths </li></ul>
  41. 41. Pathophysiology and Pathogenesis - hallmark is profound immunodeficiency resulting from progressive qualitative and quantitative -deficiency of the subset of t helper cells or inducer cells with CD4 molecule on its surface w/c serves as primary cellular receptor for HIV
  42. 42. Clinical Manifestations a.Acute HIV syndrome - in 50%-70% of indiv. with primary infection - high levels of viremia measured in million of copies of HIV RNA/ml that last for several wks. - 3-6 weeks after primary infection - fever, pharyngitis, lmphadenopathy, meningitis, encephalitis, mucocutaneous ulceration - Most will recover spontaneously w/ mildly depressed CD4+ T cells
  43. 43. b.Asymptomatic stage - Median time for untreated pats. - 10 yrs. - Rate of progression is directly correlated w/ HIV RNA levels c.Symptomatic dse - More severe & life threratening complic. of HIV infec. occurs with CD4+ T cell counts <200/µL - 60% of deaths among - due to P. carinii & viral hepatitis
  44. 44. <ul><li>- Respiratory </li></ul><ul><ul><ul><ul><li>- sinusitis, acute bronchitis </li></ul></ul></ul></ul><ul><ul><ul><ul><li>- one of the most frequent complic. </li></ul></ul></ul></ul><ul><ul><ul><ul><li>- most common - pneumonia due to S pneumoniae/H. influenzae and P. carinii (25%) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>- Pneumococcal vaccine - recommended as prophylaxis </li></ul></ul></ul></ul><ul><ul><ul><ul><li>- IV pentamidine is the tx of choice </li></ul></ul></ul></ul><ul><li> - Cardiovascular </li></ul><ul><li> - Dilated cardiomyopathy either as a direct consequence of HIV infec. or a late complic. or a consequence of IFN α tx w/c is reversible when stopped </li></ul><ul><li>- edema and shortness of brea </li></ul><ul><li>Others: Chaga’s, KS, cryptococcosis, pericardial effusions in advanced stage </li></ul>
  45. 45. - Oropharynx and GIT * Thrush - candida * Hairy leukoplakia - EBV * Aphthous ulcers * Esophagitis * Diarrhea cauased by Shigella,Salmonella, * Shigella, Campylobacter -Kidney and GUT * HIV-assoc. nephropathy * dysuria, heamturia or pyuria * Condyloma lata – most common presentation of syphilis in HIV pats.
  46. 46. Advanced HIV dis. - CD4+ T cells count falls below a critical level <200/µL & pat. becomes susceptible to opportunistic dse Long term nonprogressors Those who had been infected with HIV for long periods (>10yrs) whose CD4 + T cell counts move w/in normal range & remained stable over the years who had not received antiretroviral tx
  47. 47. Diagnosis and Lab Monitoring depends on demonstrations of Ab to HIV & or direct detection of HIV or one of its components ELISA - enzyme immunoassay (EIA) - standard screening test - Sensitivity 99.5%, - nonspecific - 10% of EIA (+) pat . developed HIV infec.
  48. 48. Western blot - Confirmatory test If western blot patterns of reactivity do not fall into the (+) or (-) categories - considered “indeterminate” - can be repeated in one month HIV RNA levels – determine the prognosis and assess the response to antiviral tx P24 antigen capture assay – detects viral protein p24 in blood PCR, Nucleic acid sequenced based assay
