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1. CANDIDIASIS
DR.HAMISI MKINDI,MD.
TO DOWNLOAD CONTACT: hermyc@live.com

2. CANDIDIASIS

3. Introduction
• Candidiasis is an opportunistic infection caused by candida, a
type of fungi. Fungi are eukaryotic organisms found in the form
of yeasts,molds, or dimorphic fungi. Candida is a form of yeast.
• They can be found in the oral cavity, gastrointestinal tract, vagina,
penis,or other parts of the body.
• Species of candida include: C.albicans,C glabrata,
C.tropicalis,C.krusei,C. parapsilosis

4. Introduction…..
• Candidemia remain potentially fatal infection that result in significant
morbidity despite recent advances in antifungal.
• According to ( science direct.com-economic burden vol.21,5,2020)suggests
that candidemia is the fourth most leading cause of blood stream ‘
• The incidence of candidemia and intensive care is steadily increasing due
to the use of invasive procedures, intravascular catheters and many more.

5. BURDEN OF DISEASE
• Candida spp have been the fourth most common organisms recovered
from blood of hospitalized patients in US during the recent decades
when the widespread use of antibiotics was introduced.(M.A.Pfaller et
al epidemiology of invasive candidiasis 2017)
• David W Denning et al 2018 reports that ,globally recurrent
vulvovaginal candida affects about 138M women annually with global
annual prevalence of 3871 per 100000 women.
• 372 M women are affected by recurrent vulvovaginal candidiasis over
their lifetime and 25-34 years age group has highest prevalence of 9%

6. EPIDEMIOLOGY
• In East africa C. albicans are the most prominent spcc with prevelence of
69.3% followed by candida glabrata 12.9%.
• In Tanzania non.candida albican spcc wer reported to contribute about 37%
of candida vaginitis cases.(Martha et al 2019)
• Untreated candidiasis usually leads to disseminated candidiasis such
as osteomyelitis,arthritis,endocarditis, pericarditis, and meningitis.
• C.albicans is known to be the most common cause of candidiasis,
nonetheless increasing incidence of candidemia caused by non albicans
candida has also being reported and their potential to cause outbreaks
,higher resistance to antifungal drugs, and the ability to cause recurrent
infections has led to this scrunity.

7. • C.albicans 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
• Candida species are common colonizers of the human skin,vagina,and
the gut.

8. •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 with a partner having Candida vaginitis.
•There is relatively high incidence of carriage on the skin of
health care workers hence they can transmit the infection to
others

9. HOST FACTORS
•CUTANEOUS AND MUCOSAL FACTORS
•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.
iv. Low subq fat-has ant fungal activity

10. 2. Immune cells
•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 antigen
presentation to T cells and therefore to activation of specific
immunity.

11. Virulence factors
1. Adhesions
2. Biofilm
3. Polymorphism(yeast/pseudophal forms)
4. Invasins(Als3 in hyphae-attache to cadherin)
5. Secreted hydrolases
6. Hemolysins(degraded hb to obtain elemental iron)
7. Metabolic adaption

12. VIRULENCE FACTORS
• Adhesion of C.albicans to host tissues is a requisite for infection.
• Attachment of C.albicans to receptors on host tissues is aided by the
expression of a family of cell wall adhesions known as agglutinin like
sequences which comprise of eight genes of which ALS3 is the most
prominent as it is hyphal specific.
• The production of hyphae is a hallmark of the initiation of biofilm
formation followed by accumulation of an extracellular
polysaccharide matrix as biofilm matures.

13. VIRULENCE FACTORS
• The non adherent yeast cells are released from the biofilm into the
surrounding where they can colonize other surfaces.
• Dispersion of the biofilms associated cells carries great clinical
significance as released cells can initiate formation of new biofilms
or disseminate into host tissues hence associated with candidemia
and disseminated invasive disease.
• Quorum sensing or cell to cell communication
• C.albicans produces several extracellular released enzymes such as
lipases and esterases as well as hemolysin that are crucial for host
tissue invasion and nutrient acquisition

14. • These enzymes can directly induce damage to host cells, facilitate
hyphal growth for invasion of tissue,increase adherence following
exposure of receptor sites and degrade antibodies and other host
defense proteins.

