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Candidiasis 2016


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class presentation at BMC

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Candidiasis 2016

  1. 1. CANDIDIASIS Presenter:B.H MSUMI
  2. 2. BURDEN OF DISEASE  Candidiasis is a fungal infection caused by Candida  The most interesting period in the history of candida infections began in 1940 when the widespread use of antibiotics was introduced  Since then the incidence of practically all forms of candida infections has risen abruptly  Candida spp have been the fourth most common organisms recovered from blood of hospitalized patients in US during the recent decades  Between 2000 and 2005 the incidence of candidaemia related hospitalizations per 100000 population rose by 52%
  3. 3.  The burden of this disease in terms of morbidity,mortality and expense is considerable.  The emerging candida infections have included not only bloodstream infection but also arthritis,myositis ,peritonitis etc  There is significant increase in reports on the incidence and manifestations of candida infections caused by non- albicans species
  4. 4. PATHOGENS  Candida spp are asexual yeast of genus ascomycetes and genetically diploid with presence of 8 chromosomes  They are small(4 to 6um),thin walled,ovoid cells(blastospores) that reproduce by budding  They grow well in vented routine blood culture bottles and on agar plate and do not require special fungal media for cultivation  About 8%-15% of nosocomial blood stream infections are reported to be caused by candida species
  5. 5.  out of more than 200 species the most commonly encountered in medical practices are C.albicans,C.guilliermondii,C.krusei,C. tropicalis,C.parapsilosis,C.pseudotropi calis,C.lusitaniae,C.dubliniensis and C.glabrata
  6. 6. Predisposing factors  Immunocompromised state i.e. AIDS, malignancies i. e. lymphomas, leukemia, conditions like diabetes mellitus, TB etc.  Prolonged use of antibiotics, anticancer drugs & anti-inflammatory drugs  Low birth weight neonates  Therapeutic procedures eg. organ transplantation, open heart surgery, artificial heart valves, indwelling catheters e.g. urinary & parenteral drug administration.  Burn patients
  7. 7. EPIDEMIOLOGY AND ECOLOGY  C.albicans organisms have been recovered from soil,animals ,hospital environments,inanimate objects and food  Non-albicans species may live in animal or non animal environment as well  The organisms are normal commensals of humans  Commonly found on skin,GI tract expectorated sputum,female genital tract and in urine of patient with indwelling catheter
  8. 8.  There is relatively high incidence of carriage on the skin of health care workers  Although the vast majority of candida infections are of endogenous origin human to human transmission is possible  Examples are thrush of the newborn,which may be acquired from the maternal vagina  Balanitis in the uncircumcised man, which may be acquired through contact
  10. 10. HOST DEFENCE 1. Cutaneous and mucosal physical barriers 2. Immune cells
  11. 11. 1. Cutaneous and mucosal physical barrier  Primary resistance to fungal invasion and colonization is contributed by mucosal and cutaneous physical barriers which include i. Antifungal activity of saliva and sweat ii. The mechanical barrier of the skin and mucous membranes which prevent entry of fungi iii. The competition for space and nutrients by normal microbiota of the skin and mucus membranes which limit growth of potent pathogen
  12. 12. 2. immune cells  Considering the interaction between host and pathogen,immune cells are the major antagonists to survival of fungal pathogens inside the host  The main cell populations involved in recognition of C.albicans during the innate immune response include monocytes,macrophages and neutrophils  Dendritic cells are crucial for processing of and antigen presentation to T cells and therefore to activation of specific
  13. 13. Cell population and pattern recognition receptors(PRRs) involved in candida recognition PRRs monocyte macroph age neutrophi l Dendritic cell CD4+ T cell TLR2 + TLR4 + + TLR6 + + + TLR9 + + + MR + + + Dectin-1 + + + + + Dectin-2 + + + + DC-SIGN + + + CR3 + + + Galectin +
  14. 14. Virulence factors 1. Adhesins 2. Polymorphism 3. Biofilm 4. Invasins 5. Secreted hydrolases 6. Metabolic adaption
  15. 15. 1.adhesins  They have special sets of (GPI)-linked cell surface glycoproteins that allow it to adhere to the surfaces of microorganisms.  These glycoproteins are encoded by 8 sets of agglutinin-like sequence (ALS) genes, ranging from Als1-7 and Als9.  For adhesion, the Als3 gene appears to be the most important as it is upregulated during an infection of oral and vaginal epithelial cells.  Also, it helps with biofilm formation by helping with adhesion to each other
  16. 16. 2.polymorphism  polymorphic fungus that can grow in several different forms, primarily yeast, pseudohyphae, and hyphae.  For its pathogenicity, its ovoid-shaped budding yeast and parallel-walled true hyphae forms are the most important.  The hyphae form is more prevalent for an infection, while the yeast form is believed to be important in the spread  The role of pseudohyphae is not very well understood, other than being an intermediate form between yeast and hyphae .  Several factors can cause a change in morphology, such as pH differences, temperature changes, carbon dioxide levels, starvation, and quorum-sensing molecules (farnesol, tyrosol, and dodecanol
  17. 17. 3 .Biofilm  Candida albicans have the ability to form biofilms on living and non-living surfaces, such as mucosal membranes and catheters, respectively.  After the adherence of yeast cells to the surface, there is development of hyphae cells in the upper part of the biofilm.  Eventually, this leads to a more resistant, mature biofilm and the dispersion of yeast cells – both contributing to the pathogen’s virulence.
