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Clin Med II Infectious Disease Lecture 1 – Fungal Diseases – Spirochetal Diseases – Mycobacterial Diseases.

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Presentation on theme: "Clin Med II Infectious Disease Lecture 1 – Fungal Diseases – Spirochetal Diseases – Mycobacterial Diseases."— Presentation transcript:

1 Clin Med II Infectious Disease Lecture 1 – Fungal Diseases – Spirochetal Diseases – Mycobacterial Diseases

2 Fungal Diseases – Candidiasis – Cryptococcosis – Histoplasmosis – Pneumocystis

3 (A)Candida albicans. (B)Fusarium spp. (C)Aspergillus fumigatus (arrow, conidia). (D)Cryptococcus neoformans (arrows, capsule). (E)Coccidioides spp (single arrow, arthroconidia; dotted arrow, spherule with endospores). (F)Histoplasma capsulatum, budding intracellular yeast forms.

4 Candiasis  Common normal flora  Can become opportunistic pathogen  Numerous risk factors  If no underlying cause found, persistent candidiasis  possible HIV infection

5 Cutaneous Candiasis  Superfically denuded, beefy red lesions  Usually in skin folds with satellite papules and pustules  Often with pruritis which may be severe  Labs—budding yeast clusters and pseudohyphae under high-power microscopy after 10% KOH prep  Culture can confirm diagnosis  Read—differential diagnosis in text

6 Cutaneous Candiasis


8 Cutaneous Candidiasis  General Treatment – Keep area dry, expose to air, discontinue offending agent if possible  Paronychia/Nails – Clotrimazole 1% solution topically BID or thymol 4% in ethanol topically QD  Skin – Hydrocortisone 1% cream BID with either Nystatin ointment BID or clotrimazole cream 1% BID  Vulvar/Anal Mucous Membranes –  Vaginal—fluconazole 150 mg PO x 1 dose; or intravaginal clotrimazole, miconazole, terconazole, or nystatin  Recurrent/Intractable – long term suppressive therapy; may be non-albicans on culture and respond to oral itraconazole 200 mg BID for 2-4 weeks

9 Cutaneous Candidiasis  Balanitis – more common in uncircumsised men  Topical nystatin ointment for mild lesions  Soaking in dilute aluminum acetate 15 minutes BID  Chronicity or relapses—reinfection from sexual partner  Mastitis – lancinating pain and nipple dermatitis in lactating women  oral fluconazole 200 mg PO QD or topical gentian violet 0.5%  Prognosis – varies from easily cured to recurrent or intractable

10 Oral Candidiasis  Usually present with mouth and/or throat discomfort  Creamy white, curd-like patches overlying erythematous mucosa  +/- angular cheilitis

11 Oral Candidiasis  Diagnosis—clinical; may do wet prep with KOH  Treatment—listed in text—fluconazole, ketoconazole, clotrimazole, nystatin  In patients with HIV, longer courses of therapy are needed  0.12% chlorhexidine or hydrogen peroxide—local relief  Refractory cases—oral itraconazole or voriconazole  Nystatin powder to dentures TID-QID for several weeks

12 Mucosal Candidiasis  Esophageal involvement—most frequent type of significant mucosal disease  Substernal odynophagia, gastroesophageal reflux, nausea without substernal pain  Oral candidiasis—often associated but not always present  Diagnosis—best confirmed by endoscopy with biopsy and culture  Treatment—depends on severity of disease  If able to swallow and adequate oral intake—PO fluconazole or itraconazole solution for 10-14 days  If significantly ill or fluconazole-refractory—oral or IV voriconazole, IV amphotericin B, IV capsofungin, IV anidulafungin, or IV micafungin

13 Mucosal Candidiasis  Vulvovaginal—occurs in 75% of women in their lifetime  Acute vulvar pruritis, burning vaginal discharge, dyspareunia  Diagnosis—often clinical; can confirm with KOH prep or culture  Treatment—Intravaginal topical azole preparations (see text) or single dose of fluconazole 150 mg orally  Recurrence is common—see maintenance therapy

14 Mucosal Candidiasis

15 Candidal Funguria  Usually resolves with antibiotic discontinuance or removal of bladder catheters  Asymptomatic—treatment not indicated  Symptomatic funguria—oral fluconazole 200 mg PO QD x 7-14 days  Newer generation azoles and echinocandins not recommended