15. Clinical manifestations
The discussion of these clinical manifestations is facilitated by their subdivision
into mucocutaneous and systemic involvement.
These clinical manifestations is facilitated by their subdivision into:-
1. Mucocutaneous eg Vulvovaginal, Oral candidiasis, Angular cheilitis,
Oesophagitis , Balanitis , Balanoposthitis , Chronic mucocutaneous candidiasis.
2. Systemic involvement, eg Candidemia and septicemia, Candiduria,
Endocarditis , Pulmonary candidiasis, Meningitis, Nosocomial candidiasis,
Arthritis ,Osteomyelitis.

16. SKIN CANDIDIASIS
• When an overgrowth of Candida develops on a skin,an infection can
occur.
• Candidiasis of skin can cause a red, itchy rush to form most
commonly in the fold of the skin.
• In some cases blisters and pustules may occur.
• These symptoms can usually be treated with improved hygiene and
antifungal creams or powder.

17. ORAL CANDIDIASIS

18. Candida Vaginitis or vulvovaginal candidiasis
(epidemiology)
Vulvo vaginal candidiasis is the fungal infection of the female lower genital tract.
According to Martha et al2015, is estimated that about 75% of women are affected with candida vaginitis at least
once during their lifetime with 15% of these casespresent with cyclic recurrent type which is defined as four or
more episodes of candida vaginitis in a year.
A study done in Aghakhan Kenya reported C.albicans species as the prominent species with prevalence of 69.3%
followed by C.glabrata12.9%.In Tanzania,non –candida albicans species were reported to contribute about 37% of
candida vaginitis cases.
A study done by Martha F. et al in 2015, whereby a study of 300 pregnant mothers was done to determine the
patterns of candida spp.causing vaginitis.
Laboratory confirmed candida vaginitis was detected in 65.7% of symptomatic pregnant mothers.Candida albicans
was the most predominant detected candida .72(24%)patients were diagnosed to have candida vaginitis caused
by non candida albicans.The predominant non candida albicans detected was candida tropicalis.

19. All isolated Candida albicans were highly susceptible to azole
antifungal agents.However C.krusei were highly resistant to
fluconazole and susceptible to other azole agents.
C.Glabrata and C.tropicalis are the commonest non albicans strains and
are more resistant to conventional therapies
Candida organisms gain access to the vaginal lumen and secretions
predominantly from the adjacent perianal area

20. RISK FACTORS OF VAGINAL CANDIDIASIS
 Loss of normal vaginal flora
 Diminished glycogen stores
 Immunosuppresion
 Sexual intercourse(oral receptive sex)
 Tight fitting undergarments leading to increased temperature
moisture,and local irritation
 Hygiene
 Increased PH

21. Candida Vaginitis/VVC Cont.
•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.
•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 (oral antibiotics), diminished glycogen stores (DM,
pregnancy and hormone replacement), increase of vaginal pH
(menstrual blood or semen) or tight-fitting undergarments
causing increase temp, moisture, and local irritation.

22. Candida Vaginitis/VVC Cont.
Clinical symptoms include
•leukorrhea,
•severe vaginal pruritus,
•external dysuria and
•dyspareunia.
•Gyn exam may reveal vulvar erythema and edema, vaginal
erythema, and thick cottage-cheese .

24. Is an opportunistic infection of the esophagus caused by
Candida albicans.
The disease usually occurs in patients with
 Immune suppression ( Malignancy, Diabetes, AIDS)
 Immunosuppressive drug therapy including post-
chemotherapy, broad spectrum antibiotics therapy
and corticosteroids in blood dyscrasia

25. Clinical Presentation
•Odynophagia (painful swallowing)
•Dysphagia (difficulty swallowing)
•Diffuse retrosternal pain
•Occasional nausea and vomiting

26. Therapy
• Fluconazole 200 mg p/o daily (preferred) x 14–21 days
• Itraconazole solution 200 mg p/o daily x 14–21 days
• Itraconazole also available in capsule but better absorption
with liquid formulation
• Ketoconazole rarely used due to erratic absorption

27. 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
If no Response to Fluconazole
•Check medication adherence
•Reconsider diagnosis
•Refer for (or do) endoscopy
•Consider resistance to azole therapy – especially if repeated
courses of azole treatment or if maintenance therapy used.

