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Edit Comment Close Premium member Presentation Transcript OPPORTUNISTIC INFECTIONS IN IMMUNODEFICIENT PATIENTS : OPPORTUNISTIC INFECTIONS IN IMMUNODEFICIENT PATIENTSDEFINITION: DEFINITION IMMUNODEFICIENCY DISEASES ARE CONDITIONS WHERE THE DEFENSE MECHANISMS OF THE BODY ARE IMPAIRED LEADING TO REPEATED MICROBIAL INFECTIONS OF VARYING SEVERITYCLASSIFICATION OF IMMUNODEFICIENCY DISORDERS: CLASSIFICATION OF IMMUNODEFICIENCY DISORDERS B CELL DISORDERS T CELL DISORDERS B + T CELL DISORDERS COMPLEMENT DISORDERS DISORDERS OF PHAGOCYTOSISNORMAL BARRIERS TO INFECTION: NORMAL BARRIERS TO INFECTION TYPE OF DEFENSE SPECIFIC LESION CELLS INVOLVED ORGANISM DISEASE PHYSICAL BARRIER BREAKS IN SKIN SKIN EPITHELIAL CELLS STAPHYLOCOCCI/STREPTOCOCCI CELLULITUIS EMPTYING OF FLUID COLLECTIONS OCCLUSION OF ORIFICES LUMINAL EPITHELIAL CELLS GRAM NEGATIVE BACILLI OVERWHELMING BACTEREMIA LYMPHATIC DISEASE NODE DISSECTION LYMPH NODES STAPHYLOCOCCI/STREPTOCOCCI CELLULITISNORMAL BARRIERS TO INFECTION: NORMAL BARRIERS TO INFECTION TYPE OF DEFENSE SPECIFIC LESION CELLS INVOLVED ORGANISM DISEASE SPLENIC CLEARANCE OF ORGANISM SPLENECTOMY SPLENIC R.E CELLS S.PNEUMONIAE,H.INFLUENZAE SEPSIS PHAGOCYTOSIS LACK OF GRANULOCYTES GRANULOCYTES STAPHYLOCOCCI/STREPTOCOCCI BACTEREMIA HUMORAL IMMUNITY LACK OF ANTIBODY B CELLS S.PNEUMONIAE,H.INFLUENZAE PNEUMONIA CELLULAR IMMUNITY LACK OF T CELLS T CELLS & MACROPHAGES M.TUBERCULOSIS,LISTERIA T.BOPPORTUNISTIC INFECTIONS ASSOCIATED WITH A.I.D.S: OPPORTUNISTIC INFECTIONS ASSOCIATED WITH A.I.D.S PARASITIC P.CARINII PNEUMONIA TOXOPLASMOSIS CRYPTOSPORIDIOSIS ISOSPORIASIS GENERALISED STRONGYLOIDIASISOPPORTUNISTIC INFECTIONS ASSOCIATED WITH A.I.D.S: OPPORTUNISTIC INFECTIONS ASSOCIATED WITH A.I.D.S VIRAL CMV HERPES SIMPLEX PAPOVA ADENOOPPORTUNISTIC INFECTIONS ASSOCIATED WITH A.I.D.S: OPPORTUNISTIC INFECTIONS ASSOCIATED WITH A.I.D.S BACTERIAL MYCOBACTERIAL INFECTIONS LEGIONELLOSIS NOCARDIA & ACTINOMYCETES SALMONELLOSIS CAMPYLOBACTER INFECTIONOPPORTUNISTIC INFECTIONS ASSOCIATED WITH A.I.D.S: OPPORTUNISTIC INFECTIONS ASSOCIATED WITH A.I.D.S MYCOTIC CANDIDOSIS CRYPTOCOCCOSIS ASPERGILLOSIS HISTOPLASMOSISPNEUMOCYSTIS CARINII: PNEUMOCYSTIS CARINII One of the most common causes of infection. Initial AIDS defining illness Infection with p. carinii represent reactivation of latent infection PCP is most commonly seen amomgst those who have previous bout of infection & who have fewer than 200 CD4+ T cells.PNEUMOCYSTIS CARINII: PNEUMOCYSTIS CARINII This lung is as solid as liver because of Pneumocystis carinii pneumonia (PCP). There is diffuse consolidation. PCP is typical of immunocompromised patients, particularly those with AIDS.PNEUMOCYSTIS CARINII: PNEUMOCYSTIS CARINII The best way to make the diagnosis of Pneumocystis carinii pneumonia is to perform a Gomori methenamine silver (GMS) stain on the lung tissue or bronchoalveolar lavage (BAL) fluid. The cyst wall is stained, and the organisms appear as crushed ping-pong balls, or crescent shapes, or folded spheres, or flattened beach balls, or deflated tennis balls, or....PNEUMOCYSTIS CARINII: PNEUMOCYSTIS CARINII CLINICAL FEATURES : PNEUMONIA FEVER WITH NON PROD. COUGH RETROSTERNAL CHEST PAIN WHICH IS WORSE ON INSPIRATION XRAY= B/L CHEST INFILTRATESEXTRA PULMONARY MANIFESTATIONS OF PNEUMOCYSTIS CARINII: EXTRA PULMONARY