FUNGAL INFECTIONS.pptx

FUNGAL INFECTIONS
MUHAMMED ALFAS M
PHARM D

DEFENITION :
• Fungi are ubiquitous microorganisms that differ from bacteria in their
cellular structure, and this makes them naturally resistant to antibacterial
agents .Fungi are broadly divided into yeasts and moulds. Yeasts are typically
round or oval shaped microscopically, grow flat round colonies on culture
plates and reproduce by forming buds from their cells. Moulds (e.g.
Aspergillus , Mucor) appear as a collection or mass (mycelium) of individual
tubular structures called hyphae that grow by branching and longitudinal
extension.
• There are hundreds of species of fungi found in the environment , but some
are mainly act as human pathogen .
• Fungal spore are spread by air, water and direct contact with infected source.
Humans usually become infected by inhalation of airborne spores or by
inoculation into traumatized skin and mucous membrane.
• This increase can be attributed, in part, to the growing numbers of
immunocompromised hosts as a result of organ transplants, cancer
chemotherapy, and the acquired immunodeficiency syndrome (AIDS)
epidemic.

• fungi are a cause of superficial infections of the skin and mucous
membranes. In some susceptible hosts whose immune system is
heavily compromised, deep-seated infections involving organs like
lungs and brain can manifest as ‘difficult to cure’ infections, for
example, pulmonary aspergillosis or cryptococcal meningitis.
1. Superficial fungal infection .
2. Invasive fungal infection .

SUPERFICIAL FUNGAL INFECTIONS
• Superficial fungal infections are benign infections of the skin, scalp
and nails caused by Candida albicans or dermatophytes.
• It grow in dark and moist areas and invade various parts of the body.
These infections are easily treatable in immunocompetent individuals.
• Superficial mycoses are among the most common infections in the
world and the second most common vaginal infections in North
America. Mucocutaneous candidiasis can occur in three forms—
oropharyngeal, esophageal, and vulvovaginal disease—with
oropharyngeal and vulvovaginal disease being the most common.
Over the past 15 to 20 years, the occurrence rates of some fungal
infections have increased dramatically. The prevalence of fungal skin
infections varies throughout different parts of the world, from the most
common causes of skin infections in the tropics to relatively rare
disorders in the United States.

VULVOVAGINAL CANDIDIASIS
FUNGUS
• Vulvovaginal candidiasis (VVC) refers to infections in
individuals
with or without symptoms who have positive vaginal cultures
for Candida species. Depending on episodic frequency, VVC
can be classified as either sporadic or recurrent.
This classification is essential to understand the
pathophysiology, as well as the pharmacotherapy, of VVC.
Furthermore, VVC may be defined as uncomplicated, which
refers to sporadic infections that are susceptible to all forms of
antifungal therapy regardless of the duration of treatment, or
complicated, in which consideration of factors affecting the
host, microorganism, and pharmacotherapy all have an
essential role in successful treatment.
Complicated VVC includes recurrent VVC, severe disease,
non– Candida albicans candidiasis, and host factors, including
diabetes mellitus, immunosuppression, and pregnancy.

PATHOPHYSIOLOGY
• C. albicans is the major pathogen responsible for VVC, accounting for 80%
to 92% of symptomatic episodes.
• Candida species can act as commensal members of the vaginal flora.
Asymptomatic colonization with Candida species has been found in 10% to
20% of women of reproductive age. Candida organisms are dimorphic;
blastospores are responsible for colonization (transmission and spread),
whereas germinated Candida forms are associated with tissue invasion and
symptomatic infections.To colonize the vagina, Candida species must be
able to attach to the mucosa. The attachment process is complex. Not only
are candidal surface structures important for attachment, but appropriate
receptors for attachment must be present in the epithelial tissue. Not all
women have the same range of receptors, which may explain variation in
colonization. Changes in the host’s vaginal environment or response are
necessary to induce a symptomatic infection. Unfortunately, in most cases
of symptomatic VVC, no precipitating factor can be identified

