Chapter 19 Rickettsiae - PowerPoint by gabyion

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									          Chapter 19: Rickettsiae
•   Family: Rickettsiaceae
•   Genera: Rickesttsia
•   5 categories of Rickettsial disease
    1.   Typhus
    2.   Scrub Typhus
    3.   Trench Fever
    4.   Spotted Fever
    5.   Q Fever
• General Characteristics
  – Small obligate intracellular parasites
     • Grow ONLY inside living host cells
  – Ultrastructure resembles Gram-negative bacilli
  – Human transmission via arthropod vector-borne
     • Rodents → arthropods (lice, ticks, fleas, mites) → humans &
       rodents (continues life cylce)
  – Rickettsial diseases are generalized infections, w/
    RASH usually being the prominent feature
• Structural features simliar to typicla
  prokaryotic bacteria
• Small, rodlike or coccobacillary shape
• Typical double-layered, Gram-negative
  cell wall.
• Stain poorly in Laboratory; best visualized
  under light microscope w/ either Giemsa
  or Macchiavello stain
•    Pathogenesis
    1.   Insect vectors for human transmission: arthropods such as
         fleas, ticks, mites, or lice
    2.   Rodents, humans, or arthropods: all can serve as reservoirs
    3.   Multiply in salivary glands of ticks/mice & gut of lice/fleas
    4.   Affinity for endothelial cells of small blood vessels of
         circulatory system – Bloodstream affinity in humans
    5.   Causes obstruction of blood flow → tissue necrosis
    6.   ***Site of Bite = Eschar (encrusted ulcer) → necrotic tissue:
         –   Site of bite = point @ which Rickettsia enters the body – becomes
    7.   Following bite, organisms taken into body by “phagocytosis-
         like” process
    8.   Organisms multiply in both nucleus & cytoplasm of host cell
    9.   Host cells die, Rickettsia spread thru-out body via bloodstream
         or lymphatics
         –   Focal thrombi (blood clots) form in organs incl. skin
         –   Small hemorrhages & hemodynamic disturbances create sx’s of illness
• Pathogenesis cont’d:
  – Except for agents of Trench Fever & Epidemic
    Typhus, Rickettsia are zoonotic disease agents for
    which humans are accidental hosts
  – After bite, predilection for cells that line small blood
    vessels (endothelial cells); bacterial multiply and
    spread along the blood vessels
  – s/sx’s result from inflammation and swelling of
    small blood vesssels
     • Blockage +/or reduced blood flow, come leakage of blood
       into surrounding tissues => produces spots and rashes seen
       w/ most Rickettsial diseases
•    Clinical
    1.   Rock Mountain Spotted Fever
         –      Etiological agent = Rickettsia ricketsii
         –      m/c rickettsial disease in US, especially found in South Central states &
                along Mid-Atlantic coast (high incidence in N. & S. Carolina); also found in
         –      Reservoir = rodents (mice, rats)
         –      Vector = Tick Bite
                   Rickettsia in saliva of tick, transfer to humans after bite
                   Human infection initiated by bite of infected wood or dog tick
         –      Highest frequency of disease during warmer months, parallels tick activity
         –      Sx’s develop ~7 days after tick bite
                   High fever & malaise, then rash – initially macular, but becomes petechial
                    or hemorrhagic
                   Rash starts on extremities, esp. palms and soles; then rapid spread to entire
                   Fever, rash, NO eschar >>> DEATH (hypotension, convulsions, cardiac arrest)
         –      Untreated cases – vascular disturbances w/ myocardial or renal failure
         –      Epidemiology: children <15 yoa; peak = 5-9 yrs.