  49. 49. <ul><li>Treatment </li></ul><ul><li>- antiretroviral therapy </li></ul><ul><li>- combination tx or HAART is the cornerstone mgt. of HIV </li></ul><ul><li>- suppression of HIV replication an impt. component in </li></ul><ul><li>prolonging life as well as improving quality of life </li></ul><ul><li>- Reverse transcriptase inhibitors : </li></ul><ul><ul><ul><li>a. Nucleoside analogues – zidovudine, didanosine, zalcitabine, stavudine, lamivudine </li></ul></ul></ul><ul><ul><ul><li>b. Nucleotide analogues – tenofovir </li></ul></ul></ul><ul><ul><ul><li>c. Nonnucleoside reverse transcriptase inhibitors </li></ul></ul></ul><ul><ul><ul><ul><li>- Irapine, delavirdine, efavirenz </li></ul></ul></ul></ul><ul><ul><ul><li>None of these drugs should be used as monotherapy </li></ul></ul></ul>
  50. 50. <ul><li>Indications for Initiation of Antiretroviral therapy </li></ul><ul><li>Acute infection syndrome </li></ul><ul><li>Chronic infection </li></ul><ul><ul><ul><li>Symptomatic </li></ul></ul></ul><ul><ul><ul><li>Asymptomatic </li></ul></ul></ul><ul><ul><ul><ul><li>CD4+ T cell count <350/µL or decreasing </li></ul></ul></ul></ul><ul><ul><ul><ul><li>HIV RNA >50,000 copies/ml or increasing </li></ul></ul></ul></ul><ul><li>Indications for changing antiretroviral Therapy </li></ul><ul><li>- <1-log drop in plasma HIV RNA by 4 wks. ffg start of tx </li></ul><ul><li>- A reproducible signif. inc. from nadir of plasma HIV RNA level not attributable to intercurrent infec., vaccination or test methodology </li></ul><ul><li>- Persistently declining CD4+ T cell no. </li></ul><ul><li>- Clinical deterioration </li></ul><ul><li>- Side effects </li></ul>
  51. 51. Influenza Virus
  52. 52. <ul><li>Influenza Virus </li></ul><ul><li>~ family Orthomyxoviridae </li></ul><ul><li>~ RNA virus </li></ul><ul><li>~ 8 RNA segments mutate or recombine resulting in new strains of viruses </li></ul><ul><li>~ lipid memb. composed of </li></ul><ul><ul><li>* 2 spikes of glycoprotein </li></ul></ul><ul><ul><li>- heamagglutinin (H) </li></ul></ul><ul><ul><li>- neuraminidase (N) </li></ul></ul><ul><ul><li>* one membrane channel protein (M2) </li></ul></ul>
  53. 53. Types: * Influenza A - isolated in 1933 - most severe type causing pandemics - hosts are humans, swine, horses * Influenza B - isolated in 1939 - usually mild illness * Influneza C - isolated in 1950 usually no s/s
  54. 54. INFLUENZA A ~ classified by Hemagglutinin (H) & Neuraminidase (N) sub-types ~ Current circulating strains: H1N1 & H3N2 ~ Human subtypes include H1N1, H3N2, H1N2, & H2N2 ~ Avian subtypes: H1 to H15 & N1 to N9 ~ Bird  human H5N1, H9N2, H7N7, H7N2, H7N3
  55. 55. <ul><li>Why H5N1 is of particular concern? </li></ul><ul><li>* It mutates rapidly </li></ul><ul><li>*cause severe disease in humans </li></ul><ul><li>Infected animals excrete virus for => 10 days orally & in feces </li></ul><ul><li>Antigenic drift – point mutations accumulated during virus replication </li></ul><ul><li>* Antigenic shift – hybrid virus emerges when cell infected w/ 2 different influenza viruses </li></ul><ul><li>* Human, avian, swine, equine are hosts </li></ul>
  56. 56. <ul><li>AVIAN INFLUENZA </li></ul><ul><li>~ Avian influenza “bird flu” </li></ul><ul><li>~ Infectious disease of birds </li></ul><ul><li>~ Caused by influenza type A strains </li></ul><ul><li>~ 1st identified in Italy </li></ul><ul><li>~ Wide spectrum of symptoms </li></ul><ul><li>~ Migratory waterfowl/wild ducks </li></ul><ul><ul><li>* natural reservoir </li></ul></ul><ul><ul><li>* most resistant to infection </li></ul></ul><ul><li>~ Domestic poultry like chickens & turkeys are susceptible </li></ul><ul><li>~ Direct or indirect contact of domestic flocks w/ wild migratory waterfowl implicated as frequent cause of epidemics </li></ul>