MANIFESTATIONS OF PNEUMOCYSTIS CARINII Acute otitis media Retinitis Visceral cystic calcifications Necrotizing vasculitis Intestinal obstruction Lymphadenopathy Bone marrow involvement Ascites ThyroiditisLAB EVALUATION OF PNEUMOCYSTIS CARINII: LAB EVALUATION OF PNEUMOCYSTIS CARINII Mild leukocytosis For HIV patients, a WBC count of 4000-6000/uL may represent an elevation Serum LDH is often elevated Decline in PaO2 & increase in (a – A ) gradient. Definite diagnosis req. demonstration of trophozoites or cyst form in samples obtained from induced sputum or broncho alveolar lavage.TOXOPLASMOSIS: TOXOPLASMOSISTOXOPLASMOSIS: TOXOPLASMOSIS Toxoplasma gondii Intracellular parasite that infects various warm-blooded animals Infection from humans usually from ingestion of undercooked meat or exposure to cat feces Can infect any organ but most commonly infects the brain and eye Orrick, J.: Opportunistic Infections in HIV/AIDSTOXOPLASMOSIS: TOXOPLASMOSIS Clinical presentation Fever, headache, seizures, mental status changes Diagnosis Presumptive: CT Scan of head showing “ring-enhancing lesions” in patient with positive Toxoplasma IgG Definitive: brain biopsy required (rarely done) Orrick, J.: Opportunistic Infections in HIV/AIDSTOXOPLASMOSIS: TOXOPLASMOSIS This is a Toxoplasma abscess in the brain, which would appear as a ring-enhancing lesion with CT scan.TOXOPLASMOSIS: TOXOPLASMOSIS This is a Toxoplasma gondii pseudocyst in the myocardium of a patient with AIDS. Toxo is an opportunistic infection of immunocompromised adults. It may also be a congenital infectionTOXOPLASMOSIS: TOXOPLASMOSIS This is a Toxoplasma abscess in the brain, which would appear as a ring-enhancing lesion with CT scan.CT scan with contrast: CT scan with contrastCRYPTOSPORIDIOSIS: CRYPTOSPORIDIOSISCRYPTOSPORIDIOSIS: CRYPTOSPORIDIOSIS Cryptosporidiosis, Microsporidia, & Isospora belli are most common opportunistic protozoa that infect G.I.T Present in a variety of ways varying from self limited / intermittent diarrhea to severe life threatening diarrhea in severely immunocompromised patientsCRYPTOSPORIDIOSIS: CRYPTOSPORIDIOSIS CLINICAL FEATURES : Diarrhea Abdominal pain Nausea/Vomiting Biliary tract diseaseCRYPTOSPORIDIOSIS: CRYPTOSPORIDIOSIS The little blue organisms lined up along the brush border of the small intestinal epithelium are Cryptosporidia. This infection causes diarrhea in immunocompromised hosts.CRYPTOSPORIDIOSIS: CRYPTOSPORIDIOSIS Cryptosporidium infection is best diagnosed by stool exam. Three cysts are seen in the center with this acid fast stainCRYPTOSPORIDIOSIS: CRYPTOSPORIDIOSIS MICROSCOPIC: Intracellular but extracytoplasmic organism in parasitophorus vacuole. 4-5 uM oocyst with 4 naked sporozoites inside ( no sporocyst ). Mild to moderate villous atrophy , crypt dilation & lymphoplamacytic infiltrate. Jejunum usually most heavily infiltratedCRYPTOSPORIDIOSIS: CRYPTOSPORIDIOSIS DIAGNOSIS : Special stains : 1) modified Kinyoun acid fast stain on stool sample. 