  18. 18.  In the process of biofilm formation, Bcr1, Tec1 and Efg1 function as important transcriptional factors .  Recent studies show that biofilms protect C. albicans colonization from neutrophil attack and deter the formation of reactive oxygen species
  19. 19. 4 invasins  Along with adhesion, Als3 proteins can function as invasins that help with the invasion of C. albicans into host epithelial and endothelial cells.  Another important invasin gene is Ssa1, which normally codes for heat-shock proteins.  Basically, these specialized proteins on the pathogen’s surface mediate binding to host ligands, such as E-cadherin on epithelial cells and N-cadherin on endothelial cells, and it induces host cells to engulf the fungal pathogen(induced endocytosis).  Another method of invasion is the active penetration of C. albicans into host cells by an unknown mechanism involving hyphae (active penetration)
  20. 20. 5. Secreted hydrolases  secrete 3 main classes of hydrolases: proteases, phospholipases and lipases.  It is proposed that these hydrolases help facilitate the pathogen’s active penetration into host cells and the uptake of extracellular nutrients from the environment.  There are about 10 known secreted aspartic proteases (Sap1-10),
  21. 21.  Their exact contribution to pathogenicity is controversial.  For phospholipases, there are 4 major classes (A, B, C, and D), and all 5 members of the B class are involved with the disruption of a host cell surface.  Thirdly, lipases are consisted of 10 members (LIP1-10), and studies show that there is decreased virulence in their absent
  22. 22. 6. Metabolic adaption  Are usually found in the gastrointestinal microbiome of healthy individuals, and in this environment, nutrient levels are relatively high.  However, during niche changes in the course of an infection, available nutrient levels will also change.  Consequently, the fungus can quickly undergo metabolic adaption, such as their glycolysis, gluconeogenesis, and starvation responses .  For example, in the case of candidemia,C. albicans infect the bloodstream, which is typically rich in glucose.
  23. 23.  Nevertheless, it might be phagocytosed into a macrophage or neutrophil, where it’s surrounded by ROS, RNS, and AMPs  In response, C. albicans quickly switch from its glycolysis to starvation response with the activation of the glyoxylate cycle.  Due to this flexibility, C. albicans can infect almost every organ in a human host through the bloodstream, providing candidemia’s higher mortality rate.
  24. 24. Pattern recognition receptors(PPRS) sensing candida associated molecular patterns Candida pathogen associated molecular pattern (PAMPS) are recognized by specific PRRS from three major families a) Toll-like receptors(TLRS) b) C-type lectin receptors (CLRS) c) Nucleotide binding domain,leucine rich repeat containing receptors(NLRS)
  25. 25. PRRs Candida PAMP Tall like receptors TLR2 phospholipomannan TLR4 Mannan O-linked mannosil residues TLR9 CpG-Oligodeoxynucleotides
  26. 26. C –type lectin receptors Mannose receptor Mannan N-linked mannosal residue Dectin -1 Beta-1,3-Glucan Dectin-2 High mannose structures(man9G1cNAc2) DC-SIGN High mannose structures Galectin-3 Beta-1,2-mannosides
  27. 27. Clinical manifestations  As the frequency of diseases due to Candida has increased a relatively large numbers of manifestations which were previously either not recognized or extremely infrequent,have become well documentated  The discussion of these clinical manifestations is facilitated by their subdivision into mucocutaneous and systemic involvement
  28. 28. Candida Vaginitis  It is estimated that 75% of women in childbearing years will experience at least one yeast infection.  The organism can be isolated from up to 20% of asymptomatic women of childbearing years, some of whom are celibate.  Candida vaginitis infection is not considered to be a STD but can be spread sexually.