• Complicated VVC : It occurs in patients who are immunocompromised or
have uncontrolled diabetes mellitus.These individuals need a more
aggressive treatment plan.Current recommendations are to lengthen therapy
to 10 to 14 days regardless of the route of administration. Therapeutic
options include those listed in un complicated treatment plan . however,
regimens should be continued for 10 to 14 days. A study of oral
fluconazole therapy in women with complicated VVC demonstrated that
cure rates increased from 67% with single-dose therapy to 80% when the
150 mg dose of fluconazole was repeated 72 hours after the initial dose.
• Recurrent Vulvovaginal Candidiasis :Recurrent vulvovaginal candidiasis
(RVVC) is defined as having more than four episodes of VVC within a 12-
month period. A proper diagnosis should be obtained to rule out other
infections or nonmycotic contact dermatitis. RVVC is best treated in two
stages: an initial intensive stage followed by prolonged antifungal therapy to
achieve mycologic remission. The Infectious Diseases Society of America
recommends 10 to 14 days of induction therapy with a topical or oral azole,
followed by 150 mg of fluconazole once weekly for 6 months for recurring
Candida VVC.

ANTIFUNGAL-RESISTANT VULVOVAGINAL CANDIDIASIS
• Resistance to azole antimycotics should be considered in individuals who have
persistently positive yeast cultures and fail to respond to therapy despite
adherence to prescribed regimens.These infections can be treated with boric
acid or 5-flucytosine
• Boric acid is administered as a 600 mg intravaginal capsule daily for 14 days
of induction therapy, followed by a maintenance regimen of one capsule
intravaginally twice weekly.
• Boric acid is administered as a 600 mg intravaginal capsule daily for 14 days
of induction therapy, followed by a maintenance regimen of one capsule
intravaginally twice weekly

OROPHARYNGEALAND ESOPHAGEAL CANDIDIASIS
• Oropharyngeal candidiasis (OPC), or thrush, is a common and localized
infection of the oral mucosa caused by the yeast Candida. C. albicans, a
common oral commensal organism, is the most frequent infecting species.
OPC is also referred to as candidiasis (or the more correct but less
commonly used term candidosis). The infection may extend into the
esophagus, causing esophageal candidiasis.
• Candida carriage increases under immunocompromised
conditions and also among hospitalized patients . Even in
the era of highly active antiretroviral therapy (HAART)
up to 80% of human immunodeficiency virus (HIV)-
infected persons may demonstrate oral yeast
colonization. The organism is capable of transition to a
pathogen causing symptomatic mucosal infections in
association with predisposing host factors

• C. albicans is the predominant colonizing Candida species (70%-80%), but any of
the non-C. albicans species such as C. glabrata and C. tropicalis which may
account for 5% to 8%, respectively, can be colonizers.
RISK FACTORS FOR THE DEVELOPMENT OF OROPHARYNGEAL OR ESOPHAGEAL
CANDIDIASIS

Pathophysiology
• The pathogenesis of OPC is most clearly elucidated in the setting of HIV
infection. There appear to be several levels of immune defense against the
development of OPC in HIV-infected persons, and they involve both
systemic and local immunity. The primary line of host defense against C.
albicans is cell-mediated immunity (CMI) at the mucosal surfaces, which is
mediated by CD4 T cells.
• When the number of CD4 T cells drops too low, recruitment of these cells to
the oral cavity is impaired. The CD4 T-cell count is the hallmark predictor
for development of OPC. similar immunosuppression, such as lymphoma
and bone marrow transplant.
• When the primary line of defense fails, the secondary host defenses become
crucial. These include the CD8 T cells, salivary cytokines, and other innate
immune cells, such as the neutrophils, macrophages, and epithelial cells
(with anti-Candida activity).
• The problem with the CD8 T cells is caused more by a dysfunction of the
microenvironment, specifically, reduction in the E-cadherin adhesion
molecule that promotes migration of the cells through mucosal tissues