  57. 57. AVIAN INFLUENZA IN BIRDS ~ carry the viruses in their intestines ~ shed the virus in their saliva, nasal secretions, & feces ~ contact with contaminated secretions or excretions or w/ surfaces that are contaminated w/ secretions ~ Domestic birds infected w/ direct contact w/ infected waterfowl or poultry ~ contact w/ surfaces (dirt/cages) or materials contaminated w/ virus
  58. 58. AVIAN INFLUENZA IN HUMANS ~ Risk is low; usually do not infect humans ~ From contact with infected poultry or surfaces contaminated with secretions/excretions from birds ~ Spread of avian virus from one person to another has been very rare
  59. 59. <ul><li>AVIAN INFLUENZA TIMELINE </li></ul><ul><li>* 1890 </li></ul><ul><ul><li>`1st recorded influenza pandemic </li></ul></ul><ul><li>* 1918 </li></ul><ul><ul><li>` “Spanish Flu” pandemic caused by H1N1 virus </li></ul></ul><ul><li>* 1957 </li></ul><ul><ul><li>` “Asian Flu” due to H2N2 influenza virus </li></ul></ul><ul><li>* 1968 </li></ul><ul><ul><li>` “Hongkong Flu” H3N2 virus </li></ul></ul><ul><li>* May 21, 1997 </li></ul><ul><ul><li>` H5N1 1st isolated from human px in Hongkong </li></ul></ul><ul><li>* March 2005 </li></ul><ul><ul><li>` Bird flu has spread to 10 countries including Democratic People’s Republic of Korea and killed 50 M chicken </li></ul></ul>
  60. 60. <ul><li>* July 2005 </li></ul><ul><ul><li>` Philippines report its 1st case in a town North of the capital, Manila Aug 2005 </li></ul></ul><ul><ul><li>` Lancet - Oseltamivir (Tamiflu) less side effects and no evidence of resistance </li></ul></ul><ul><ul><li>` Poultry outbreaks noted in Russia, Kazakhstan and ` Tibet </li></ul></ul><ul><ul><li>* Oct 2005 </li></ul></ul><ul><ul><li>` Greece becomes the 1st EU country w/ bird flu infection detected in one turkey </li></ul></ul><ul><ul><li>` WHO reiterates the level of pandemic alert remains unchanged at phase 3 but don’t confirm whether it is the H5N1 strain </li></ul></ul>
  61. 61. <ul><li>CLINICAL FEATURES </li></ul><ul><li>~ Incubation period : 3-7 days </li></ul><ul><li>~ Case to case intervals in household clusters is 2-5 days </li></ul><ul><li>~ Initial symptoms </li></ul><ul><ul><li>* Fever (> 38C) </li></ul></ul><ul><ul><li>* Lower respiratory tract symptoms </li></ul></ul><ul><ul><li>* Rarely conjunctivitis </li></ul></ul><ul><ul><li>* Diarrhea </li></ul></ul><ul><li>~ Other symptoms </li></ul><ul><ul><li>* Abdominal pain </li></ul></ul><ul><ul><li>* pleuritic pain </li></ul></ul><ul><ul><li>* Bleeding from nose and gums </li></ul></ul>
  62. 62. <ul><li>~ Clinical course </li></ul><ul><ul><li>* Dyspnea develop 5 days after onset of illness </li></ul></ul><ul><ul><li>* Respiratory distress, tachypnea and crackles </li></ul></ul><ul><ul><li>* Bloody sputum </li></ul></ul><ul><ul><li>* pneumonia </li></ul></ul><ul><li>~ CXR </li></ul><ul><ul><li>* Diffuse, multifocal, or patchy infiltrates </li></ul></ul><ul><ul><li>* Interstitial infiltrates </li></ul></ul><ul><ul><li>* Segmental or lobular consolidation w/ air bronchograms </li></ul></ul><ul><ul><li>* Pleural effusions uncommon </li></ul></ul><ul><ul><li>* Limited microbiologic data indicating that it is a primary viral pneumonia </li></ul></ul>
  63. 63. <ul><li>~ Progression to respiratory failure </li></ul><ul><ul><li>* Diffuse, bilateral ground glass infiltrates </li></ul></ul><ul><li>(+) ARDS (6 days from onset) </li></ul><ul><li>~ Complications </li></ul><ul><ul><li> * Multiorgan failure </li></ul></ul><ul><ul><li>* Cardiac dilatation and SVT </li></ul></ul><ul><ul><li>* VAP </li></ul></ul><ul><ul><li>* Pulmonary hemorrhage </li></ul></ul><ul><ul><li>* Pneumothorax </li></ul></ul><ul><ul><li>* Sepsis </li></ul></ul>
