Candidiasis is a fungal infection caused by Candida species. Since the 1940s when antibiotics became widespread, cases of candidiasis have risen significantly. Candida is now the fourth most common cause of bloodstream infections in hospitalized patients in the US. The burden of candidiasis in terms of morbidity, mortality, and costs is considerable. Common manifestations include vaginal candidiasis, chronic mucocutaneous candidiasis, and bloodstream infections. Host defenses against Candida include physical barriers and immune cells such as macrophages and neutrophils. Candida virulence factors that enhance its pathogenicity include adhesins, polymorphism, biofilms, invasins, secreted hydrolases, and metabolic adaptation.

1. CANDIDIASIS
Presenter:B.H MSUMI

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.  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. 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.  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. 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. 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.  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

9. PATHOGENESI
S AND
IMMUNOLOGY

10. HOST DEFENCE
1. Cutaneous and mucosal physical
barriers
2. Immune cells

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. 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. 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. Virulence factors
1. Adhesins
2. Polymorphism
3. Biofilm
4. Invasins
5. Secreted hydrolases
6. Metabolic adaption

16. 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

17. 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

18. 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.

19.  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

20. 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)

22. 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),

23.  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

24. 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.

25.  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.

26. 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)

27. PRRs Candida PAMP
Tall like receptors
TLR2 phospholipomannan
TLR4 Mannan
O-linked mannosil residues
TLR9 CpG-Oligodeoxynucleotides

28. 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

30. 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

33. 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.

34. 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.

35. 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.

36. 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.

37. 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.

38. 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

39.  .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.

40.  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

41. 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

42.  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

43.  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)

44.  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

45. 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.

46. 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

47. 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

48. Clinical Presentation
 Odynophagia (painful swallowing)
 Dysphagia (difficulty swallowing)
 Diffuse retrosternal pain
 Occasional nausea and vomiting
 Oral candidiasis often present but not
required

49. 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

50. 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

51. 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

52. 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

53.  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

54.  Conclusion: The prevalence of oral
candida infection was significantly
higher in patients with CD4+ cell
counts less than 200 cells/µl.

55. 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

56. 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.

57. 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.

58. 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.

59. .Oral thrush usually occurs with CD4
counts of <300 cells/µL and is not
an AIDS-defining illness.

60.  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

61. 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

62. 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

64. 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

65. 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

66. 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

67. 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)

68. 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

69. 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.

70.  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.

71. 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.

72. 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.

73. 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

74. 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

75. 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

76. 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.

77. 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

78.  Germ tube test(Reynold’s-Braude
phenomenon)
 Biochemical tests
 Fungal culture
 Typing of candida stains
 Immunodiagnosis

79. Differential diagnosis
 Abdominal abscess
 Aspengillosis
 Cryptococcus
 Bacterial sepsis