  29. 29. Candida Vaginitis Cont.  Factors that favor increased rates of asymptomatic vaginal colonization are pregnancy, oral contraceptives, uncontrolled DM, and frequent STD clinic visits.  C. albicans strains account for 85-92% of those strain isolated from the vagina.  C. glabrata and C. tropicalis are the commonest non-albicans strains and are more resistant to conventional therapies.
  30. 30. Candida Vaginitis Cont.  Candida organisms gain access to the vaginal lumen and secretions predominately from the adjacent perianal area.  Risk factors for yeast infections are: loss of normal vaginal flora (po antibiotics), diminished glycogen stores (DM, pregnancy, BCP, and hormone replacement), increase of vaginal pH (menstrual blood or semen) or tight-fitting undergarments causing increase temp, moisture, and local irritation.
  31. 31. Candida Vaginitis Cont.  Clinical symptoms include leukorrhea, severe vaginal pruritus, external dysuria, and dyspareunia. Odor is unusual.  Gyn exam may reveal vulvar erythema and edema, vaginal erythema, and thick cottage-cheese D/C.  The diagnosis is made by have a normal pH4-4.5 and positive results on microscopic exam (yeast buds and pseudohyphae).  Culture is only use with symptomatic patients with negative findings on microscopic exam.
  32. 32. Candida Vaginitis Cont.  Most treatment are effective; topical azoles are more effective than nystatin.  For uncomplicated infections any topical agent as well as oral diflucan will treat candida.  Complicated infections can be treated with lotrinmin 500mg vag. supp 1 weekly or Diflucan 150mg po day 1 and 3.  For pregnant patients must receive topical azole therapy applied for 7 days, can not use oral diflucan.
  33. 33. Namkinga et al 2005  Cross sectional study done at ilala municipal hospital in Dar es Salaam, Tanzania  Subjects: 464 women presenting with complaints of genital infections.  Results: Of the 464 women examined, 177 (38.1%) had abnormal vaginal discharge, 68(14.7%) had genital ulcers, 272 (58.6%) had genital pruritis, 18 (3.9%) had genital warts and 58 (12.5%) had chancre
  34. 34.  .The prevalencies of VC, bacterial vaginosis, HIV, T vaginalis, N. gonorrhoeaeand syphilis were 45%, 48.4%, 22%, 93%, 1.5% and 4.3%, respectively. The occurrence of VC was positively associated with HIV, (OR=1.81, 95% CI (1.0-2.67), bacterial vaginosis; (OR=2.6, 95%CI (1.7-3.9), genital pruritis; (OR=1.8 1, 95%CI (1.2- 2.7) genital discharge; (OR=1.867, 95% (1.28-2.73) and negatively with T. vaginalis (OR=0.27, 95% CI (0.12 - 0.6), occupation (OR=0.65, 95%CI (0.35-0.86)) and with education (OR=0.43, 95% CI (0.11-0.73). There were increased but non-significant odds for VC in patients with syphilis (OR=1.6 95%CI (0.6-4.3) and venereal warts (OR=2.5 95% CI (0.92-6.8) VC was not associated with N. gonorrhoeae, genital ulcers, age at first intercourse, number of sexual partners, marital status or antibiotic usage.
