Transcript Lyme Disease

Clin Med II
Infectious Disease
Lecture 1 – Fungal Diseases
– Spirochetal Diseases
– Mycobacterial Diseases
Fungal Diseases
– Candidiasis
– Cryptococcosis
– Histoplasmosis
– Pneumocystis
(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.
Candiasis
 Common normal flora
 Can become opportunistic
pathogen
 Numerous risk factors
 If no underlying cause
found, persistent candidiasis
 possible HIV infection
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
Cutaneous Candiasis
Cutaneous Candiasis
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
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
Oral Candidiasis
 Usually present with
mouth and/or throat
discomfort
 Creamy white, curd-like
patches overlying
erythematous mucosa
 +/- angular cheilitis
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
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
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
Mucosal Candidiasis
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
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
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
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
Candidal Endocarditis
Candidal Endocarditis
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
Cryptococcus
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.
 http://thorax.bmj.com/content/53/7/554.full
Cryptococcosis
Cryptococcosis
 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
Cryptococcosis
Cryptococcosis
Cryptococcosis
Cryptococcosis
 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
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
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
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
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
Histoplasmosis
Histoplasmosis
 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
Histoplasmosis
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
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
Subacute/Chronic Progressive
Pulmonary Histoplasmosis
 Older patients
 Various lesions
on radiographs
 Heals with
fibrosis
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
Complications of Pulmonary
Histoplasmosis
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
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
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
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
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
Pneumocystosis
Pneumocystosis
 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%
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
Spirochetal Diseases
– Lyme Disease
– Syphilis
– Rocky Mountain Spotted Fever
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
Primary Syphilis
 Stage of Invasion
 Typical lesion is changre
at sites of inoculation
 Initial small erosion 1090 days after
inoculation; develops
into painless superficial
ulcer with clean base and
firm, indurated margins
 Regional lymph node
enlargement
 Heals without treatment;
may scar
Primary Syphilis
 Darkfield microscopy and
immunofluorescent
staining can help
visualize pathogen
 Read—Nontreponemal
antigen tests vs.
Treponemal antibody
tests
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
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
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—1st prenatal visit
 Repeat in 3rd trimester if high risk
 Patients who have other STDs
 Patients who have known or suspected contact with
patients who have syphilis
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
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
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
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
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
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
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
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
For your reading…
 Neurosyphilis
 Syphilis in HIV patients
 Syphilis in pregnancy
 Congenital syphilis
 When to Refer/Admit
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
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
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%)
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
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
Lyme Disease—Prevention
 No human vaccine
available
 Preventive measures
 Prophylactic antibiotic
guidelines—in text
 Treatment—Table 34-4
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
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
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
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
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
Mycobacterial Diseases
– Tuberculosis
– Atypical Mycobacterial Disease
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
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
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
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
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
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
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?
Atypical Mycobacterial
Diseases
 10% of mycobacterial
infections
 Among the most
common opportunistic
infections in HIV patients
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
Questions?