  64. 64. <ul><li>~ Laboratory findings </li></ul><ul><ul><li>* Leukopenia-lymphopenia </li></ul></ul><ul><ul><li>* Thrombocytopenia </li></ul></ul><ul><ul><li>* Elevated anminotransferase levels </li></ul></ul><ul><ul><li>* Hyperglycemia </li></ul></ul><ul><ul><li>* Elevated creatinine </li></ul></ul><ul><ul><li>* Inc. risk of death w/ dec. platelet & leukocyte </li></ul></ul><ul><li>~ Virologic diagnosis </li></ul><ul><ul><li>*viral isolation </li></ul></ul><ul><ul><li>*Detection of H5-specific RNA </li></ul></ul><ul><ul><li>*Avian influenza A infection is assoc. w/ high frequency of virus detection & higher viral RNA levels </li></ul></ul><ul><ul><li>*2-15 days- interval detection of viral RNA in throat-swabs & 4-8 days in pharyngeal swabs </li></ul></ul>
  65. 65. <ul><li>~ Laboratory Tests </li></ul><ul><ul><li>* usually diagnosed by virus isolation </li></ul></ul><ul><li>~ Presence of virus confirmed by </li></ul><ul><ul><li>* ELISA </li></ul></ul><ul><ul><li>* RT-PCR </li></ul></ul><ul><li>~ Serology may be helpful </li></ul>
  66. 66. <ul><li>MANAGEMENT </li></ul><ul><li>~ Hospitalized in isolation </li></ul><ul><ul><li>* clinical monitoring </li></ul></ul><ul><ul><li>* Appropriate diagnostic testing </li></ul></ul><ul><ul><li>* Antiviral therapy </li></ul></ul><ul><ul><li>~ Ventilatory support </li></ul></ul><ul><li>~ Oxygen </li></ul><ul><li>~ Nebulizers and high air flow O2 masks </li></ul><ul><li>~ Supportive care & antibiotics for secondary infections </li></ul><ul><li>~ Antivirals (amantadine) effective in reducing mortality </li></ul><ul><li>~ Treatment Prophylaxis AMANTADINE (Influenza A only) </li></ul><ul><li>~ RIMANTADINE (Influenza A only) </li></ul><ul><li>~ Oseltamivir </li></ul>
  67. 67. SEVERE ACUTE RESPIRATORY SYNDROME (SARS)
  68. 68. SARS <ul><li>SARS coronavirus </li></ul><ul><li>Natural reservoir not yet identified </li></ul><ul><li>Incubation period: 1-14days </li></ul><ul><li>Prodromal symptoms of fever > 38 0 C , malaise, myalgia and headache </li></ul><ul><li>With in 3 days non productive cough may follow with or without respiratory distress </li></ul>
  69. 69. Clinical Diagnosis of SARS <ul><li>SUSPECT CASE: </li></ul><ul><li>Person w/ respiratory illness of unknown etiology presenting after Nov. 1 2002 a the ffg. </li></ul><ul><ul><li>Fever (>38 0 C) AND </li></ul></ul><ul><ul><li>One or more clinical finding of respiratory illness including cough, shortness of breath AND </li></ul></ul><ul><ul><li>One of the ffg exposure during the 10 days prior to onset of symptoms: </li></ul></ul><ul><ul><ul><li>Close contact with a person who is a suspect or probable case of SARS </li></ul></ul></ul><ul><ul><ul><li>History of travel to an area w/ recent local transm. of SARS </li></ul></ul></ul><ul><ul><ul><li>Residing in an area w/ recent local transm. of SARS </li></ul></ul></ul>
  70. 70. <ul><li>PROBABLE CASE: </li></ul><ul><li>A suspect case w/ radiographic evidence of infiltrates consistent w/ pneumonia or respiratory distress syndrome(RDS) on chest x-ray </li></ul><ul><li>A suspect case of SARS that is (+) for SARS coronavirus by one or more assays </li></ul><ul><li>A suspect case of SARS with autopsy findings consistent the pathology of RDS w/out an identifiable cause </li></ul>Clinical Diagnosis of SARS