  35. 35.  Conculsion: The high prevalence of vaginal candidiasis among women with genital infections should be taken into account when updating policies concerning syndromic management of sexually transmitted diseases. More gender specific approach to syndromic management of sexually transmitted infections in females should be considered.  East African Medical Journal Vol.82(3) 2005: 139-144
  36. 36. Chronic Mucocutaneous Candidiasis  Hereditary immunodeficiency disorder results in failure of the patient's T lymphocytes to produce cytokines that are essential for expression of cell-mediated immunity to Candida  Most forms of CMC begin in infancy or within the first 2 decades; rarely, the onset may be after the age of 30 years  Characterised by cellular immunodeficiency and endocrinopathies – skin or mucosal disease.  Infections of the scalp; skin; nails; and membranes lining the mouth, eyes, digestive tract & reproductive tract
  37. 37.  The different forms of CMC are generally categorized as follows:  familial CMC, autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED)  Chronic localized candidiasis, chronic mucocutaneous candidiasis with thymoma, candidiasis with keratitis, and candidiasis with hyper-IgE syndrome
  38. 38.  The first manifestation is usually oral thrush followed by nail infections and then skin involvement  There is a broad spectrum of severity, ranging from chronic involvement of an isolated nail to a severely disfiguring form((Candida granuloma)
  39. 39.  In recent years has been the discovery of certain,specific innate immunity defects that result in CMC  Briefly, the genes discovered so far include AIRE (21q) (APECED), STAT3, DOCK8 (9p ), TYK2 (19p), CARD9 (9q), Dectin-1 (12p), IL17RA (22q), IL17F (6p), STAT1 (2q), and IL12Rβ1 (19p).  Hematogenous disseminated candidiasis is rare, probably due to intact, functional neutrophils
  40. 40. Management  Management can be difficult, and relapse is common following discontinuation of therapy.  Topical therapies are not usually effective in patients with CMC.  Treatment of oral involvement in CMC can be aided by therapy with clotrimazole troches or oral nystatin solution.  Treatment falls into 3 main categories: antifungal agents, immunologic therapies, and combination therapy.
  41. 41. Esophageal candidiasis  is an opportunistic infection of the esophagus caused by Candida albicans. The disease usually occurs in patients in  immune suppression ( Malignancy,Diabetes,AIDS)  immunosuppressive drug therapy including post- chemotherapy broad spectrum antibiotics therapy and corticosteroids  in blood dyscrasia  Occurs in 20–40% of patients with AIDS  Patients usually have CD4 <100 cells/mm3
  42. 42. However, it can also occur in patients with no predisposing risk factors, and is more likely to be asymptomatic in those patients. It is also known as candidal esophagitis or monilial esophagitis
  43. 43. Clinical Presentation  Odynophagia (painful swallowing)  Dysphagia (difficulty swallowing)  Diffuse retrosternal pain  Occasional nausea and vomiting  Oral candidiasis often present but not required
  44. 44. First Line Therapy  Fluconazole 200 mg po daily (preferred) x 14–21 days  Itraconazole solution 200 mg po daily x 14–21 days ◦ Itraconazole also available in capsule but better absorption with liquid formulation ◦ Ketoconazole rarely used due to erratic absorption
  45. 45. Second Line Therapy  Amphotericin B 0.3-0.7 mg/kg IV daily ◦ Or lipid formulations of amphotericin  If available, can also use ◦ Echinocandins  Caspofungin, micafungin ◦ Alternative azoles with increased activity against fluconazole-resistant Candida  Voriconazole, posaconazole, itraconazole
  46. 46. Treatment  Assess response to therapy within 5–7 days  Continue therapy for 14–21 days after clinical improvement  Use intravenous drugs for patients unable to swallow
  47. 47. If no Response to Fluconazole  Check medication adherence  Reconsider diagnosis  Refer for endoscopy  Consider resistance to azole therapy – especially if repeated courses of azole treatment or if maintenance therapy used
  48. 48.  Study conducted at KCMC Gwakisa et al (2016)  Prevalence of oral candida was 42.0% (132/314). Age group 6-27 years accounted for half of the infections (49/98). A significantly higher prevalence of candida infection (66.7%; 24/36) was obseved among patients with <200 cells/µl than in those with 200-500 cells/µl or >500 cells/µ
  49. 49.  Conclusion: The prevalence of oral candida infection was significantly higher in patients with CD4+ cell counts less than 200 cells/µl.