16 Disseminated Candidiasis  Non-albicans species account for over 50% of blood isolates and have different resistance patterns  See text for recommended drugs for each species  Hepatosplenic Candidiasis—from aggressive chemo and prolonged neutropenia in patients with underlying hematologic cancers  Fever and abdominal pain weeks after chemotherapy  Negative blood cultures—neutrophil count often recovered  Elevated alkaline phosphatase  Fluconazole or lipid formulation of amphotericin B

17 Disseminated Candidiasis  Problematic diagnosis  Candida isolated from mucosa without invasive disease  Blood cultures positive only 50% of the time in disseminated infection  Decision to treat for Candida – based on each patient  Antifungal therapy is rapidly changing based on addition of new agents and emergence of non-albicans species  Less critically ill and no recent azole exposure—fluconazole 800 mg IV initially, then 400 mg IV daily  More severe illness or recent azole exposure—echocandin  Continue treatment for 2 weeks after last + blood culture and resolution of signs and symptoms of infection  Once patients are clinically stable, IV therapy can be changed to oral

18 Candidal Endocarditis  Rare—usually with exposure to healthcare setting  Increased frequency on prosthetic valves in the first few months after surgery  Diagnosis—culturing candida from emboli or vegetations at the time of valve replacement  Therapy—amphotericin usually considered optimal along with aggressive surgical intervention  High risk patients undergoing induction chemotherapy, bone marrow transplantation, or liver transplant, prophylaxis with antifungal agents can help prevent invasive fungal infections

19 Candidal Endocarditis


21 Cryptococcosis  Cryptococcosis neoformans— an encapsulated budding yeast found worldwide in soil and on dried pigeon dung  Cryptococcosis gatii—related species that can also cause disease  Transmitted via inhalation  Clinically apparent cryptococcal pneumonia is rare in immunocopmetent patients  Most common cause of fungal meningitis

22 Cryptococcus

23 Cryptococcosis  Pulmonary disease: simple nodules  widespread infiltrates  respiratory failure  Three main patterns on CXR in immunocompetent pts  solitary or multiple masses of more than 5 mm in diameter  patchy, segmental or lobar air space consolidation  nodular or reticulonodular interstitial changes  Immunosuppression affects pattern of pulmonary involvement--in AIDS patients interstitial changes are common and often also have lymphadenopathy. 

24 Cryptococcosis

25  Disseminated disease: can involve any organ, but CNS disease predominates  Headache is usually the first symptom of meningitis  Confusion, mental status changes, cranial nerve abnormalities, nausea, vomiting  +/- Nuchal rigidity and meningeal signs  C gatii – neurologic signs due to space occupying lesions  Primary C neoformans infection of skin can mimic bacterial cellulitis  Can see clinical worsening with improved immunologic status

26 Cryptococcosis



29  Respiratory tract disease—diagnosed by culture of respiratory secretions or pleural fluid  Meningeal/CNS disease—lumbar puncture is preferred diagnostic procedure  Increased opening pressure, variable pleocytosis, increased protein, decreased glucose  Gram stain of CSF—budding, encapsulated fungal cells  Cryptococcal capsular antigen in CSF and culture together establish diagnosis in over 90% of cases  MRI is more sensitive than CT in finding CNS abnormalities such as cryptococcomas

30 Cryptococcosis  Initial azole therapy—not recommended for acute cryptococcal meningitis  IV amphotericin B initially x 2 weeks, followed by 8 weeks of oral fluconazole  Can add flucytosine—improved survival but increased risk for toxicity  Frequent repeated LPs or ventricular shunting if there is high CSF pressure or hydrocephalus  Switching from IV amphotericin B to oral fluconazole—  Favorable clinical response (decreased temperature, improvement in headache, N/V, and MMSE score)  Improvement in CSF biochemical parameters  Conversion of CSF culture to negative

31 Cryptococcosis  Similar regimen for non-AIDS patients with cryptococcal meningitis – continue until CSF cultures are negative and CSF antigen titers are below 1:8  Maintenance antifungal therapy is important after acute episode in HIV cases  Fluconazole 200 mg/daily is preferred maintenance therapy  Possible to stop secondary prophyalxis with fluconazole in pts with AIDS who have had good response to antiretroviral therapy  Patients without AIDS—6-12 months of fluconazole as maintenance therapy

32 Cryptococcosis  Poor prognostic factors for cryptococcosis:  Activity of predisposing conditions  Increased age  Organ failure  Lack of spinal fluid pleocytosis  High initial antigen titer  Decreased mental status  Increased ICP  Disease outside the nervous system