CLINICAL PRESENTATION OF OROPHARYNGEAL AND ESOPHAGEAL CANDIDIASIS
OROPHARYNGEAL CANDIDIASIS ESOPHAGEAL CANDIDIASIS
Symptoms : Symptoms are diverse and range
from none to a sore, painful mouth, burning
tongue, metallic taste, and dysphagia and
odynophagia with involvement of the
hypopharynx
Symptoms :Typically, the symptoms are
dysphagia, odynophagia, and retrosternal chest
pain but can be asymptomatic in some
patients; although rare, epigastric pain can be
the dominant symptom
Signs :Signs are variable and can include
diffuse erythema and white patches on the
surfaces of the buccal mucosa, throat, tongue,
or gums; constitutional signs are absent
Signs : Constitutional signs, including fever,
occasionally occur; physical findings can
range from a few to numerous white or beige
plaques of variable size
Plaques can be hyperemic or edematous, with
ulceration in more severe cases
Most advanced cases can occur with increased
mucosal friability and narrowing of lumen
Uncommon complications include perforation
and aortic–esophageal fistula formation

OROPHARYNGEAL CANDIDIASIS ESOPHAGEAL CANDIDIASIS
Laboratory tests : Scraping of an active
lesion for microscopic examination can
help confirm the diagnosis (presence of
pseudohyphae and budding yeast) but is
usually not necessary
Cultures are not necessary because
isolation of Candida species does not
distinguish between colonization and true
infection; cultures can be taken in patients
responding poorly to therapy to determine
the infecting species and to predict likely
drug resistance
Laboratory tests : The best test is upper
GI endoscopy (more useful than barium
swallow); helps exclude other causes of
esophagitis (eg, viral, aphthous ulcers);
diagnosis is confirmed by the histologic
presence of Candida species in biopsy
lesions taken during endoscopy
Cultures to look for drug-resistant
Candida species are warranted in patients
who require endoscopy

THERAPEUTIC OPTIONS FOR MUCOSAL
CANDIDIASIS

MYCOTIC INFECTIONS OF THE SKIN,
HAIR, AND NAILS
• Superficial cutaneous mycoses affect up to 20% to 25% of the global
population.65 The usual pathogens are the dermatophytes classified by
genera: Trichophyton, Epidermophyton, and Microsporum.
• Dermatophytes have the ability to penetrate keratinous structures of the
body and therefore infections are limited to hair, nails and skin. These
infections affect both male and female genders and all races.
• Risk factors for the development of an infection include prolonged exposure
to sweat or soaking in water, maceration, intertriginous folds, sharing
personal belongings such as combs, close living quarters
• Diagnosis usually is based on patient history, as well as the physical
examination. Diagnostic tests include direct microscopic examination of a
specimen after the addition of KOH or fungal cultures.

TINEA PEDIS TINEA MANUUM
Tinea pedis, also known as athlete's foot or foot ringworm
is an infection of the feet affecting soles, interdigital clefts
of toes, and nails with a dermatophyte fungus.
Tinea pedis is characterized by erythema, scaling,
maceration, and/or bulla formation. In most cases of
epidermal dermatophytosis, the infection occurs initially on
the feet, and, in time, spreads to sites such as the inguinal
area (tinea cruris), trunk (tinea corporis), hands (tinea
manuum).
Tinea manuum is a superficial fungal infection of one or
infrequently both hands, and can involve the feet (tinea
pedis). The infection presents with dry and hyperkeratotic
palmar surface of the hand. The fingernails, when
involved, may present with vesicles and scaling. Contact
dermatitis, eczema, psoriasis and callus formation should
be in the differential diagnosis
Tinea is also called ringworm, and manuum refers to it
being on the hands.