•   Clinical
    2. Typhus Group
       Louseborne (epidemic) Typhus
      –   Etiological agent = Rickettsia prowazekii
      –   Transmission: person-to-person by infected human body louse
          that excretes organisms in feces
          •    Introduction of pathogen form lice facilitated by scratching the louse
          •    Ex. Infected human → louse bites human and becomes infected;
               sheds Rickettsia in feces → bites another human → feces on skin,
               scratching forces Rickettsia into wound → 2nd human now becomes
          •    ***Disease is NOT maintained in the louse population; lice serve as
               VECTORS, transmitting organism to humans
      –   Epidemics occur under conditions of displacement of people,
          crowding & poor sanitation
      –   Sx’s: high fever, chills, severe HA; rash possible
      –   Duration of Disease: ~2 weeks; more severe in ederly
      –   Complications: CNS (neurological involvement) dysfunction and
•       Clinical
    –     Note: Brill-Zinsser Disease (recrudescent typhus): mild
          form of typhus – occurs in pts who previously recovered from
          1° infection; is latent infection, m/likely maintained in
          reticuloendothelial system; “carrier form”
    2. Typhus Group
             Endemic (Murine) Typhus Fever
          –   Etiological agent = Rickettsia typhi
          –   Reservoir = Rodents (Rats)
          –   Vector = flea feces or bite
          –   Transmission: thru skin, respiratory tract, conjunctiva
          –   Milder form of Epidemic Typhus
          –   Natural infection is found in rats/mice and sporadically
              transmitted to humans; no human-to-human transfer
          –   rare in US d/t good rodent control
•   Clinical
    3. Scrub Typhus Group
      –   Etiological agent: Rickettsia tsutsugamushi
      –   Reservoir = rodents
      –   Vector = mite bite
      –   Typically seen in SE Asia and S. Pacific region
      –   Clinical: maculopapular rash, Eschar; untreated
          cases can lead to DEATH
•   Distiguishing Characterisitics
    –   Grows in cytoplasmic vacuoles
    –   Stimulated by low pH of phagolysosome, but
        resistant to host degradative enzymes
    –   Extremely resistant to heat and drying; persists
        outside host for long periods
    –   Causes disease in livestock (cattle, etc.)
    –   NOT transmitted to humans by arthropods; but
        organism has been recovered from ticks.
    –   Human infection usually follows inhalation of
        infected dust in barnyards, slaughterhouses, etc
• Clinical
   – Q Fever group
       •   Etiological agent = Coxiella burnetti
       •   Reservoir = cattle, sheep, rodents, ticks
       •   Vector = contaminated aerosol (i.e., if a cow sneezes!)
       •   C. burnetti enters the body via mucous membranes, abrasions &
           GIT via consumption of milk for infected animals
             – Zoonosis b/c animal direclty transmits the organism to humans
             – Reproduction w/in RT and dissemination is possible (untreated cases)
             – Sx’s: high fever, cough, pneumonia, hepatitis – all self-limiting usually;
               rarely – endocarditis (scarring of hrt. valves) and scarring of liver
             – Classic Q fever is an interstitial pneumonitis, complicated by
               hepatitis, myocarditis, or encephalitis
       • Laboratory Dx: Serological assays
       • Treatment: Antimicrobials
• Laboratory Identification/Dx
   – Serologic Procedures ONLY
        • Demonstration of rickettsia-specific Ab response during the course of the
        • ↑ in specific Ab’s between acute & convalescent stages of infection
   – NO culture – dangerous & difficult
        • Do not want to handle it in lab setting!
   – Most diagnoses made by pt. hx & clinical signs
• Treatment & Prevention
   –   Antimicrobials effective in eradication
   –   Early tx is absolutely necessary
   –   No vaccines
   –   Person cleanliness/hygiene
   –   Eliminate/reduce an. reservoir & avoid/reduce contact w/ arthropod
        • Delousing, rodent-proofing buildings, removing brush in tick- or mite-infested
        • Wearing proper clothing, using tick repellants
        • Frequent inspection of body for lice & subsequent removal
•       Similar to Rickettsia; but these organisms parasitize
        leukocytes & grow in cytoplasmic vacuoles –
        formation of inclusion known as morulae
•       Clinical Disease = Ehrlichosis
    –     Reservoir = rodents (mice, rats)
    –     Vector = Ticks
    –     Etiological agents
          1.   E. chaffeensis: causes Human Monocytic Ehrlichiosis (HME)
          2.   Anaplasma phagocytophilum: causes Human Granulocytic