  50. 50. Oropharyngeal candidiasis  A common local infection.  Host: infants, older adults who wear dentures, patients treated with antibiotics, chemotherapy, or radiation therapy to the head and neck, and cellular immune deficiency states.  Symptoms: white curd like lesions on tongue,gums and buccal mucosa, cottony feeling, loss of taste, pain on eating and swallowing, asymptomatic
  51. 51. The following are the 5 types of oropharyngeal candidiasis (OPC): Membranous candidiasis: This is one of the most common types and is characterized by creamy-white curdlike patches on the mucosal surfaces. Erythematous candidiasis: This is associated with an erythematous patch on the hard and soft palates.
  52. 52. Chronic atrophic candidiasis (denture stomatitis): This type is also thought to be one of the most common forms of the disease. The presenting signs and symptoms include chronic erythema and edema of the portion of the palate that comes into contact with dentures.
  53. 53. Angular cheilitis: An inflammatory reaction, this type is characterized by soreness, erythema, and fissuring at the corners of the mouth . Soreness and cracks at the lateral angles of the mouth (angular cheilitis) are a frequent expression of candidiasis in elderly individuals.
  54. 54. .Oral thrush usually occurs with CD4 counts of <300 cells/µL and is not an AIDS-defining illness.
  55. 55.  Diagnosis: Gram stain or KOH preparation on the scrapings. Budding yeasts with or without pseudohyphae.  Rx: ◦ Clotrimazole troche (10 mg troche dissolved five times per day) ◦ Nystatin suspension (400,000 to 600,000 units four times per day) - Nystatin troche (200,000 to 400,000 units four to five times per day), - For 7 to 14 days
  56. 56. Candidaemia and disseminated candidiasis  It is an invasive fungal infection in deep seated tissue or other normally sterile sites  When candida is in your blood stream the condition is called candidaemia  Documented by histopathology and/or microbiological culture  Usually begins with candidemia(but only about 50% of cases candidermia can be proven
  57. 57. Pathogenesis  Candida spp may enter the blood stream from colonization and growth on an intravascular catheter or by translocation across gut mucosa  Translocation is enhanced by fungal overgrowth commonly associated with broad spectrum antibiotic use  Epithelial injury secondary to trauma or surgery in the GIT also facilitates this
  58. 58. Risk factors  immunosuppressed patients ◦ Hematologic malignancies ◦ Recipients of solid organ or hematopoietic stem cell transplants ◦ Those given chemotherapeutic agents for a variety of different diseases  intensive care patients ◦ Trauma and Burn patients, ◦ Neonatal units ◦ Central venous catheters ◦ Total parenteral nutrition ◦ Broad-spectrum antibiotics ◦ High APACHE II scores ◦ Renal failure requiring hemodialysis ◦ Abdominal surgical procedures ◦ Gastrointestinal tract perforations and anastomotic leaks
  59. 59. Symptoms and sign  Vary from minimal fever to a full-blown sepsis syndrome  Clinical clues: ◦ characteristic eye lesions (chorioretinitis, endophthalmitis), ◦ skin lesions, ◦ much less commonly, muscle abscesses. ◦ signs of multiorgan system failure may present: kidneys, heart, liver, spleen, lungs, eyes, and brain
  60. 60. Treatment Fluconazole  Remain effacious in candidaemia  Loading dose 800mg followed 400mg daily in haemodynamically stable pts  Available as iv/po  Widely studied for prophylaxis in ICU pts
  61. 61. Prevention strategies Prophylaxis  Treating patients with multiple risk factors for infection with no documented micro or histological evidence Pre-emptive  Those with documented micro or histological evidence (fungal colonization)
  62. 62. Candida Prophylaxis POPULATION RECOMMENDATION Solid-organ transplant recipients Fluconazole: 200-400 mg (3-6 mg/kg) daily or LAMB: 1-2 mg/kg/day for 7-14 days Intensive care unit patients with high risk in units with high risk Fluconazole: 400 mg (6 mg/kg) daily Patients with chemotherapyinduced neutropenia Fluconazole: 400 mg (6 mg/kg) daily or Posaconazole suspension: 200 mg 3 times daily or Caspofungin: 50 mg daily or Itraconazole: oral, 200 mg once
  63. 63. John dottis et al 2009,philadelphia  Type of study  retrospective analysis of demographic data, clinical features, therapeutic procedures and outcomes associated with Candida bloodstream infections (BSIs) that occurred at the Children’s Hospital of Philadelphia between 1997–2009.