TINEA CRURIS TINEA CORPORIS
Tinea cruris is an infection of the proximal thighs and
buttocks. It is referred to as “jock itch” and is more
common in males.
Tinea cruris and tinea pedis often occur concurrently. High
humidity and warm temperatures along with wet or tight-
fitting clothes contribute to the development of tinea cruris.
The scrotum and penis often are spared from infection. The
lesions are red, scaling with raised borders. Itching and
burning are the most common patient complaint.
Tinea corporis, also known as ringworm, is an infection of
the glabrous skin of the trunk, extremities, or face. Lesions
of tinea corporis may be singular or multiple and appear as
round, scaly lesions with central clearing and a raised
border with sharp margination. The border may exhibit
pustules.

TINEA CAPITIS TINEA BARBAE
Tinea capitis is a mycotic infection involving the scalp, hair
follicles, and adjacent skin that primarily affects children
Approximately, 90% to 95% of tinea capitis cases are due to
Trichophyton tonsurans. Inanimate objects such as hats,
brushes, or pillowcases are often the source of transmission
particularly in the setting of poor hygiene. Viable organisms
can be recovered from shed hairs for up to a year. The
lesions are characterized by irregular, frequently well-
demarcated areas of alopecia with scaling. The alopecia is a
result of infected hairs breaking off a few millimeters from
the scalp; sometimes called “black dot alopecia.
Tinea barbae affects the hairs and follicles of beards and
mustaches of adult men and hirsute women. The differential
diagnosis included bacterial folliculitis, contact dermatitis,
perioral dermatitis, pseudofolliculitis barbae and herpes
simplex. One clue to the diagnosis of tinea barbae is that
hair removal with shaving is painless. Treatment is similar
to that for tinea capitis

PITYRIASIS VERSICOLOR ONYCHOMYCOSIS (TINEA UNGUIUM)
Hyper- and hypopigmented scaly patches characterize
pityriasis versicolor, which is also known as tinea versicolor.
It is caused by yeasts of the Malassezia genus which with the
exception of Malassezia pachydermatis, are all lipophilic. The
seborrheic areas (scalp, face, back and front of the trunk) of
the human body. This is not considered a contagious infection
given the source is normal flora. Lesions are described as
well-demarcated and scaling thin plaques with various degrees
of pigmentation. Most patients are asymptomatic or may
complain of mild pruritis. Many are concerned about the
cosmetic appearance and possible contagion.
Onychomycosis is a fungal infection of the nail apparatus and
is the most common single cause of nail dystrophy, affecting
up to 8% of the general population and accounting for up to
50% of all nail problems. Onychomycosis more commonly
affects the toenails. This can be because of the slower growth
of toenails (three times slower than fingernails), making it
easier for fungi to establish infection. Onychomycosis has a
significant impact on quality of life, both functional and
psychosocial. In addition, the affected nails can disrupt the
integrity of the surrounding skin, potentially increasing the
risk of secondary bacterial infections.

TREATMENT OF MYCOSES OF THE SKIN, HAIR, AND NAILS

Invasive Fungal Infections
Invasive fungal infection refers to rare cases in which the fungus spreads throughout
the body via the blood stream and invades other organ systems. Once established,
invasive fungal infections are extremely difficult to cure and, as a result, the associated
death rate is extremely high.
 General Patterns of Susceptibility and Interpretive Breakpoints of Candida Species

General Patterns of In-Vitro Susceptibility of Non-Candida Fungal
Pathogens
 PATHOGENESIS AND EPIDEMIOLOGY
• Systemic mycoses caused by primary or pathogenic fungi include histoplasmosis,
coccidioidomycosis, cryptococcosis, blastomycosis, paracoccidioidomycosis, and sporotrichosis.
• In contrast, mycoses caused by opportunistic fungi such as C. albicans, Aspergillus species,
Trichosporon, Torulopsis (Candida) glabrata, Fusarium, Alternaria, and Mucor generally are found
only in the immunocompromised host.