               Anaplasmosis (HGA)
    –     Clinical features: acute fever, myalgia; moderate-to-severe
          leukopenia and thrombocytopenia; NO rash, usually
    –     Dx: Ab assays, PCR
    –     Treatment: Antimicrobial
        Trench Fever Group
• NOT intracellular parasite; can be cultured
  on artificial media
• Etiological agent = Rochalimaea
• Reservoir = humans
• Vector = body louse (lice)
• WWW I & II; virtually none today
          Chapter 20: Fungi
• Mycology: the study of fungi
  – Fungi are widespread in nature; ~200,000
    species identified
  – Most fungi involved in decomposition of
    organic matter & play important role in
    recycling organic compounds in nature
  – Fungi are Eukaryotic organisms
    • Unicellular morphology (=Yeast) or
      Mulitcellular morphology (= Mold)
• Yeasts (Unicellular morphology)
   – Single, oval or spherical fungal cell
   – Reproduction: Asexual by budding
   – Budding
       • Division of nucleus
       • Passage of one nucleus to a bud the “balloons” out from the mother
       • Formation of wall between the bud and mother cell
       • Daughter cell = bud or blastospore
       • Daughter cell initially smaller than mother cell; but, it will increase in
         size & produce own buds
• Molds (Filamentous morphology)
   – Multicellular – filamentous or tubular structures
   – Reproduction: asexual or sexual (main discriminating feature)
• Growth of mold
  – Germination of Condium (=asexual reproductive unit in fungi) –
    send out a filament that grows by elongation @ its tip
  – Hyphae – elongated filament; the basic structure of growing
  – Mycelium – multiple branches of hypae; mass of hypae
  – Many nuclei located w/in each hypae
  – Formation of Septae = “cross-walls” w/in hypae
  – Conidia – terminal ends of hyphae; “seeds” for new colonies;
    molds reproduce by developing conidia on the hyphae
• Sexual reproduction
  – 2 reproductive bodies connect & haploid cells fuse to form
    diploid cells (spores) – meiosis
  – Resulting diploid cells become Spores = reproductive elements
    formed from sexual reproduction
  – Rare among the human fungal pathogens
•       Dimorphic Fungi
    –     Dimorphism: the property of having 2
          morphological shapes; dimorphic fungi have
          capability of 2 distinct forms – dependent on
         •   Temperature Dependent
             1. Yeast form: 37°C
             2. Mold or mycelial form: 25°C
•       General characteristics
    – Cell wall: rigid & thick; NO PG
    – 1° component is presence of sterol in cell wall
    – No locomotion: non-motile
•    Distinguishing Morphological Characteristics
    –     Size, presence of a capsule, cell wall thickness, spores or
          conidia production
• Growth Conditions
  –   Molds: aerobic
  –   Yeasts: facultative anaerobes
  –   Acid pH (4.0 → 6.0)
  –   Selective Laboratory Media
       • Sabouraud’s Dextrose Agar (SDA) – low pH
       • Dermatophyte Test Media (DTM) – turns red in presence of all
       • Birdseed Agar – specific for ID of Cryptococcus neoformans ( agar
         turns brown); all other Crytpococcus spp – turn it white
  – Minimal Media
       • Corn Meal Agar (ID of spore formation: production of terminal
  – Slide cultures – undisturbed growth
  – Colonial Morphology
       • Molds – dry, cotton-like masses
       • Yeast – moist, opaque, creamy colonies
         Mycoses (Fungal Diseases)
1.       Superficial Mycoses
     •     “surface infection”
     •     Fungal diseases that grow on surface of skin & nails
2.       Cutaneous Mycoses or Dermatomycoses
     •     Fungal infections of keratinous structures – outer layers of
           skin, nails, in hair shafts
3.       Subcutaneous Mycoses
     •     Infections that penetrate below the skin & involve the
           subcutaneous CT and bone tissue
4.       Systemic or Deep Mycoses
     •     Infections of internal organs – from disseminated disease
5.       Opportunistic Mycoses
     •     Infections in compromised or immunosuppressed
• ONLY contagious fungal infection/disease in
  humans; not associated w/ death, just
  uncomfortable symptoms and characteristic
• Dermatophytes – fungi that invade keratinized
  & cutaneous areas of the body
  – Nails, hair and skin
• 3 Major Genera
  – Microsporum
  – Tichophyton = m/c dermatophyte fungus
  – Epidermophyton
•       Mode of Infection
    –     Hyphae grows into keratinized tissues of epidermis, into hair
          shaft, or into finger/toe nail
    –     Growth outward from infection site in concentric circles
    –     Enzyme production – keratinase, elastase and collagenase
•       Clinical Infections
    1.    Tinea capitis (ringworm of scalp) – Trichophyton &
          Microsporum spp.