  71. 71. LABORATORY EVALUATION OF SUSPECT SARS CASE <ul><li>BASELINE ASSESSMENT </li></ul><ul><li>CXR </li></ul><ul><li>Pulse oximeter </li></ul><ul><li>Blood Exam (CBC, blood culture, ALT,AST,BUN, crea, Na, K, creatine kinase, acute serum for serology, ABG </li></ul><ul><li>Respiratory specimen </li></ul><ul><ul><li>Sputum G/S and C/S, AFB smears, tracheal aspirates </li></ul></ul>Nasopharyngeal & oropharyngeal swabs for viral work up BAL & pleural tap specimens Legionella AFB smear & culture Viral culture & PCR
  72. 72. TREATMENT <ul><li>EMPIRIC ANTI-MICROBIAL THERAPY </li></ul><ul><li>at time of admission use broad spectrum antibiotics for the treatment of pneumonia with atypical coverage </li></ul><ul><li>ROLE OF ANTIVIRALS AND SYSTEMIC STEROIDS </li></ul><ul><li>The efficacy of RIBAVARIN in SARS treatment is largely anecdotal </li></ul><ul><li>There is no role for RIBAVARIN in the prophylaxis or prevention of SARS </li></ul>
  73. 73. TREATMENT <ul><li>Preemptive treatment w/ RIBAVARIN of suspected SARS patients, not fulfilling all diagnostic criteria but with close contacts w/ proven SARS, is NOT RECOMMENDED </li></ul><ul><li>The role of systemic steroids is unclear </li></ul><ul><li>SUPPORTIVE MANAGEMENT </li></ul><ul><li>Adequate hydration </li></ul><ul><li>treatment of secondary infection </li></ul><ul><li>Use of mucolytics, expectorants, and cough suppressants </li></ul><ul><ul><li>is discouraged </li></ul></ul>
  74. 74. AMEBIASIS
  75. 75. AMEBIASIS <ul><li>E. Histolytica </li></ul><ul><li>Food and water </li></ul><ul><li>90% asymptomatic </li></ul><ul><li>PATHOGENESIS </li></ul><ul><li>Trophozoites invade tissues and attach to mucosa --- mucosal microulceration with normal intervening mucosa --- “flask shaped” ulcer </li></ul>
  76. 76. Clinical Syndrome <ul><li>INTESTINAL AMEBIASIS </li></ul><ul><li>Asymptomatic cyst passer </li></ul><ul><li>AMEBIC COLITIS </li></ul><ul><li>2 to 6 wks after cyst ingestion </li></ul><ul><li>Abdominal pain, diarrhea, scanty stools with blood and mucus </li></ul><ul><li>TOXIC MEGACOLON – severe pain, high fever, profuse diarrhea </li></ul><ul><li>POST AMEBIC COLITIS </li></ul>
  77. 77. Clinical Syndrome <ul><li>AMEBIC LIVER ABSCESS </li></ul><ul><li>Travellers (+) for ameba, develops abscess w/in 5 mos. in 95% of cases </li></ul><ul><li>Normal liver enzymes </li></ul><ul><li>“ anchovy paste” necrotic contents </li></ul><ul><li>Complete resolution w/in 6 mos. in 2/3 of patients </li></ul><ul><li>Complications: </li></ul><ul><ul><li>Rupture into pleural spaces, peritoneum,pericardium </li></ul></ul><ul><ul><li>Hepatobroncial fistula </li></ul></ul>
  78. 78. Diagnosis <ul><li>Stool exam </li></ul><ul><ul><li>Hematophagous trophozoites (definitive) </li></ul></ul><ul><li>Culture </li></ul><ul><li>Serology – ELISA, Agar gel diffusion </li></ul><ul><li>Radiography- UTZ, CTscan, MRI </li></ul>
  79. 79. TREATMENT <ul><li>INTESTINAL AMEBIASIS </li></ul><ul><li>TISSUE AMEBICIDE – METRONIDAZOLE </li></ul><ul><ul><li>Does NOT eradicate the cyst </li></ul></ul><ul><ul><li>Disulfuram-like reaction </li></ul></ul><ul><li>LUMINAL AMEBICIDE – IODOQUINOL, PAROMOMYCIN, DILOXANIDE FUROATE </li></ul><ul><ul><li>for eradication of cyst with colitis and abscess </li></ul></ul><ul><ul><li>Treatment for asymtomatic carrier </li></ul></ul><ul><ul><li>Poorly absorbed, increase concentration in bowel </li></ul></ul>
  80. 80. TREATMENT <ul><ul><li>AMEBIC LIVER ABSCESS </li></ul></ul><ul><ul><li>METRONIDAZOLE + luminal agent </li></ul></ul><ul><ul><li>EMETINE, CHLOROQUINE – 2 nd line drugs </li></ul></ul><ul><ul><li>INDICATION for ASPIRATION </li></ul></ul><ul><ul><li>Rule out pyogenic abscess </li></ul></ul><ul><ul><li>Failure of respond clinically w/in 3-5days </li></ul></ul><ul><ul><li>The threat of immenent rupture </li></ul></ul><ul><ul><li>Prevention of rupture of L lobe abscess in the pericardium </li></ul></ul><ul><ul><li>Does not accelerate healing </li></ul></ul>