DIAGNOSIS
• evaluation of clinical symptoms :
serologic tests, and histopathologic examination and culture of clinical specimens.
TREATMENT
Invasive Mycoses
classified broadly as prophylaxis, early empirical therapy, empirical therapy, and
secondary prophylaxis or suppression..
Prophylactic therapy with topical, oral, or intravenous antifungal agents.
Prevention or treatment of infections caused by Candida and Aspergillus species in
patients taking cytotoxic chemotherapy : Antifungal therapy is given
Early empirical therapy systemic antifungal agents at the onset of fever and neutropenia
Empirical therapy with systemic antifungal agents is administered to granulocytopenic
patients with persistent or recurrent fever
Secondary prophylaxis (or suppressive therapy) is the administration of systemic
antifungal agents (generally prior to and throughout the period of granulocytopenia) to
prevent relapse of a documented invasive fungal infection.

PROPHYLAXIS OF FUNGAL INFECTION IN THE HIV-
INFECTED PATIENT
• Fluconazole : Cryptococcosis and local Candida
infections, including esophagitis, in HIV-infected
patients.
 HISTOPLASMOSIS
• It is caused by inhalation of dust-borne microconidia of the
dimorphic fungus H. capsulatum.
• Exist two dimorphic varieties : H. capsulatum, the small-
celled (2–5 microns) form (var. capsulatum) the largecelled
(8–15 microns) form (var. duboisii)
 PATHOPHYSIOLOGY

 CLINICAL MANIFESTATIONS AND THERAPY OF HISTOPLASMOSIS

Histoplasmosis in HIV-Infected Patients
• Adult patients with AIDS demonstrate an acute form of disseminated
disease that resembles the syndrome
seen in infants and children.
• Progressive disseminated histoplasmosis (PDH) can occur as the direct
result of initial infection or because of the reactivation of dormant foci.
• PDH is characterized by fever (75% of patients), weight loss, chills,
night sweats, enlargement of the spleen, liver, or lymph nodes, and
anaemia.

 DIAGNOSIS
• Direct examination or by histologic study of blood smears or tissues should raise strong suspicion of
infection with H. capsulatum because colonization does not occur as with Aspergillus or Candida infection.
• Suspected disseminated or chronic cavitary histoplasmosis two to three blood, sputum, and bone marrow
cultures and stains should be obtained using the lysis centrifugation technique
• Radioimmunoassay (RIA), which measures immunoglobulin M (IgM) and immunoglobulin G (IgG)
antibodies against a histoplasmin extract
BLASTOMYCOSIS
• It is a systemic fungal infection caused by Blastomyces dermatitidis, a dimorphic fungus that infects
primarily the lungs.
• Can present with a variety of pulmonary and extrapulmonary clinical manifestations. Pulmonary disease can
be acute or chronic and can mimic infection with tuberculosis, pyogenic bacteria, other fungi, or malignancy
• Approximately 40% of patients with blastomycosis present with skin, bone and joint, or genitourinary tract
involvement without any evidence of pulmonary disease
• Pulmonary infection probably occurs by inhalation of conidia, which convert to the yeast form in the lung.
 CLINICAL PRESENTATION
• fever, shaking chills, and productive, purulent cough, with or without hemoptysis, in immunocompetent
individuals.
Sporadic pulmonary blastomycosis : low-grade fever, night sweats, weight loss, and productive cough that
resembles tuberculosis rather than bacterial pneumonia

PATHOPHYSIOLOGY
Chronic pulmonary blastomycosis: fever,
malaise, weight loss, night sweats, chest pain,
and productive cough.
LABORATORY AND
DIAGNOSTIC TESTS
Direct microscopic visualization: of the large,
multinucleated yeast with single, broad-based
buds in sputum or other respiratory specimens
following digestion of cells and debris with 10%
potassium hydroxide.
Histopathologic examination of tissue biopsies
and culture of secretions also should be used to
identify B. dermatitidis