33 Histoplasmosis  Histoplasma capsulatum— dimorphic fungus isolated from soil contaminated with bird or bat droppings in endemic areas  Infection takes place by inhalation of conidia  In lungs, conidia convert to small budding cells that are engulfed by phagocytes  Proliferates and undergoes lymphohematogenous spread to other organs

34 Histoplasmosis

35  Most cases are asymptomatic or mild and go unrecognized— incidental radiographs may show calcifications in lungs, spleen  Symptomatic—mild, influenza-like illness; 1-4 days  Moderately severe symptomatic infections— diagnosed as atypical pneumonia—fever, cough, and mild central chest pain; 5-15 days

36 Histoplasmosis

37 Acute Histoplasmosis  Frequently in epidemics  Marked prostration, fever, and comparatively few pulmonary complaints  May last from 1 week to 6 months but is rarely fatal

38 Progressive Disseminated Histoplasmosis  Often in pts with HIV or other immunosuppresion  Fever and multiple organ system involvement  CXR—miliary pattern  Can have fulminant presentation  Fever, dyspnea, cough, weight loss, prostration, oropharyngeal mucous membrane ulcerations, hepatosplenomegaly, IBD-like symptoms

39 Subacute/Chronic Progressive Pulmonary Histoplasmosis  Older patients  Various lesions on radiographs  Heals with fibrosis

40 Chronic Progressive Disseminated Histoplasmosis  Middle-aged to elderly men with no known condition causing immunosuppression  Similar presentation to acute disseminated histoplasmosis  Can be fatal if not treated

41 Complications of Pulmonary Histoplasmosis

42 Histoplasmosis—Labs  Anemia of chronic disease  Bone marrow involvement  Elevations in alkaline phosphatase, LDH, ferritin, AST  Sputum culture rarely positive except in chronic disease  Antigen testing of bronchoalveolar lavage  Antigen testing of urine and serum  Blood or bone marrow cultures  Biopsy of affected organs

43 Histoplasmosis--Treatment  Progressive localized disease and mild-moderately severe nonmeningeal disease  itraconazole 200-400 mg/d orally divided BID  Treatment of choice—overall response rate 80%  More severe illness  IV amphotericin B  AIDS-related histoplasmosis  Lifelong suppressive therapy with itraconazole  No evidence that antifungal agents improve granulomatous or fibrosing mediastinitis

44 Pneumocystosis  Pneumocystis jiroveci – worldwide distribution  Symptomatic disease is rare in general population, but most people have had asymptomatic infections by a young age  Overt infection—interstitial plasma cell pneumonia  Epidemics of primary infections — infants with comorbid conditions  Sporadic cases in older children and adults with altered immunity  Transmission unknown—most likely airborne  Pneumocystis pneumonia (PCP) occurs in up to 80% of AIDS patients without prophylaxis and is a major cause of death

45 Pneumocystosis  Extrapulmonary findings are rare  Sporadic form of disease—abrupt onset of fever, tachypnea, shortness of breath, cough  Pulmonary findings on exam may be slight and disproportionate to degree of illness and CXR findings  Adult pts may present with spontaneous pneumothorax  AIDS pts will have other evidence of HIV-related disease

46 Pneumocystosis  CXR—varying findings—most commonly show diffuse “interstitial” infiltration  No pleural effusions  ABG—can be normal; usually hypoxemia and hypocapnia  Isolated elevation or rising levels of LDH—sensitive but not specific  Serologic tests—unhelpful  elevated (1-3)-β-D-glucan has reasonably good sensitivity and specificity for diagnoses of PCP  Cannot be cultured—may be stained from sputum

47 Pneumocystosis


49  Can start empric therapy if disease suspected clinically  Oral TMP-SMZ is preferred agent because of low cost and high bioavailability  Second-line—Clindamycin/Primaquine, Dapsone/TMP, Pentamidine, Atovaquone  Continue therapy 5-10 days before changing agents  Duration of treatment—14 days for non-AIDS patients, 21 days for AIDS patients  Supportive O2 therapy to maintain pulse oximetry >90%