  81. 81. MALARIA
  82. 82. <ul><li>P. vivax- relatively common, prefer reticulocytes </li></ul><ul><li>P. ovale- unusual outside africa, invades reticulocytes </li></ul><ul><li>P. malariae -less common </li></ul><ul><li>P. falciparum- invade RBC of all ages </li></ul><ul><li> - high levels of parasitemia </li></ul>GENETIC DISORDERS confirming protection against malaria Sickle cell disease Thalassemia Glucose 6 phosphate dehydrogenase deficiency
  83. 83. PATHOGENESIS / Life Cycle <ul><li>Female Anopheles mosquito bite Sporozoites </li></ul><ul><li>blood liver (exoerythrocytic/intrahepatic/ </li></ul><ul><li>preerythrocytic phase) </li></ul><ul><li> schizonts merozoites </li></ul><ul><li> erythrocytes </li></ul><ul><li>intraerythrocytic cycle: 48Hfor P. vivax </li></ul><ul><li> P. ovale </li></ul><ul><li> P. falciparum </li></ul><ul><li> 72 H for P. malariae </li></ul><ul><li> </li></ul>
  84. 84. PATHOGENESIS / Life Cycle <ul><li>trophozoites schizonts merozoite </li></ul><ul><li> gametocytes </li></ul><ul><li> (sexual forms) </li></ul><ul><li>ingested by anopheles after a meal </li></ul><ul><li> ZYGOTE </li></ul><ul><li> Oocyst </li></ul><ul><li> sporozoite </li></ul><ul><li> </li></ul>
  85. 85. Clinical features <ul><li>Non specific: headache, fatigue, body malaise, paroxysms of fever spike(regular intervals), chills, rigors </li></ul><ul><li>Anemia, splenomegaly </li></ul><ul><li>SEVERE FALCIPARUM MALARIA: </li></ul><ul><ul><li>CEREBRAL MALARIA </li></ul></ul><ul><ul><ul><li>Coma – characteristic and ominous feature </li></ul></ul></ul><ul><ul><li>HYPOGLYCEMIA </li></ul></ul><ul><ul><li>LACTIC ACIDOSIS </li></ul></ul><ul><ul><li>NON CARDIOGENIC PULMONARY EDEMA </li></ul></ul><ul><ul><li>RENAL IMPAIRMENT </li></ul></ul><ul><ul><li>HEMATOLOGIC ABNORMALITY </li></ul></ul><ul><ul><li>ASPIRATION PNEUMONIA </li></ul></ul><ul><ul><li>BACTERIAL SUPERINFECTION </li></ul></ul>
  86. 86. Clinical features <ul><li>TRANSFUSION MALARIA </li></ul><ul><ul><li>No pre erythrocytic stage </li></ul></ul><ul><li>MALARIA IN PREGNANCY </li></ul><ul><ul><li>Congenital Malaria (<5%) </li></ul></ul><ul><ul><ul><li>Related to parasitic density in maternal blood and placenta </li></ul></ul></ul><ul><li>MALARIA IN CHILDREN </li></ul><ul><li>CHRONIC COMPLICATIONS </li></ul><ul><li>TROPICAL SPLENOMEGALY (Hyperactive malarial splenomegaly) </li></ul><ul><li>QUARTAN MALARIAL NEPHROPATHY </li></ul><ul><li>BURKITT’S LYMPHOMA AND EBV INFECTIONS </li></ul>
  87. 87. DIAGNOSIS <ul><li>Demonstration of asexual forms of parasite in blood smears </li></ul><ul><ul><li>THIN BLOOD SMEARS, THICK BLOOD SMEARS </li></ul></ul><ul><li>PREVENTION </li></ul><ul><li>CHEMOPROPHYLAXIS </li></ul><ul><ul><li>Travellers should start at least 1 wk before departure & continue for 4 wks after leaving the endemic area </li></ul></ul>MEFLOQUINE 250mg po for 1week DOXYCYCLINE 100mg po (alternative) CHLOROQUINE 300mg po 1 week
  88. 88. TREATMENT CHLOROQUINE <ul><li>drug of choice for benign cases </li></ul><ul><li>schizonticidal, gametocidal </li></ul>SULFADOXINE PYRIMETHAMINE (Fansidar) for chloroquine resistant MEFLOQUINE Active against blood stages and schizonts HALOFANTRINE <ul><li>Alternative for chloroquine resistant P. falciparum </li></ul><ul><li>lengthening of PR and QT intervals </li></ul>TETRACYLINE/ DOXYCYCLINE <ul><li>weak antimalarial activity, use in combination </li></ul>