COCCIDIOIDOMYCOSIS
• It is caused by infection with Coccidioides immitis
• Coccidioides immitis grows in the soil as a mold, and mycelia proliferate during the rainy season. During the
dry season, resistant arthroconidia form and become airborne when the soil is disturbed.
• feeling of tiredness, loss of smell and taste, fever,
cough, headaches, rash, muscle pain, and joint pain
• Chronic fibrocavitary disease: cough (sometimes
productive of mucus), fevers, night sweats, and weight
loss.
• Valley fever: erythema nodosum and erythema
multiforme of the upper trunk and extremities in
association with diffuse joint aches or fever
• Disseminated disease: skin, lymph nodes, bone,
and meninges, although the spleen, liver, kidney, and
adrenal gland also can be involved.
• CNS infection: headache, weakness, changes in
mental status (lethargy and confusion), neck
stiffness, low-grade fever, weight loss, and
occasionally, hydrocephalus.
 DIAGNOSIS
• microscopic detection : cells in body fluids,
exudates, sputum and biopsy tissue
• PCR
• Serologic analysis : fungal antigen or
host IgM or IgG antibody produced against the fungus
Imaging
• Chest X-rays : demonstrate lung opacification, pleural
effusions, or enlargement of lymph nodes associated with
the lungs
• CT scans

TREATMENT
SPECIFIC AGENTS
• chronic pulmonary or disseminated infections: Azole antifungals, primarily fluconazole and
itraconazole
• Respiratory failure because of infection with Coccidioides species, those with rapidly progressive
coccidioidal infections, or women during pregnancy: Amphotericin B
• Specific antifungals: intravenous amphotericin B (0.5 to 1.5 mg/kg per day), ketoconazole (400 mg/day
orally), intravenous or oral fluconazole (usually 400 to 800 mg/day, although dosages as high as 1200
mg/day have been used without complications), and itraconazole (200 to 300 mg orally twice daily or
three times daily, as either capsules or solution).
• Amphotericin B: rapidly progressive disease
PRIMARY RESPIRATORY INFECTION
• Commonly prescribed therapies: oral azole antifungals at their recommended doses for courses of
therapy ranging from 3 to 6 months
• Diffuse pneumonia with bilateral reticulonodular or miliary infiltrates: amphotericin B, Consolidation
therapy with oral azoles
INFECTIONS OF THE PULMONARY CAVITY
• Symptomatic patients can benefit from oral azole therapy.

• disease located outside the lungs : 400 mg/ of an oral azole
• Amphotericin B is an alternative therapy ,Patients with worsening lesions or with disease in the vertebral column.
EXTRAPULMONARY (DISSEMINATED) DISEASE
Nonmeningeal Disease
Meningeal Disease
• Fluconazole 400 mg/day : coccidioidal meningitis.
• Itraconazole 400 to 600 mg/day : comparably effective
• The intrathecal dose: amphotericin B ranges from 0.01 to 1.5 mg daily to weekly
CRYPTOCOCCOSIS
It is a noncontagious, systemic mycotic infection caused by the ubiquitous encapsulated soil yeast Cryptococcus
neoformans, which is found in soil, particularly in pigeon droppings, although disease occurs throughout the world,
even in areas where pigeons are absent. Infection is acquired by inhalation of the organism.
• cough, rales, and shortness of breath
• AIDS patients, the symptoms of cryptococcal meningitis
are nonspecific ,fever and headache are common
• Headache, fever, nausea, vomiting, mental status changes,
and neck stiffness generally are observed
• Less common symptoms include visual disturbances
(photophobia and blurred vision), papilledema, seizures,
and aphasia.
 Laboratory Tests
CSF opening pressure generally is elevated.
CSF pleocytosis (usually lymphocytes), leukocytosis, a
decreased glucose concentration, and an elevated CSF
protein concentration.
There is also a positive cryptococcal antigen (detected by
LA).