          –   Initial Sx: inflammation & itching of the scalp
          –   Mode of Infection: hypae spread into keratinized areas of scalp &
              hair follicle → fungal growth weakens the hair → breakage @
              shaft → ALOPECIA (hair loss): localized & spotty
          –   Associated mostly w/ children (high transmission)
•    Clinical Infection
    2.   Tinea Barbae (ringworm of the beard)
         –   Infection site – bearded areas
         –   Superficial lesion – scaly
         –   Severe infection – development of deep pustules
         –   Result – permanent hair loss
    3.   Tinea pedis (ringworm of the foot, “Athlete’s Foot”) – m/c in
         adolescents & adults
         –   Trichophyton rubrum, Trichophyton mentagrophytes,
             Epidermophyton floccosum
         –   Sx’s – foot lesions
         –   Mode of infection – growth between toes of small fluid-filled
             vesicles → vesicles rupture → development of shallow lesion that
             itch; may become infected with bacterial (2° bacterial infection)
         –   Predisposing conditions – public showers, swimming pools,
             failure to dry between toes.
•    Clinical Infections
    4.   Tinea curis (ringworm of the groin, “Jock Itch”)
         –   E. floccosom & T. rubrum
         –   Sx’s – lesions in groin or perianal area → red, scaly, itchy and
             often dry
         –   Predisposing factors – moisture in the groin area; wet bathing
             suits, athletic supporter, tight fitting pants/slacks and obesity
    5.   Tinea corporis (ringworm of the body)
         –   E. floccosum, spp. of Trichophyton & Microsporum
         –   Infection site – non-hairy areas of the body
         –   Sx’s – lesions are reddened, scaly, w/ papular eruptions
    6.   Tinea unguium (ringwom of nails - onychomycosis)
         –   T. rubrum
         –   Infection sites – fingernails and toenails
         –   Initial Sx’s – superficial white patches on nail beds: puffy & chalky
         –   Later Sx’s – thickening of the nail, accumulation of cheesy debris,
             cracking and discoloration of the nail
• Diagnosis
  – Clinical signs and symptoms
  – Microscopic ID from tissue scraping samples: presence of
     • Tissue scraping + 10% KOH (heated, then stain added) → presence
       of septate hyphae visible under microscope
  – Macroscopic ID
     • Culture: Dermatophyt Test Media (DTM) – turns RED
     • Culture: Sabouraud’s Dextrose Agar (SDA)
• Treatment
  – Non-Rx: salves/ointments – for symptomatic relief
  – Good hygiene
  – Oral antibiotic therapy
  – Topical antifungal agent
  Note: re-infection may occur over & over => not good host immune
             Subcutaneous Mycoses
•    Fungal source = normal inhabitants of soil or organic
•    Introduction to host – wound or abrasions of skin
•    Deeper infection – penetration to below skin
•     Clinical Infections
    1.   Sporotrichosis (“Rose Gardner’s Disease”)
         –    Causative agent = Sporothrix schenckii
         –    Mode of infection – traumatic implantation of fungus into skin →
              painless papule @ inoculation site → enlargement to form
              ulcerated lesion → then possible spread to regional lymph nodes
              = Lymphocutaneous sporotrichosis
    2.   Lymphocutaneous Sporotrichosis
         –    Mode of infection – fungus form multiple nodules after being
              spread by draining lymph node channels → nodules may ulcerate
              → untreated lesions last for years
         –    Occupational Risk Groups = horticulturists, foresters,
              gardeners, farmers & basket weavers
              Systemic Mycosis
• “True pathogens” – infect normal, healthy individuals
• “Opportunisitic pathogens” – infect debilitated +/or
  immunocompromised individuals
• Mode of Infection – inhalation of spores → lower
  respiratory tract → germinate into yeast → asymptomatic
  or 1° pulmonary infection that parallels TB →
  disseminated to other organs d/t compromised defense
• NO person-to-person transmission; only airborne route
  to humans from fungal spores
   – Fungi growing in soil or on an. droppings produce conidia that be
     aerosolized and carried by air-borne route to humans
              Systemic Mycosis
•   Clinical Diseases
    1. Coccidioidomycosis
      –   Chronic, necrotizing mycotic infection of the lungs;
          resembles TB pathologically
      –   Begins as a bronchopneumonia w/ its inflammatory
      –   Disseminated to many site in immunocompromised pt’s:
          skin, bones, meninges, liver, spleen
      –   Causative agent: Coccidiodes immitis
          •   Dimorphic fungus that grows in soil of SW US
          •   Spore = Arthrospores – inhaled into alveoli and terminal
              bronchi, where they enlarge into “spherules”
          •   Spherules fill w/ endospored, which are released to form more
          •   In Arizona – 50% chance (after 10 yrs) person w/ (+) serology
              to this b/c of exposure, NOT necessarily the disease
                  Systemic Mycosis
•    Clinical Diseases
    1.   Coccidioidomycosis
         –   Epidemiology
                 SW US, particularly San Joaquin and Sacramento Valley of
                  California, areas around Tucson and Phoenix in Arizona
                 High incidence of infection & disease may follow dust storm
                 Coccidioidomycosis = Valley Fever = San Joaquin Valley Fever =
                  Desert Rheumatism
         –   Pathogenesis
                 Inhalation of arthroconidia leads to 1° infection
                   •   Asymptomatic in 60% individuals
                   •   40%: self-limiting influenza-like illness – fever, malaise, cough,
                       arthralgia, HA
         –   Laboratory DX
             1.   Culture: specimen from sputum; exudate from cutaneous lesions;
                  CSF, blood, urine, tissue biopsies
             2.   Serology – IgM Ab detection w/ latex agglutination
             3.   Coccidioidin Skin Test (+)
             4.   Chest X-Ray analysis – hilar lymphadenopathy along w/
                  pulmonary infiltrates, pneumonia, pleural effusions or nodules
                 Systemic Mycosis
•    Clinical Diseases
    2.   Histoplamosis
         –   m/c fungal disease in US
         –   Acute, necrotizing, caseous granuloma of the lungs
         –   Causative agent = Histoplasma capsulatum
                Dimorphic fungus found in nature
                Multiplies extensively in areas where bird feces accumulate
         –   Fungus grows in soil → formation of conidia → airborne →
             inhalation into the lungs → germination into yeast-like cells →
             engulfed by alveolar macrophages
         –   Infection – acute, but benign and self-limiting; or chronic,
             progressive and fatal
                Usu. Self-limiting flu-like syndrome (fever, chills, myalgia, HA, non-
                 productive cough
         –   Dissemination = rare; but can occur – to reticuloendothelial
             tissues (liver, spleen, BM lymph nodes)
              Systemic Mycosis
•   Clinical Diseases
    2. Hitoplasmosis
      –   Laboratory Dx
           Culture – specimens include sputum, urine, scrapings from
            superficial lesions, BM aspirates
           Microscopic examination of fungus in macrophages
           Serology – Tests for Ab’s to Histoplasmin Ag or yeast cells
           Skin Test – Histoplasmin (+)
      –   Epidemiology
           most prevalent in Ohio & Mississippi River Valleys,
            including Central and Eastern States
           KC = high risk area
           Reservoir = Soils laden w/ bird, chicken, or bat droppings =
            rich sources of the fungus (natural habitat)
              Systemic Mycosis
•   Clinical Diseases
    3. Blastomycosis
      –   Chronic granulomatous and suppurative disease of the
          lungs, resulting in small areas of consolidation
      –   Causative agent = Blastomyces dermatitidis
      –   Fungus produces microconidia in soil, which become
          airborne and inhaled in lungs
           Germination into yeast cells
           Dissemination is rare, but can occur – skin, bone, GU tract
      –   M/c in South Central and South Eastern US
      –   M/c clinical presentation = pulmonary infiltrate w/ fever,
          malaise, cough, myalgia, night sweats
      Opportunistic Mycoses
• Endogenous type infection – caused by
  normal flora of respiratory tract, mouth,
  intestinal tract and vagina
• Opportunistic Infection
  – Overgrowth of normal flora → inflammation of
    epithelial surfaces (m/c = oral cavity and
    vagina) → dissemination to internal organs
             Opportunistic Mycoses
•    Clinical Diseases
    1.   Cryptococcosis
         –   1° disease of lungs w/ granulomas and consolidation
         –   Rapidly spreads to the meninges and brain, causing
         –   Etiological agent = Cryptococcus neoformans
                Only systemic fungus that is NOT dimorphic