2) Looks like wrinkled tissue paper.ISOSPORA BELLI: ISOSPORA BELLI World wide G.I. Coccidian Endemic in some tropical/ sub tropical countries. Fecal - oral transmission of sporocysts.ISOSPORA BELLI: ISOSPORA BELLI CLINICAL FEATURES Acute mild to profuse non bloody, watery diarrhea. Resolves in 2 wks in immunocompetent persons. Lasts wks ,months or years in immunocompromised patients. Low grade peripheral eosinophillia.ISOSPORA BELLI: ISOSPORA BELLI MICROSCOPIC : 25 - 30 uM ellipsoid oocyst with 2 internal spherical sporocysts & 4 banana shaped sporozoites within each sporocyst. Small bowel villous atrophy. Crypt hyperplasia. Intraepithelial lymphocytes. Sub nuclear loose fitting parasitophorus vacuole.ISOSPORA BELLI: ISOSPORA BELLI SPECIAL STAINS : Modified kinyoun acid fast stain of stool specimen. Alcian blue added to H & E of biopsies ; Tissue Giemsa gives best contrast.STRONGOLYDES STERCOLALIS: STRONGOLYDES STERCOLALIS Smallest of intestinal nematodes. Geographic distribution similar to hookworm. Filariform larvae penetrate skin & follow trans-pulmonary route ; auto infection possible .STRONGOLYDES STERCOLALIS: STRONGOLYDES STERCOLALIS CLINICAL FEATURES : Intestinal infection only symptomatic with large worm loads. Peptic ulcer like pain aggravated by eating. Peripheral eosinophillia. Malabsorbtion. Fever,dyspnea,cough. Disseminated in immunosuppresed patients.STRONGOLYDES STERCOLALIS: STRONGOLYDES STERCOLALISSTRONGOLYDES STERCOLALIS: STRONGOLYDES STERCOLALIS MICROSCOPIC: Larvae has curved tail & is very similar to hookworm. But has shorter buccal cavity. Longer primitive genitalia. May see calcified worm fragments in histologic sections of colon.STRONGOLYDES STERCOLALIS: STRONGOLYDES STERCOLALIS DIAGNOSIS : Identification of 0.75 - 1.0 cm rhabditiform larvae. Prominent genital primordium in stool,duodenal aspirate or jejunal biopsy. Eggs usually not seen.STRONGYLOIDES STERCOLALIS FRAGMENTS OF WORM IN INTESTINAL MUCOSA: STRONGYLOIDES STERCOLALIS FRAGMENTS OF WORM IN INTESTINAL MUCOSASTRONGYLOIDES STERCOLALIS FRAGMENTS OF WORM IN INTESTINAL MUCOSA: STRONGYLOIDES STERCOLALIS FRAGMENTS OF WORM IN INTESTINAL MUCOSASTRONGYLOIDES STERCOLALIS MULTIOLE PARTIALLY CALCIFIED WORM FRAGMENTS: STRONGYLOIDES STERCOLALIS MULTIOLE PARTIALLY CALCIFIED WORM FRAGMENTSPNEUMOCYSTIS CARINII: PNEUMOCYSTIS CARINII At higher magnification, the granular pink exudate of Pneumocystis carinii pneumonia is seen. The exudate consists of edema fluid, protein, Pneumocystis organisms, and dead macrophages. One can see why gas exchange is severely compromised.VIRUSES: VIRUSESCYTOMEGALOVIRUS: CYTOMEGALOVIRUS CLINICAL FEATURES : Enveloped ds DNA herpes virus. Ubiquitous – can infect almost any body site. Serious disease in immuno compromised patients especially in HIV. Pneumonitis.CYTOMEGALOVIRUS: CYTOMEGALOVIRUS MICROSCOPIC : Enlarged cells with OWL’S EYE eosinophillic nuclear inclusion & marginated chromatin. Granular cytoplasmic inclusions. Interstitial pneumonia, diffuse alveolar damage.CYTOMEGALOVIRUS H & E IMMUNOPEROXIDASE: CYTOMEGALOVIRUS H & E IMMUNOPEROXIDASEHERPES SIMPLEX VIRUS I & II: HERPES SIMPLEX VIRUS I & II CLINICAL FEATURES : HSV I = 1) primary infection usually asymptomatic. 2) Rare kerato conjuctivitis, resp. infection, infection of any part of skin or mucosa. 