CANDIDA INFECTIONS
• Candida species are yeasts that exist primarily as small (4–6 microns), unicellular, thin-walled, ovoid cells that
reproduce by budding.
• On agar medium, they form smooth, white, creamy colonies resembling staphylococci. Although there are more
than 150 species of Candida, eight species—C. albicans, C. tropicalis, Candida parapsilosis, C. krusei, Candida
stellatoidea, C. guilliermondii, C. lusitaniae, and C. glabrata— are regarded as clinically important pathogens in
human disease.
• 13 Yeast forms, hyphae, and pseudohyphae can be found in clinical specimens
1. HEMATOGENOUS CANDIDIASIS
Hematogenous candida endophthalmitis, which has a characteristic finding of single or multiple fluffy white cotton
ball-like chorioretinal lesions often extending into vitreous, is the most fulminant manifestation of systemic
candidiasis and may result in blindness

• Dissemination of C. Albicans can result in infection in single or multiple organs, particularly the kidney, brain, myocardium,
skin, eye, bone, and joints.
• multiple micro- and macroabscesses are formed.
1. Patients present with the acute onset of fever, tachycardia, tachypnea, and occasionally, chills or hypotension.The clinical
presentation generally is indistinguishable from that seen with sepsis of bacterial origin..
2. Patients develop intermittent fevers and are ill only when febrile.
3. Patient manifests progressive deterioration of their condition with or without fever.
4. Hepatosplenic candidiasis often is manifested only as fever while the patient remains neutropenic (1000WBCs/mm3)
• Candida protein antigens, serum antibodies to
Candida, and antibodies to cell wall components such
as mannan
• cultures of the skin, mouth, sputum, feces, or urine
• imaging studies can detect the presence of abscess or
microabscesses in the liver and spleen
• peptide nucleic acid (PNA)
• fluorescence in situ hybridization (FISH)
 Laboratory Tests

CANDIDURIA
Within the urinary tract, most common lesions are either Candida cystitis or hematogenously disseminated renal abscesses.
Candida cystitis often follows catheterization or therapy with broad-spectrum antimicrobial agents
 DIAGNOSIS : of Candida cystitis can be problematic because of the frequent presence of Candida pseudohyphae and
yeast cells in urine specimens secondary to urethral colonization.
 TREATMENT
• Initial therapy : should focus on removal of urinary catheters whenever possible
• Fluconazole 200 mg/day for 14 days
• Bladder irrigation with amphotericin B (50 mg in 500 mL sterile water instilled twice daily into the bladder via a three-way
catheter)
ASPERGILLOSIS
Aspergillosis is an infection caused by a type of mold (fungus). The illnesses resulting from aspergillosis infection usually
affect the respiratory system, but their signs and severity vary greatly. The mold that triggers the illnesses, aspergillus, is
everywhere — indoors and outdoors.
 CLINICAL MANIFESTATIONS
Cough , Wheezing, Coughing up blood , Shortness of breath , Fever, Stuffy nose, Runny nose, Headache, Chest pain, Skin lesions

Allergic Bronchopulmonary Aspergillosis
• BPA, which is almost always caused by A. fumigatus,
is characterized by severe asthma with wheezing,
fever, malaise, weight loss, chest pain, and a cough
productive of blood-streaked sputum.
• Recurrent episodes of severe asthma, the disease
usually progresses to fibrosis and bronchiectasis with
granuloma formation.
• When Aspergillus conidia become trapped in the
viscous mucus of asthmatic patients, BPA develops.
• An immunoglobulin E (IgE)-mediated (type I) immune
reaction results in bronchospasm, eosinophilia, and
immediate skin reactivity.
• administration of parenteral corticosteroids clears lung
infiltrates
• Itraconazole 200 mg twice daily for 16 weeks

 Aspergilloma
• Aspergillus infections of the sinuses most commonly
occur as saprophytic colonization (aspergillomas or
“fungus balls”) of previously abnormal sinus tissue
• Infection usually is localized in the maxillary sinus and
rarely is associated with local invasion of adjacent
bone or brain tissue
• Sinus aspergillosis also can present as allergic sinusitis
with nasal drainage of brownish mucous plugs
• Therapy with corticosteroids and surgery
• Combination of antifungal and surgical therapy
generally is required
• Diagnosis of aspergilloma : chest radiographs, on
which aspergillomas appear as a solid rounded mass,
sometimes mobile, of water density within a spherical
or ovoid cavity and separated from the wall of the
cavity by an airspace of variable size and shape.
• Chest pain, dyspnea, and sputum production
• Hemoptysis : because of ulceration of the epithelial
lining of the cavity with formation of granulation
tissue.