50 Pneumocystosis  Primary prophylaxis should be given to HIV pts with CD4 counts <200 cells/mcL, CD4 percentage <15%, weight loss, or oral candiasis  Secondary prophlyaxis—to pts with a history of PCP until they have had a durable virologic response to antiretroviral therapy for at least 6 months and CD4 count persistently >200 cells/mcL  Prognosis—varies greatly depending on treatment  Endemic infantile form—20-50% mortality without early and adequate treatment, only 3% with early treatment  Sporadic immunodeficienty form—nearly 100% mortality without treatment, 10-20% in AIDS patients with treatment, 30-50% in other immunodeficient patients with treatment  Recurrences common in immunodeficient patients without prophylaxis

51 Spirochetal Diseases – Lyme Disease – Syphilis – Rocky Mountain Spotted Fever

52 Syphilis  Complex disease caused by Treponema pallidum  Transmission most frequently during sexual contact  Major clinical stages— early (infectious) and late, separated by a symptom-free latent phase

53 Primary Syphilis  Stage of Invasion  Typical lesion is changre at sites of inoculation  Initial small erosion 10- 90 days after inoculation; develops into painless superficial ulcer with clean base and firm, indurated margins  Regional lymph node enlargement  Heals without treatment; may scar

54 Primary Syphilis  Darkfield microscopy and immunofluorescent staining can help visualize pathogen  Read—Nontreponemal antigen tests vs. Treponemal antibody tests

55 Primary Syphilis  Penicillin remains preferred treatment; Doxycycline, Rocephin or Tetracycline can be used for secondary treatment  Table—34-3  Jarisch Herxheimer Reaction—fever and aggravation of symptoms in hours following treatment  Resolves spontaneously in 24 hours  Patients with infectious syphilis must abstain from sexual activity for 7-10 days after treatment  Patients sexually exposed in the last 3 months should be treated even if seronegative; if over 90 days, base treatment on serologic testing

56 Primary Syphilis  Monitor treated pts clinically and serologically Q 3-6 mo  Screen for HIV at time of diagnosis  Failure of nontreponemal titers to decrease 4x by 6 mo – high risk for treatment failure  Failure of titers to decrease 4x by 6-12 mo – repeat HIV screening, consider lumbar puncture, retreat  Persistent signs and symptoms or 4x or greater increase in in nontreponemal titers – failed therapy or reinfection

57 Screening for Syphilis  Avoidance of sexual contact—only 100% reliable method  Latex or polyurethane condoms  Men who have sex with men—screening every 6-12 mo  High-risk individuals—every 3-6 months  Pregnant women—1 st prenatal visit  Repeat in 3 rd trimester if high risk  Patients who have other STDs  Patients who have known or suspected contact with patients who have syphilis

58 Secondary Syphilis  Appears from a few weeks to 6 months after development of chancre  Dissemination of Treponema pallidum  systemic signs and/or infectious lesions distant from inoculation site

59 Secondary Syphilis  Rash—nonpruritic, macular, papular, pustular, follicular, or combinations of any of these types  Generalized; involve palms and soles in 80%  May see annular lesions or mucous membrane patches  Condyloma lata  Meningeal, hepatic, renal, bone, and joint invasion  Alopecia and uveitis






65 Secondary Syphilis  Serologic tests positive in almost all cases  Moist cutaneous and mucous membrane lesions show pathogen on darkfield examination  Transient CSF pleocytosis in 30-70%  Immune complex hepatitis or nephritis  Treatment—Same as primary syphilis unless CNS or ocular disease present, in which case treatment for neurosyphilis given

66 Latent Syphilis  Clinically quiescent phase after disappearance of secondary lesions  Early latent syphilis—first year after primary infection  May relapse to secondary syphilis if undiagnosed or inadequately treated  90% of relapses occur within first year after infection  Relapse is almost always accompanied by rising titer  Late latent syphilis—noninfectious; over 1 year  No clinical manifestations; only significant labs are positive serologic tests  Can last from months to a lifetime

67 Latent Syphilis  Early latent syphilis treatment—same as primary syphilis unless CNS disease present  Late latent syphilis treatment—Table 34-3  If CNS involvement, perform LP and start neurosyphilis treatment of positive  Repeat nontreponemal serologic tests at 6, 12, 24 mo  HIV screen, LP, and retreat if:  titers increase 4x  initially high titers fail to decrease 4x by 12-24 mo  signs and symptoms consistent with syphilis develop

68 Tertiary Syphilis  May occur at any time after secondary syphilis  Late lesions – possible delayed hypersensitivity reaction  Localized gummatous reaction  Diffuse inflammation (usually of CNS and large arteries  Gummas may involve any area or organ of the body  Most common types of involvement—skin, mucous membranes, skeletal system, eyes, respiratory system, GI system, cardiovascular system, nervous system