3) Recurrence trigerred by sun light , fever or illness. HSV II = 1)Acquired via sexual contact or by neonates during vaginal delivery to mom with active genital lesions. HERPETIC WHITLOW Wide spread disseminated disease in immuno compromised patients.HERPES SIMPLEX VIRUS I & II SKIN H & E: HERPES SIMPLEX VIRUS I & II SKIN H & EHERPES SIMPLEX VIRUS I & II MULTI NUCLEATED CELLS WITH NUCLEAR MOLDING & MARGINATION OF CHROMATIN : HERPES SIMPLEX VIRUS I & II MULTI NUCLEATED CELLS WITH NUCLEAR MOLDING & MARGINATION OF CHROMATINHERPES SIMPLEX VIRUS I & II Ground glass nuclei with margination of chromatin in LIVER: HERPES SIMPLEX VIRUS I & II Ground glass nuclei with margination of chromatin in LIVERADENO VIRUS: ADENO VIRUS CLINICAL FEATURES : Non enveloped ds DNA virus. Upper & lower RTI , conjunctivitis , hemorrhagic cystitis, colitis in AIDS , gastroenteritis in children; may be asymptomatic. MICROSCOPIC : Bronchiolar necrosis, coagulative necrosis, hyaline membranes, diffuse alveolar damage. Infected nuclei of bronchial epithelium & alveoli appear smudged or may have a round , eosinophillic nuclear inclusion with surrounding halo & marginated chromatin.ADENO VIRUS: ADENO VIRUSADENO VIRUS: ADENO VIRUSADENO VIRUS: ADENO VIRUSSlide 55: THANK YOU By : Dr Ravi JainOPPORTUNISTIC INFECTIONS IN IMMUNODEFICIENT PATIENTS – PART II: OPPORTUNISTIC INFECTIONS IN IMMUNODEFICIENT PATIENTS – PART IIBACTERIA: BACTERIAMYCOBACTERIA TUBERCULOSIS: MYCOBACTERIA TUBERCULOSIS CLINICAL CLASSIFICATION : PRIMARY T.B. = exogenous first infection; usually self limiting. PROGRESSIVE T.B. = inadequate acquired immunity; progression or original infection. POST PRIMARY T.B. = endogenous reactivation.MYCOBACTERIA TUBERCULOSIS: MYCOBACTERIA TUBERCULOSIS MACROSCOPIC : PRIMARY T.B. = Ghon focus; single sub pleural nodule, above or below interlobar fissure & enlarged hilar caseous lymph nodes. PROGRESSIVE T.B. = cavitations & progression of initial or reactivation nodule; consolidation or miliary spread can occur. POST PRIMARY T.B. = apical lesion; miliary spread can occur.MYCOBACTERIA TUBERCULOSIS: MYCOBACTERIA TUBERCULOSIS MICROSCOPIC : PRIMARY/POST PRIMARY T.B. = necrotizing granulomatous inflammation, airway based . PROGRESSIVE T.B. = necrotizing granulomatous inflammation with cavitation & spread thru out lung; pleura commonly involved.MYCOBACTERIA TUBERCULOSIS: MYCOBACTERIA TUBERCULOSISMYCOBACTERIA TUBERCULOSIS: MYCOBACTERIA TUBERCULOSIS Mycobacteria can also be stained with auramine and viewed with fluorescence microscopy, in which acid fast bacilli now appear as glowing yellow rods. This method is easier to use to screen for mycobacteria and is the method routinely used in sputum specimens sent to the laboratory.MYCOBACTERIA TUBERCULOSIS: MYCOBACTERIA TUBERCULOSIS This is an acid fast stain of Mycobacterium tuberculosis (MTB). Note the red rods--hence the terminology for MTB in histologic sections or smears: acid fast bacilli.MYCOBACTERIA TUBERCULOSIS: MYCOBACTERIA TUBERCULOSIS This spleen shows a miliary pattern of granulomatous inflammation, with numerous small tan granulomas. This suggests a poor immune response. This patient had AIDS. The infection turned out to be Mycobacterium avium-intracellulare (MAI), also known as Mycobacterium avium-complex (MAC).MYCOBACTERIA – AVIUM COMPLEX: MYCOBACTERIA – AVIUM COMPLEX CLINICAL FEATURES : Opportunistic infections in A.I.D.S Other risk factors include COPD, bronchiectasis & pneumoconioses. Also found in patients without underlying lung disease ( non smoking women ): more benign course.MYCOBACTERIA – AVIUM COMPLEX: MYCOBACTERIA – AVIUM COMPLEX MACROSCOPIC : Can cause upper lobe cavitary lesion. Non cavitating form may be associated with local bronchiectasis. MICROSCOPIC : Necrotizing granulomatous inflammation most