  89. 89. TREATMENT <ul><li>drug resistance : if parasitemia does not decrease below </li></ul><ul><li>25% of admission value in 48H or if parasetemia </li></ul><ul><li>has not cleared by 7 days </li></ul>QUININE/ QUINIDINE <ul><li>acts mainly on trophozoites, gametocidal, no liver activity </li></ul><ul><li>1 st line drug for falciparum malariae </li></ul><ul><li>Adverse effect: cinchonism, arrythmias </li></ul>PRIMAQUINE <ul><li>acts on intrahepatic hypnozoite, prevent relapse </li></ul><ul><li>gametocidal vs P. falciparum </li></ul><ul><li>radical cure for P. vivax and ovale </li></ul>ARTESENUATE/ ARTEMETHER <ul><li>more rapid activity than other drugs </li></ul><ul><li>No action on liver stages </li></ul>
  90. 90. FILARIAL INFECTIONS
  91. 91. FILIRIAL INFECTIONS <ul><li>NEMATODES- dwell in subcutaneous tissues and lymphatics </li></ul><ul><li>Transmitted by mosquitoes and arthropods </li></ul><ul><li>LYMPHATIC FILIRIASIS </li></ul><ul><li>Wucheria bancrofti - vector: Culex, Aedes </li></ul><ul><li>Brugia malayi – vector: anopheles </li></ul><ul><li>PERIODICITY </li></ul><ul><ul><li>NOCTURNAL </li></ul></ul><ul><ul><li>SUBPERIODIC FORMS </li></ul></ul>
  92. 92. MANIFESTATIONS: <ul><li>Asymptomatic microfilaremia </li></ul><ul><li>Hydrocele – scrotal elephantiasis </li></ul><ul><li>Acute lymphangitis and lymphadenitis with high fever – “filarial fevers” </li></ul><ul><li>Regional lymph nodes – enlarged, indurated, inflamed, thrombophlebitis </li></ul><ul><li>Genital lymphatic involvement </li></ul><ul><li>Chyluria – rupture of renal lymphatics </li></ul>
  93. 93. DIAGNOSIS: <ul><li>Detection of microfiliriae in the blood/hydrocele fluid </li></ul><ul><ul><li>Direct method or concentration method ( Knott’s concentration technique ) </li></ul></ul><ul><ul><li>Eosinophilia – support the diagnosis </li></ul></ul><ul><li>TREATMENT: </li></ul><ul><li>DIETHYLCARBAMAZINE(DEC)- 6mg/kg/day for 2-3wks </li></ul><ul><li>IVERMECTIN –alternative </li></ul>
  94. 94. ONCOCERCIASIS (“river blindness”) <ul><li>Oncocerciasis volvulus </li></ul><ul><ul><li>Transmission: skin bite of infected black fly with deposition of infective larvae </li></ul></ul><ul><ul><li>Damage is secondary to microfilariae </li></ul></ul><ul><li>FEATURES: </li></ul><ul><li>SKIN: rash, papular eruption, premature wrinkling, </li></ul><ul><li>redundant skin </li></ul><ul><li>ONCHOCERCOMATA –subcutaneous nodule containing adult </li></ul><ul><li>worm common over coccyx, sacrum </li></ul><ul><li>LYMPH NODES </li></ul><ul><ul><li>lymphadenopathy- inguinal and femoral areas </li></ul></ul><ul><ul><li>hanging groin </li></ul></ul>
  95. 95. ONCOCERCIASIS (“river blindness”) <ul><li>EYES </li></ul><ul><ul><li>punctate keratitis --- “snow flake” opacities </li></ul></ul><ul><ul><li>Sclerosing keratitis, anterior uveitis, iridocyclitis </li></ul></ul><ul><ul><li>optic atrophy </li></ul></ul><ul><li>DIAGNOSIS: </li></ul><ul><li>Biopsy-excise nodule, corneal scleral punch </li></ul><ul><li>TREATMENT: </li></ul><ul><li>IVERMECTIN </li></ul><ul><li>SURAMIN </li></ul><ul><li>Surgical excision of the nodules </li></ul>