  64. 64.  Among 406 Candida BSIs, Candida albicans accounted for 198 (49%), C. parapsilosisfor 99 (24%) and all other species for 109 (27%) episodes. There was no consistent change in proportion of C. parapsilosis BSIs during the study. C. parapsilosis BSI was more frequent than non-parapsilosis Candida spp. at age ≤2 years as compared with older patients [62% vs. 50%; OR=1.24, 95% CI=1.03–1.51, p=0.038]. Patients with C. parapsilosis were more likely to be mechanically ventilated within 48 hours of BSI (OR=1.38, 95% CI=1.01–1.85, p=0.047). Presence of a urinary catheter a week before infection was a protective factor for developing candidemia due to C. parapsilosis spp. (p=0.003). No significant differences were found between the two groups in presence of central intravascular catheters, co-morbidities and clinical or surgical procedures, previous administration of immunosuppressive or antifungal agents and mortality.
  65. 65. Conclusions  C. parapsilosis is the second most frequent cause of candidemia after C. albicans. While it is more frequent at the age of ≤2 years and is more likely associated with mechanical ventilation than other Candida spp., mortality does not significantly differ between those with and without C. parapsilosis candidemia.
  66. 66. BLADDER INFECTION AND COLONIZATION  Risk factors: urinary tract drainage devices; prior antibiotic therapy; diabetes; urinary tract pathology and malignancy.  Most patients with candiduria are asymptomatic.  It is difficult to differentiate between colonization and bladder infection.  Infected patients may have dysuria, frequency, and suprapubic discomfort, no symptoms.  Pyuria with a chronic indwelling bladder catheter that it cannot be used to indicate infection.
  67. 67. BLADDER INFECTION AND COLONIZATION Recommendations: IDSA  Asymptomatic candiduria rarely requires antifungal therapy, if kidney transplantation, neutropenia, low birth-weight neonates, or urinary tract manipulation.  Asymptomatic candiduria may respond to risk factor reduction by removal of bladder catheters or urologic stents, and discontinuation of antibiotics ]. If it is not possible, placement of new devices or intermittent bladder catheterization may be beneficial.  Symptomatic candiduria should always be treated.  Rx: ◦ Fluconazole 200 mg/day 7- 14 days, ◦ Azole-resistant yeast can be treated with intravenous amphotericin B 0.3-0.7 mg/kg per day for 1-7 days
  68. 68. KIDNEY INFECTION  Most commonly occurs in patients with disseminated  Acute infection ◦ Bilateral, consisting of multiple microabscesses in the cortex and medulla  Chronic infection ◦ Involve the renal pelvis and medulla with sparing of the cortex, which reflects ascending infection. ◦ The kidney is usually the only organ involved and the infection tends to be unilateral
  69. 69. KIDNEY INFECTION  Rx: ◦ Amphotericin B (0.5 to 1.0 mg/kg/day) ◦ Fluconazole (400 mg/day adjusted for renal function). ◦ At least 2 weeks ◦ removal and replacement of all intravenous catheters
  70. 70. Laboratory studies  Unfortunately, results from the routine laboratory studies are often nonspecific and not very helpful.  Clinicians are required to act definitively and early based on a high index of suspicion.  In the past, many patients with life-threatening candidiasis died without receiving antifungal therapy.  Systemic candidiasis should be suspected in patients with persistent leukocytosis and either persistent neutropenia or other risk factors and who remain febrile despite broad-spectrum antibiotic therapy.  To be effective, antifungal therapy should be provided early and empirically in such high-risk patients.
  71. 71. Specimens: swabs & scrapings from superficial lesions and/or vagina, blood, spinal fluid, tissue biopsies, urine & exudates Direct examination(microscopy) A smear taken from lesion is fixed on to microscope slides and then stained either by gram stain or by periodic acid sciff(PAS) technique Candidal hyphae and yeasts appear either dark blue(gram-stain) or red/purple
  72. 72.  Germ tube test(Reynold’s-Braude phenomenon)  Biochemical tests  Fungal culture  Typing of candida stains  Immunodiagnosis
  73. 73. Differential diagnosis  Abdominal abscess  Aspengillosis  Cryptococcus  Bacterial sepsis