common, with non necrotizing granulomas present. Organizing pneumonia & non necrotizing granulomas can be seen.MYCOBACTERIA – AVIUM COMPLEX: MYCOBACTERIA – AVIUM COMPLEX SPECIAL STUDIES : Ziehl – Nielsen stain for acid fast organisms. Auramine – Rhodamine stain more sensitive.MYCOBACTERIA – AVIUM COMPLEX: MYCOBACTERIA – AVIUM COMPLEX The lymph nodes in this mesentery, best seen at the left, are enlarged and have cut surfaces that appear yellow-tan. These nodes are filled with sheets of Mycobacterium avium-complex (MAC) organisms, and the immune response is so poor in this AIDS patient that there is no focal granuloma formation.MYCOBACTERIA – AVIUM COMPLEX: MYCOBACTERIA – AVIUM COMPLEX Microscopically, Mycobacterium avium-intracellulare infection is marked by numerous acid fast organisms growing within macrophages. Lots of bright red rods are seen, particularly in macrophages, in this acid fast stain of lymph node.LEGIONNAIRES’ DISEASE: LEGIONNAIRES’ DISEASE CLINICAL FEATURES : FIRST RECOG. IN LARGE OUTBREAK IN AMERICAN LEGION CONVENTION IN PHILADELPHIA. Acute pneumonic process with high fever , cough , chills & chest pain; gastrointestinal symptoms are prominent; renal failure is common. Renal & bone marrow transplant patients at high risk.LEGIONNAIRES’ DISEASE: LEGIONNAIRES’ DISEASE MICROSCOPIC : Acute bronchopneumonia with characteristic intra alveolar exudate of neutrophils, macrophages & karyorrhectic debris. SPECIAL STUDIES: Small , pleomorphic gram bacillus- cultured in modified MUELLER – HINTON agar. DIETERLE’S SILVER stain best for visualizing organisms; florescent studies of smears & scrapes are most sensitive for diagnosis.LEGIONNAIRES’ DISEASE ACUTE BRONCHO PNEUMONIA H & E: LEGIONNAIRES’ DISEASE ACUTE BRONCHO PNEUMONIA H & ELEGIONNAIRES’ DISEASE-DIETERLE’S STAIN: LEGIONNAIRES’ DISEASE-DIETERLE’S STAINACTINOMYCOSIS: ACTINOMYCOSIS CLINICAL FEATURES : Aspiration of oral or tonsillar organisms; patients with poor dentition or repeated tonsilitis. May present like a carcinoma. MICROSCOPIC : Abscess in lung or mediastinum ; sulphur granules found with palisadeing eosinophillic proteinaceous halo – SPLENDORE HOEPPLI REACTION.ACTINOMYCOSIS: GRAM’S STAIN: ACTINOMYCOSIS: GRAM’S STAINMYCOSES: MYCOSESMYCOSES: MYCOSES 1. SUPERFICIAL 2. CUTANEOUS 3. SUBCUTANEOUS 4. ENDEMIC (PRIMARY, SYSTEMIC): Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatitidis, Paracoccidioides brasiliensis 5. OPPORTUNISTIC endogenous - Candida (different species) - Pneumocystis carinii (?) exogenous - Cryptococcus neoformans - Aspergillus (different species) - Zygomycetes - MANY OTHER FUNGICANDIDA ALBICANS: CANDIDA ALBICANS CLINICAL: Normal flora of G.I. Tract. Intertigo,Paranochiya,Diaper rash,Thrush,Esophagitis,Balanitis & vaginitis. Immuno suppressions , steroid & antibacterial increases the risk of infection. May disseminate via hematogenous route. High mortality.CANDIDA ALBICANS: CANDIDA ALBICANS MACROSCOPIC : Superficial infection appears white & velvety with red adjacent areas. Locally invasive lesions have sharp margins with granular base & tan yellow friable base. Disseminated candidiasis is invasive infection. Involving parenchyma of at least two organs excluding mucosa of G.I/RESP./G.U.TCANDIDA ALBICANS: CANDIDA ALBICANS Budding cells with pseudohyphae seen here are characteristic for Candida infection.CANDIDA ALBICANS: CANDIDA ALBICANS With a PAS stain, the budding cells and pseudohyphae (short filaments that are not true hyphae) of Candida stain bright redCANDIDA ALBICANS: CANDIDA ALBICANS Here is a GMS stain of CandidaCANDIDA ALBICANS: CANDIDA ALBICANS A PAS stain reveals the budding cells and pseudohyphae of Candida on the surface of the tongue.CANDIDA ALBICANS: CANDIDA ALBICANS Oral candidiasis is common in immunocompromised hosts, such as those with HIV infection. There is a hairy coating of the tongue seen here mixed with a pale tan exudate.CANDIDA ALBICANS: CANDIDA ALBICANS MICROSCOPIC : Yeast's with narrow necked budding & sausage link pseudohyphae. Blastoconidia. Dense neutrophillic infiltrate in the epidermis & superficial dermis. May see a spongiform sub corneal pustule indistinguishable from psoriasis. Chronic inflammatory infiltrate in deeper levels. Disseminated forms may have leukocytoclastic vasculitis .CANDIDA ALBICANS: CANDIDA ALBICANS DIAGNOSIS : 1) SPECIAL STAIN - GOMORI’S METHENAMINE SILVER. 2) P.A.S GERM TUBE TEST 1) 95 % POSITIVE IN C.ALBICANS 2) OCCASIONALLY POSITIVE IN C.TROPICALIS 3) ALL OTHER CANDIDA ARE NEGATIVECRYPTOCOCCUS NEOFORMANS: CRYPTOCOCCUS NEOFORMANS Found in soil & pigeon droppings. Can remain viable for years.CRYPTOCOCCUS NEOFORMANS: CRYPTOCOCCUS NEOFORMANS CLINICAL FEATURES : Inhalation leads to mild pulmonary disease. Menigitis , cut. & mucocut.. Osseous & visceral infection also may occur.CRYPTOCOCCUS NEOFORMANS: CRYPTOCOCCUS NEOFORMANS This is Cryptococcus neoformans infection of the lung. There are numerous organisms that have a large mucoid capsule, giving the appearance of a clear zone around a faint round nucleusCRYPTOCOCCUS NEOFORMANS: CRYPTOCOCCUS NEOFORMANS This is a Cryptococcus neoformans meningitis stained with GMS to reveal the nuclei. In this AIDS patient, the organisms didn't even bother to make a capsule. The budding cells of Cryptococcus have a narrow base.CRYPTOCOCCUS NEOFORMANS: CRYPTOCOCCUS NEOFORMANS This is an India ink preparation of cerebrospinal fluid in a patient with Cryptococcus neoformans meningitis. Note the clear zone of the capsule around the central nucleus of the organismsCRYPTOCOCCUS NEOFORMANS: CRYPTOCOCCUS NEOFORMANS MACROSCOPIC : Slimy glistening white meninges. Cutaneous lesions, papules , pustules to solitary well circumscribed ulcerated nodule.CRYPTOCOCCUS NEOFORMANS: CRYPTOCOCCUS NEOFORMANS MICROSCOPIC : 2 - 15 uM variable sized encapsulated yeasts with single bud & narrow attachment. Often neutrophillic infiltrate , but may be granulomatous especially in immunocompetent patients.CRYPTOCOCCUS NEOFORMANS: CRYPTOCOCCUS NEOFORMANS DIAGNOSIS : Indian ink direct exam of C.S.F. Gomori methenamine silver, P.A.S, Mucicarmine or Alcian blue to detect capsule. Fontana - masson stains cell wall.ASPERGILLUS: ASPERGILLUS CLINICAL FEATURES : Disseminated opportunistic infection in immunocompromised patients. Predisposing factors : 1) neutropenia 2) malignancy 3) A.I.D.S 4) Transplant patient 5) long term steroid use Primary pulmonary infection may disseminate hematogenously to skin or skin may be primary.ASPERGILLUS: ASPERGILLUS MACROSCOPIC : Colonies begin white then become shades of yellow ,green ,brown or black depending upon the species.ASPERGILLUS: ASPERGILLUS This is a fungal abscess of the lung. Note the yellow tan material in the abscess. It is