 Invasive Aspergillosis
• Aspergillus conidia causes ivasive aspergillosis
• Phagocytes (neutrophils, monocytes, and
macrophages) rather than antibodies or lymphocytes
constitute the primary host defense system against
invasive disease with aspergillosis
• Corticosteroids
• Macrophages prevent germination of conidia and also
eradicate conidia, providing the first line of defense
against invasive disease.
• Neutrophils halt hyphal growth and dissemination and
kill mycelia, constituting a second line of defense
• Therapy with amphotericin B 0.5 mg/kg per day or
itraconazole 200 to 600 mg/day.
CLINICAL PRESENTATION
• Acute pulmonary embolus: pleuritic chest pain, fever,
hemoptysis, and friction rubs.
• The CNS, liver, spleen, heart, GI tract, pericardium,
and other body sites are involved in a substantial
minority of cases.
Diagnosis
• Demonstration of Aspergillus by repeated culture and
microscopic examination of tissue
• Galactomannan levels : Double-sandwich enzyme
immunosorbent assay (EIA)
• BG test : Detection of BG in serum uses a
chromogenic variant of the limulus amoebocyte lysate
assay.
• CT abnormalities are best documented in neutropenic
marrow transplant recipients

Patient Counseling:
• Clean the oral cavity prior to administering the topical antifungal agent. Daily fluoride rinses can help reduce the
risk of caries when using an agent containing sucrose or dextrose.
• Use the topical antifungal agent after meals, as saliva flow and mouth movements can reduce the contact time
• Troches should be slowly dissolved in the mouth, not chewed or swallowed whole, over 15-20 minutes, and the
saliva swallowed.
• Suspension should be swished around the mouth in the oral cavity to cover all areas for aslong as possible,
ideally at least 1 minute, then gargled and swallowed.
• Remove dentures while medication is being applied to the oral tissues.
• Use a suspension or buccal mucoadhesive tablet instead of a troche if xerostomia is present; if a troche is
preferred, the patient should rinse or drink water prior to dosing. For xerostomia, suggest nonpharmacologic
measures for symptomatic relief (eg, ice chips, sugarless gum or hard candy, citrus beverages).
• Dentures should be removed and disinfected overnight using an antiseptic solution (eg, chlorhexidine 0.12%-
0.2%). Disinfect oral tissues in addition to dental prosthesis.
• Complete treatment course even though symptomatic improvement can occur in 48-72 hours.
• Maintain good oral hygiene. Brush teeth daily (twice daily) and floss, rinse mouth, or brush teeth after eating
sweets.
• Stop smoking; avoid alcohol.

• Shower regularly and dry yourself completely before dressing
• Avoid wearing tight garments such as jeans, leggings and jeggings. Wear loose fitting cotton garments
• Don’t share your bed linen, towel and clothes.
• Dry the clothes inside out. Wear well dried inner garments after about 3-4 days of washing if ironing is not
possible.
• Remove waistband, wristband etc.
• In case of tinea cruris or jock itch, (fungal infections in the groin area), wear “boxer shorts” instead of the tight
fitting ones(Frenchie) that hug the groin and cut into it.
• Wear non-occlusive (open-loose) footwear like sandals etc. if possible.
• Sensitize people about the morbidities associated with obesity and encourage them to lose weight.
• Regular removal of hair on genitalia.
• Keeping scalp clean and do not share combs, hairbrushes, hats or helmets.
• Vacuuming is considered the best method if possible. Wet moping may be ideal in our country.
• Washable surfaces should be cleaned thoroughly with detergent soap and hot water.
• This should be repeated at least once daily for 4-6 weeks until all affected persons have eliminated fungal
infection.
• Please consult your dermatologist for any fungal infection and take your medicine as advised by
your dermatologist.

FUNGAL INFECTIONS.pptx

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