28. 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,
• Or asymptomatic

29. Mucocutaneous candidiasis

31. The following are the 4 types of oropharyngeal candidiasis
(OPC):-
1. Membranous candidiasis: creamy-white curdlike patches
2. Erythematous candidiasis: erythematous patch on the hard
and soft palates.
3. Chronic atrophic candidiasis (denture stomatitis)
4. Angular cheilitis

32. Therapy
- 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

33. INVASIVE CANDIDIASIS
• Candida can inter blood stream or internal organs and cause infection.
• Candida blood stream infection is termed as candidemia.
• Though candidemia it is the most invasive form, but infection can also
occur in heart,kidney,bones and other internal organs without being
detected in the blood.
• Candida albicans is the most common causative agent of candidemia.
• Non-candida albicans e.g C.glabrata also cause candidemia.
• Since 2015 there is an emerging species called C.auris with multidrug
resistance,difficult to dx and resistance to antiseptics used in hospital
settings.

34. Other forms of invasive candidiasis:
• Candida endocarditis.
• Suppurative thrombophlebitis
• Chronic diseminated candidiasis(hepatosplenic candidiasis)
• Candida osteoarticular infections.
• Candida infections of central nervous sytem.

38. Sign and symptoms
• Fever, chills that don’t improve after antibiotic treatment for
suspected bacterial infection.
• Other symptoms depend on the organ involved.
• Candida opthalmitis start as asymptomatic white retinal lesion but
progress to opacification of vitrous, irreversible scaring and
blindness(opthalmogic examination is indicated for all pt with
candidemia).

39. Diagnosis

40. • Candida species are commensals, their culture from body fluids
(sputum,vagina,urine,stool) does not signifies invasiveness.
• A characteristic lesion, histological examination and culture from
normally sterile sites(blood,CSF,pericardial fluid,biopsied tissue) are
necessary for confirmatory diagnosis.

41. diagnosis
• Invasive candidiasis is associated with high mortality especially in ICU
patients.
• In ICU patient with multiple diagnosis is difficult to diagnose invasive
candidiasis.
• Prompt initiation of antifungal has been shown to reduce mortality.
• However, impirical treatment before culture led to emergence of MDR
species.
• candida score is a bed site scoring system initiated for the purpose of
differentiating patients who would benefit from early antifungal treatment
from those whose invasive candidiasis is highly improbable.

42. Candida score

44. Laboratory examination:
• Microscopic examination:
• India ink wet mount of cerebrospinal fluid (CSF) highlights the capsule of
Cryptococcus neoformans; however, this method is insensitive (misses 50% of
cases).
• A Giemsa or Wright's stain of thick blood or bone marrow smear may detect
the intracellular Histoplasma capsulatum.
• Calcofluor white stain shows•
fungal elements in exudates and small skin
scales under a fluorescent microscope, giving them a fluorescent blue-white
appearance.

45. Histological
• Gomori methenamine-silver stain (fungi are stained dark gray to black)
• Periodic acid-Schiff reaction (fungi are stained hot pink to red)
• Gridley fungus stain (fungi are stained purplish rose with a yellow
background)

46. Culture
• must be specially ordered.
• use special media (e.g., Sabouraud's dextrose medium), enriched media (e.g.,
blood agar) with antibiotics to inhibit bacterial growth, and enriched media
with both antibiotics and cycloheximide (which inhibits many saprophytic
fungi).

47. Serologic testing
• is used to identify patient antibodies specific to the fungi.
• generally requires acute and convalescent sera.
Fungal antigen detection
• uses known antibodies to identify circulating fungal antigens in a patient's
serum, CSF, or urine.

49. Treatment of invasive candidiasis.
There are 3 major drug classes.
• Polyenes: Amphotericin B-3 to 5mg/kg IV once a day. (lipid
amphotericin B are less nephrotoxic)
• Azoles: (fungistatic effect): Fluconazole 800mg/ 12mg/kg orally or IV
once followed by 400mg/ 12mg/kg once a day.
• Echinocandins (fungicidal effect)
- caspofungin(loading dose 70mg IV then 50 mg IV once a day).
- Micafungin(100mg IV once a day).
-Anidulafungin(loading dose 200mg then 100mg IV once a day)

51. Conclusion:
• Candidemia: importance of early dx and appropriate therapy.
• Use of new diagnostic tools and clinical algorythm.
• Echinocandim first choice of treatment.
• Look for complications after CVC removal.f

52. REFERENCES
• Martha F.et al, High diversity of Candida glabrata in a Tertiary
Hospital-Mwanza Tanzania.
• Martha F et al,candida vaginitis among symptomatic pregnant
women.mwanza. Tanzania. 2019.
• Bitew and Abebaw :BMC Womens Health 2018
• Namkinga L.A et al,Prevalence and Risk Factors for vaginal candidiasis
amon women seeking primary care for genital infection in Dar es
salaam Vol.82.
• MSD MANUAL Proffesional Version.