very firm material, because it is composed of fungal hyphae. This one is due to Aspergillus. Aspergillus has a habit of colonizing previously formed cavities, such as those with tuberculosis .ASPERGILLUS: ASPERGILLUS This is Aspergillus infection of the lung. Note how the infection crosses the pleura between the lobes. Note that a small artery to the left of the yellow-brown fungal abscess is thrombosed and surrounded by hemorrhage. Aspergillus likes to invade vessels and surrounding tissues .ASPERGILLUS: ASPERGILLUS Here is an Aspergillus fungus ball in a dilated bronchusASPERGILLUS: ASPERGILLUS At higher magnification, Aspergillus hyphae are seen to branchASPERGILLUS: ASPERGILLUS Here are branching Aspergillus hyphaeASPERGILLUS: ASPERGILLUS MICROSCOPIC : 2 -4 uM septate hyphae with acute angle branching & progressive arborizing branches. Often see vascular invasion with thrombus & infarction. Neutrophillic to granulomatous reaction. Conidiophores ( fruiting bodies ) allow identification of species but are rarely seen in tissues.ASPERGILLUS: ASPERGILLUS DIAGNOSIS : Gomori’s methenamine silver stain P.A.S Speciation based on conidial arrangement. Culture is reqd. for definite arrangement.HISTOPLASMOSIS: HISTOPLASMOSIS CLINICAL FEATURES : Dimorphic fungi. Most common syst. Fungal disease in US. Acute on chronic histoplasmosis – cough, fever, night sweats, malaise, weight loss. Disseminated histoplasmosis primarily in AIDS. Mediastinal fibrosis. Chest x-ray – diffuse / patchy interstitial infiltrate.HISTOPLASMOSIS: HISTOPLASMOSIS MACROSCOPIC : Silky or hair like white to gray tan mold with tuberculate macroconidia after 10 – 30 days of incubation at 25 – 30 deg.C Spectrum of findings : Cavitary lesion ( upper lobe ) Fibrosis with emphysema Residual solitary nodule with onion skin layered appearance Enlarged necrotic & calcified hilar lymph nodeHISTOPLASMOSIS: HISTOPLASMOSIS Many fungal infections can produce a granulomatous pattern. In immunocompromised hosts, the immune response is often poor, so granulomas are poorly formed, if at all. This portion of liver demonstrates some pinpoint yellow-tan granulomas in a patient with disseminated histoplasmosis.HISTOPLASMOSIS: HISTOPLASMOSIS This is infection with Histoplasma capsulatum. Note how each macrophage is filled with numerous small organisms. The organisms have a clear zone around a central blue nucleus which gives the cell membrane the appearance of a capsule. Hence, the name of the organism.HISTOPLASMOSIS: HISTOPLASMOSIS A PAS stain highlights Histoplasma capsulatum infection in the liverHISTOPLASMOSIS: HISTOPLASMOSIS MICROSCOPIC : 2 – 4 uM oval yeasts with single eccentric nucleus & perinuclear clearing. Narrow necked single buds clustered in R.E. cells in tissue section. Surrounded by a halo giving a false impression of a capsule. 5 – 15 uM rough walled macroconidia on lactophenol cotton blue prep of colony.HISTOPLASMOSIS: HISTOPLASMOSIS DIAGNOSIS : May be difficult to convert to yeast form in culture; however culture is gold standard. H & E and fungal stains. Serology .CONCLUSION: CONCLUSION MANAGING OPPORTUNISTIC INFECTIONS is the most imp. Part in the T/t of immuno deficient patients B/c patients usually die from infections rather than original disorder.Slide 112: THANK YOU By : Dr Ravi Jain You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.