69 Tertiary Syphilis  Skin—two types of lesions  multiple nodular lesions that eventually ulcerate  solitary gummas that start as painless subcutaneous nodules and then enlarge, attach to skin and ulcerate  Mucous membranes—nodular gummas or leukoplakia  Skeleton—destructive—periostitis, osteitis, arthritis  Eyes—gummatous irits, chorioretinitis, optic atrophy, cranial nerve palsies  Respiratory system—gummatous infiltrates into larynx, trachea, and pulmonary parenchyma

70 Tertiary Syphilis  Gastrointestinal—benign, asymptomatic hepar lobatum  may have cirrhotic syndrome  Gastric involvement—diffuse infiltration or focal lesions  Cardiovascular—10-15% of late syphilis lesions; usually starts as arteritis in supracardiac aorta and progresses to:  Narrowing of coronary ostia  Scarring of aortic valves  Weakness of wall of aorta  Neurological—multiple possible manifestations  Asymptomatic  meningovascular syphilis  tabes dorsalis  general paresis

71 For your reading…  Neurosyphilis  Syphilis in HIV patients  Syphilis in pregnancy  Congenital syphilis  When to Refer/Admit

72 Lyme Disease  Most common tick-borne disease in US and Europe  Vectors and animal reservoirs vary with area  Ticks must generally feed for 24-36 hours or more to transmit infections  Most cases are in spring and summer months

73 Lyme Disease—Early Localized  Erythema migrans  1 week after bite (3-30 d)  Expands over several days  May have more homogenous appearance or central intensification  10-20% of pts have atypical lesions or do not notice lesion  Viral-like illness  Myalgias, arthralgias, headache, fatigue  +/- fever  Resolves in 3-4 weeks

74 Lyme Disease—Early Disseminated  Up to 50-60% of pts with erythema migrans—bacteremic  Secondary skin lesions in 50% of patients  Appear in days-weeks and resemble primary lesion  Malaise, fatigue, fever, headache, cervicalgia, body aches  Pathogen may sequester itself and cause focal symptoms  Cardiac (4-10%)  Neurologic (10-15%)

75 Lyme Disease—Late Persistent  Months to years after initial infection  Musculoskeletal, neurologic, and skin disease  Classic – monarticular or oligarticular arthritis  May be quite swollen but usually less painful than bacterial septic arthritis  Self-limited but can have multiple recurrences  Nervous system involvement is usually rare  subacute encephalopathy (in US) or more severe encephalomyelitis (in Europe)  Peripheral—intermittent paresthesias or radiculopathy  Cutaneous—acrodermatitis chronicum atrophicans  Bluish-red discoloration of distal extremity with swelling

76 Lyme Disease—Diagnosis  Person with exposure to tick habitat with either  Erythema migrans diagnosed by physician  At least one late manifestation and laboratory confirmation  Nonspecific abnormalities—especially early  Elevated sed rate > 20 mm/hr (50%)  Mildly abnormal LFTs (30%)  Mild anemia or microscopic hematuria – 10% or less  Serologic tests—two-test approach recommended  ELISA test - confirm with Western immunoblot assay for IgM/IgG  Suspected early disease—acute and convalescent titers

77 Lyme Disease—Prevention  No human vaccine available  Preventive measures  Prophylactic antibiotic guidelines—in text  Treatment—Table 34-4

78 Lyme Disease  Most patients respond to appropriate therapy with prompt resolution of symptoms within 4 weeks  Long term outcome generally favorable  Joint pain, memory impairment, decreased function due to pain are common subjective complaints  Refer—infectious disease specialist if atypical or prolonged  Admit—IV antibiotics  symptomatic CNS or cardiac disease  Second-degree AV block or third-degree AV block  First-degree AV block with PR interval 300 milliseconds or more

79 Rocky Mountain Spotted Fever  Most cases occur outside Rocky Mountain area  56%--North Carolina, South Carolina, Tennessee, Oklahoma, Arkansas  Endemic in Central and South America  Causative pathogen – Rickettsia rickettsii  Gram negative aerobic bacterium  Transmitted by tick bite  Increasing incidense in US

80 Rocky Mountain Spotted Fever  Most serious rickettsial disease  Severe multiorgan dysfunction and  Symptoms appear 2-14 days after bite  Characteristic rash—days 2-6 of fever  Initially on wrists and ankles  Spreads to arms, legs, and trunk for 2-3 days  Involves palms and soles  Facial flushing, conjunctival injection, hard palate lesions  10% of cases—no or minimal rash