  96. 96. LOASIS <ul><li>LOA LOA (African eye worm) </li></ul><ul><ul><li>Diurnal periodicity that peaks bet. 12 NN and 2pm </li></ul></ul><ul><ul><li>CALABAR SWELLING </li></ul></ul><ul><ul><ul><li>Episodic, evanescent localized areas of angioedema and ertyhema of extremities, secondary to hypersensitivity reaction to adult worms </li></ul></ul></ul><ul><li>DIAGNOSIS: </li></ul><ul><li>Detection of microfilariae in peripheral blood </li></ul><ul><li>Biopsy of subcutaneous tissue </li></ul><ul><li>TREATMENT </li></ul><ul><li>DIETHYLCARBAMAZINE </li></ul><ul><li>ALBENDAZOLE </li></ul><ul><li>IVERMECTIN </li></ul>
  97. 97. SCHISTOSOMIASIS
  98. 98. PATHOGENESIS/ Life Cycle <ul><li>Contact with water containing infective stage – Cercariae </li></ul><ul><li>penetrates the skin </li></ul><ul><li>transform to Schistosomules </li></ul><ul><li>migrates to the lungs </li></ul><ul><li>PORTAL VEIN </li></ul><ul><li>mature adult schistosomes pair (do not multiply, may live for 5-8yrs) </li></ul><ul><li>Venules of mesentery- S. japonicum </li></ul><ul><li>Venules of bladder/ureters- S. hematobium </li></ul>
  99. 99. PATHOGENESIS/ Life Cycle (contd…) <ul><li>Egg Deposition </li></ul><ul><ul><ul><ul><ul><li>Some swept back to the liver portal venous system </li></ul></ul></ul></ul></ul><ul><li>extruded to feces/urine </li></ul><ul><li>contact with water </li></ul><ul><li>Miracidium </li></ul><ul><li>Penetrates snail vector </li></ul><ul><ul><ul><li>Intermediate host: S. haematobium – Bulinus </li></ul></ul></ul><ul><ul><ul><li> S. japonicum – Oncomelania </li></ul></ul></ul><ul><ul><ul><li> S. Mansoni - Biomphalaria </li></ul></ul></ul><ul><ul><ul><li>Sporocyst </li></ul></ul></ul><ul><ul><ul><li>Cercariae – most infectious immediately after shedding; no longer viable 48H </li></ul></ul></ul><ul><ul><ul><li>after release </li></ul></ul></ul>
  100. 100. CLINICAL SYNDROMES <ul><li>ACUTE SCHISTOMIASIS (Katayama Fever) </li></ul><ul><li>follows initial exposure </li></ul><ul><li>Intense itchiness, fever, chills, headache, liver, angioedema, cough, abdo pain, weight loss </li></ul><ul><li>LIVER FIBROSIS (Hepatosplenic Schistomiasis) </li></ul><ul><li>Most important complication, secondary to fibroblast proliferation </li></ul><ul><li>Pathognomonic in S. mansoni and S. japonicum </li></ul><ul><li>Develops after 10-15 yrs of prolonged exposure </li></ul>
  101. 101. <ul><li>Liver fibrosis cont… </li></ul><ul><li>Pipe stem fibrosis – finger size bands of portal fibrosis </li></ul><ul><li>Perisinusoidal blockage, portal HPN, splenomegaly, esophageal and gastric varices </li></ul><ul><li>ULTRASOUND ( diagnostic method of choice) </li></ul><ul><ul><li>Dense echogenic areas of fibrotic bands surrounding the portal veins </li></ul></ul>
  102. 102. <ul><li>GLOMERULONEPHRITIS AND PULMONARY HPN </li></ul><ul><li>Due to obliteration of pulmo arterioles by granulomatous inflamation induced by shunted or embolized egg </li></ul><ul><li>Common in S. mansoni, S. japonicum </li></ul><ul><li>OTHERS </li></ul><ul><li>Schistosome Dermatitis (SWIMMER’S ITCH) </li></ul><ul><li>INFLAMMATORY POLYPS/POLYPOSIS </li></ul><ul><li>CNS INVOLVEMENT </li></ul><ul><li>CHRONIC CYSTITIS, URETERITIS, </li></ul><ul><li>PROLONGED EXCRETION OF Salmonellla/urinary carrier state </li></ul>
  103. 103. <ul><li>DIAGNOSIS </li></ul><ul><li>Identification of ova in feces (Concentration Method) </li></ul><ul><li>Immunofluorescent Ab test </li></ul><ul><li>TREATMENT </li></ul><ul><li>PRAZIQUANTEL </li></ul><ul><ul><li>Drug of choice: 20mg/Kg single or 2 doses with food </li></ul></ul><ul><ul><li>Associated with abdo pain, diarrhea, fever, lethargy </li></ul></ul><ul><ul><li>Effectiveness is evaluated by cessation of egg excretion after 2-3 months </li></ul></ul>

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