                Only true yeast unicellular pathogen of humans
         –   Epidemiology
                Occurs worldwide in nature; found in very large #’s in dry pigeon
                Usually associated w/ immunosuppression – AIDS, malignancy
                2nd m/c fungal dis in AIDS pts (after candidiasis)
                Reservoir = decomposing plant materials (soil) w/ high N content
                 from pigeon feces
         –   Pathogenesis
                Inhalation of yeast cells (encapsulated, dry, easily aerosolized)
                Influenza-like illness follows
                Immunosupressed: yeast cells multiply and disseminated to CNS
                  •    YEAST CELLS FOUND W/IN CSF
             Opportunistic Mycoses
•    Clinical Diseases
    1.   Cryptococcus
         –   S/sx’s: MAJOR clinical manifestation = chronic meningitis w/
             spontaneous remissions and exacerbations
         –   Pt presentation
                HA
                Stiff neck
                Disorientation
                Lesions in skin, lungs
         –   Laboratory Dx
                CSF pressure and protein [ ] ↑
                WBC count ↑
                Glucose [ ] normal or low
         –   Diagnosis
                Specimens from CSF, sputum, blood, urine, exudates
                Culture
                Serology
           Opportunistic Mycoses
•    Clinical Diseases
    2. Candidiasis (candidiosis)
       –   Causative agent = Candida albicans
            Normal flora of skin, vagina, and intestines
            Considered a yeast, but is Dimorphic (forms a true mycelium)
       –   Cutaneous Infections
            arise d/t host’s condition – diabetes, immunological
             deficiencies, exposure of skin to moist environment
            Mode of infection
              1. Adherence to epithelial surfaces
              2. Fungal proliferation
              3. Invasion of epithelial tissue
             Opportunistic Mycoses
•    Cutaneous Infection w/ C. ablicans
    1.   Thrush or Oral Candidiasis = Most Common Candidiasis
         –  Symptomatic appearance: white, adherent patches
            (pseudomembranes) attach to epithelial membranes of tongue,
            gums, cheeks, or throat – FUNGAL MAT formation
         – Pseudomembrane composition = yeast, hyphae, epithelial debris
         – Increased susceptibility: Newborns
         – Transmission: Vertical - Mother→Child
    2.    Vaginal Candidiasis = m/c form of vaginal infection
         – Sx’s: yellow to white milky discharge, inflammation, painful
            ulcerations & itching
         – Candidal overgrowth – related to increased glucose content of
            vaginal secretions
         – Assoc’d w/ - diabetic ♀, pregnant ♀, broad spectrum antibiotic tx
        Opportunistic Mycoses
•   Cutaneous Infection w/ C. ablicans
    3. Esophageal Candidiasis
      – Complication of AIDS patients
      – Sx’s: painful bleeding, ulcerations, nausea,
    4. General Candidiasis Infections
      – Infections of epidermal tissue – folds of skin on
        obese people (usual sites =upper legs,
        underarms); tissue that remains wet
        (dishwashers); skin covered by wet diapers
        (diaper rash)
       Opportunistic Mycoses
• Disseminated infection w/ C. albicans
  – Cutaneous infection → mutisystem disease
  – Iatrogenic – use of catheters of prosthetic devices
• Diagnosis
  – Clinical symptoms
  – Microscopic examination
  – Macroscopic examination – culture
     • SDA (white- to cream-colored colny, pasty w/ a yeasty odor
     • Corn Meal Agar – visualization of spores
• Treatment: Antifungals
             Opportunistic Mycoses
•    Clinical Diseases
    3.   Asperigellosis
         –   Causative agent = Aspergillus fumigatus
         –   Acute, invasive infection of lung – dissemination to brain, GIT,
             other organs
         –   Non-invasive lung infection gives rise to aspergilloma (Fungal
             Ball) – a mass of hyphal tissue that can form in lung cavities
             produced by other diseases, like TB
    4.   Pneumocystis Pneumonia
         –   Causative agent = Pneumocystis jiroveci
                                  Pneumocystis carnii
         –   Acute interstitial pneumonia w/ plasma cell infiltrates
         –   As disease progresses, pt. experiences weakness, dyspnea, and
             tachypnea leading to cyanosis; Death can result from
         –   m/c cause of DEATH in AIDS pts from Pneumocystis carinii

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