82 Rocky Mountain Spotted Fever  Labs—thrombocytopenia, hyponatremia, elevated AST/ALT, hyperbilirubinemia  CSF—hypoglycorrhachia, mild pleiocytosis  Severe cases—DIC  Diagnosis—immunohistologic (including PCR) studies of skin biopsies  Must do as soon as skin lesions are apparent and before antibiotics are started  Serologic tests confirm diagnosis – not valid in early disease

83 Rocky Mountain Spotted Fever  Treatment—doxycycline (chloramphenicol if pregnant)  Fever usually ends 48-72 hrs  Continue medication for at least 3 d after afebrile  Mortality rate 3-5% on average  as high as 70% in untreated elderly  Myocarditis is leading cause of death  Protective clothing, tick-repellent chemicals  No prophylactic therapy

84 Mycobacterial Diseases – Tuberculosis – Atypical Mycobacterial Disease

85 Tuberculosis  One of the world’s most widespread and deadly illnesses  20-43% of the world’s population  15 million patients in US  Disproportionately high among malnourished, homeless, and residents of overcrowded and substandard housing  More common in HIV positive patients

86 Tuberculosis  Infection by inhaling airborne droplet nuclei with viable Mycobacterium tuberculosis organisms  Tubercule bacilli are ingested by alveolar macrophages  Infection if the pathogen escapes macrophage microbicidal activity  If infection occurs, there is usually lymphatic and hematogenous dissemination before an adequate immune response is mounted

87 Tuberculosis  Primary tuberculosis—dissemination of M tuberculosis with usually no clinical signs  Progressive primary tuberculosis—in 5% of patients; inadequate immune response to contain initial infection  Latent tuberculosis—cannot transmit organism but are susceptible to reactivation of disease if immune system becomes impaired  Resistance is becoming more prevalent—15% of US cases are resistant to one or more antituberculous drugs  MDRTB outbreaks have been associated with 70-90% mortality rates and 4-16 week survival rates

88 Pulmonary Tuberculosis  Slowly progressive symptoms of malaise, anorexia, weight loss, fever, and night sweats  Chronic cough is most common pulmonary symptom  Appear chronically ill and malnourished  Chest examination may be normal or may show classic findings such as posttussive apical rales

89 Pulmonary Tuberculosis  Definitive diagnosis—recovery of pathogen from cultures or identification by DNA/RNA amplification techniques  Cultures may require 12 weeks to grow  Fiberoptic bronchoscopy, bronchial washings and transbronchial biopsies can help diagnosis in patients with suspicious symptoms but negative sputum smears  Needle biopsies of pleura—granulomatous inflammation in approximately 65% of patients

90 Pulmonary Tuberculosis  CXR—small homogenous infiltrates, hilar and paratracheal lymphadenopathy, segmental atelectasis  Pleural effusion may be sole abnormality  Cavitation—if progressive primary  Ghon and Ranke complexes in some patients  Reactivation TB—usually in apical or posterior segments of upper lobes, but other sites in up to 30%  Miliary pattern in dissemination  HIV patients—early findings resemble non-HIV patients; later disease tends toward atypical findings





95 For Your Reading…  Tuberculin Skin Testing  Be familiar with table 9-15!  Have a good idea of what is a positive test and what isn’t for common patient populations  Treatment  Know basic principles of treatment  Review table 9-16 – look at names of drugs, general monitoring tests you would order for a patient on anti-TB therapy, and which drugs (if any) have significant side effects/interactions  What would be a good maintenance regimen for latent TB?

96 Atypical Mycobacterial Diseases  10% of mycobacterial infections  Among the most common opportunistic infections in HIV patients

97 Atypical Mycobacteria  Pulmonary -- MAC causes a chronic, slowly progressive pulmonary infection resembling TB in immunocompetent pts; M kansasii can also produce clinical disease resembling TB but which progresses more slowly  Lymphadenitis – in adults usually due to TB; in children, most are due to nontuberculous mycobacteria  Skin/Soft Tissue—abscesses, septic arthritis, osteomyelitis  Disseminated—MAC can range from asymptomatic colonization to a spectrum of diseases  Treatment—rifabutin, azithromycin, clarithromycin, ethambutol—combination of 2 or more agents  Prophylaxis—for all HIV patients with CD4 counts 50 or less

98 Questions?

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