Basic Mycology Guide

MYCOLOGY
BASIC MYCOLOGY
I. STRUCTURES & GROWTH
FUNGI multicellular heterotrophic members of the plant kingdom that lack roots & stems & are referred
to as THALLOPHYTES
- bec fungi are eukaryotic organisms whereas bacteria are prokaryotic they differ in several
fundamental respects (Table 47-1)
** Eukaryotes ** Prokaryotes
- larger ribosomes (80s) - smaller ribosomes (70s)
- possess a true nucleus w/ nuclear membrane - noncompartmentalized
- compartmentalized (w/ membrane bound organelles) - ex. Bacteria
-ex. Fungi, algae, viruses, protozoa, animal & plant cells
Table 47-1 Comparison of fungi and bacteria

Feature Fungi Bacteria
Diameter Approximately 4 m (Candida) Approximately 1 m
(Staphylococcus)
Nucleus Eukaryotic Prokaryotic
Cytoplasm Mitochondria and Endoplasmic Mitochondria and Endoplasmic
reticulum present reticulum absent
Cell membrane Sterols present Sterols Absent (except
Mycoplasma)
Cell wall content Chitin Peptidoglycan
Spores Sexual and asexual spores for Endospores for survival, not for
reproduction reproduction
Thermal dimorphism Yes (some) No
Metabolism Require organic carbon; no Many do not require organic
obligate anaerobes carbon; many obligate anaerobes
2 Fungal cell structures are important medically:

1. the fungal cell wall consists primarily of chitin (not peptidoglycan as in bacteria); thus fungi are
insensitive to antibiotics such as penicillin, that inhibit peptidoglycan synthesis
2. the fungal cell membrane contains ergosterol & symosterol, in contrast to human cell membranes,
w/c contain cholesterol
2 Types of fungi:
1. yeasts = grow as single cells that reproduce by asexual budding
2. molds = grow as long filaments (hyphae) & form a mat (mycelium)
THALLUS = actively growing vegetative portion

HYPHAE = filaments or threadlike fungal structures
A. septate hyphae when hyphae form transverse walls
B. nonseptate hyphae doesnt form a transverse wall & are multinucleated (coencytic)
MYCELIA (MYCELIUM) = mass or group of countless intertwined hyphae
* TWO TYPES OF MYCELIA *
1. Aerial mycelium that part of the growth that projects above the surface of the substrate &
produce the spores
2. Vegetative mycelium that part of the growth that penetrates the substrate & absorbs food
@ Several important fungi are thermally DIMORPHIC (they form different structures at different temp.)
exist as molds in the saprophytic, free-living state at ambient temp
as yeasts in host tissues at body temp
@ Most fungi are obligate aerobes, some are facultative anaerobes; but NONE are OBLIGATE
ANAEROBES.
@ ALL fungi REQUIRE a preformed organic source of CARBON, hence their frequent association w/
decaying matter.
@ Normal habitat of fungi is the ENVIRONMENT; except Candida albicans (w/c is a part of human
normal flora)
SPORES structure set aside for reproduction

* KINDS OF SPORES *
1. SEXUAL SPORES - some fungi reproduce sexually by mating & forming sexual spores
* Fungi that exhibit a sexual phase are called perfect fungi & those that dont form sexual spores
are termed imperfect & are classified as Fungi imperfecti.
A. Ascospores = sexual spores contained/formed in special sacs called asci (ascus)
B. Basidiospores = sexual spores formed externally at the end of club-shaped structures
called basidia (basidium)
C. Zygospores = formed by conjugation between two morphologically identical cells; are
single large spres w/ thick wall
D. Oospores = sexual spores formed by heterogenous fertilization
2. ASEXUAL SPORES must fungi of medical interest propagate asexually by forming CONIDIA
(asexual spores) from the sides or ends of specialized structure (Fig. 47-1)
- some important conidia:
A. Blastospores = buds formed by a process of sprouting from the surface of the parent
cell (ex. Candida, Cryptococcus)
B. Arthrospores = spores resulting from a hyphae fragmentized into individual cells &
are the mode of transmission of Coccidioides immitis
(ex. Coccidioides)
C. Chlamydospores = large, round, thick-walled unicellular structures formed by the
enlargement of a hyphal cell & quite resistant (ex. Candida albicans)
D. Sporangiospores = are formed w/in a sac (sporangium) on a stalk by molds such as
Rhizopus & Mucor
@ CONIDIA asexual spores produced singly or in groups by specialized vegetative hyphal strands called
conidia spores
1. Macroconidia or Fuscaux large, spindle-shaped or club-shaped bodies divided into 2 or
more cells by septa
2. Microconidia small, unicellular, round, elliptical or pyriform shaped conidia
PHIALIDE a flask-shaped projection from the mycelium of certain fungi

PENICILLUS a brush-like structure arising from conidia spores
@ Though we focus on the fungi that are human pathogens, it should be remembered that fungi are used
in the production of important foods (ex. bread, cheese, wine, & beer). Fungi are also responsible for the
spoilage of certain foods, fruits, grains, vegetables, & jams, bec molds can grow in a drier, more acidic, &
higher osmotic pressure environment than bacteria.
II. PATHOGENESIS
Granulomas = is the form/response to infection w/ many fungi; are produced in the
major systemic fungal diseases
= involves a cell-mediated immune response w/c is suppressed
DELAYED HYPERSENSITIVITY SKIN TEST response to certain fungal Ags injected
intradermally
= a (+) skin test indicates exposure to the fungal Ag not a current infection
Fungi do not have endotoxin in their cell walls & do not produce bacterial-type exotoxins
Intact skin is an effective host defense against certain fungi
Fatty acids in the skin inhibit dermatophyte growth
Hormone-associated skin changes at puberty limit ringworm of the scalp caused by
Trichophyton
Normal flora of the skin & mucous membranes suppress fungi = when NF are inhibited
ex by antibiotics, overgrowth of fungi such as C. albicans can occur
= mucous membrane of the nasopharynx trap inhaled fungi
@ The transmission & geographic locations of some important fungi are described in Table 47-2:
Table 47-2 transmission of some important fungi
Genus Habitat Form of Organism Portal of Entry Endemic Geographic
Transmitted Location
Coccidioides Soil Arthrospores Inhalation into lungs Southwestern USA AND
Latin America
Histoplasma Soil (associated Micronidia Inhalation to lungs Mississipi and Ohio River
w/ bird feces) Valleys
Blastomyces Soil Microconidia Inhalation to lungs States east of Mississipi
River
Paracoccidioides Soil Uncertain Inhalation to lungs Latin America
Cryptococcus Soil (associated Yeast Inhalation to lungs Worldwide
w/ pigeon feces)
Aspergillus Soil and Conidia Inhalation into lungs Worldwide
vegetation
Candida Human body Yeast Normal flora of skin, Worldwide
mouth, gastrointestinal
tract, and vagina
III. FUNGAL TOXINS & ALLERGIES

In addition to mycotic infections, there are 2 other kinds of fungal disease:
1. mycotoxicoses = caused by ingested toxins
= among the most potent hepatotoxins: a) amanitin
b) phalloidin
= ergotism is an mycotoxicosis caused by mold Claviceps purpura
= aflatoxins, an ingested toxins produced by Aspergillus flavus, that cause liver
damage & tumors in animals & human hepatic carcinoma
2. allergies = to fungal spores

= are manifested primarily by an asthmatic reaction (rapid bronchoconstriction
mediated by IgE), eosinophilia, & a wheal & flare immediate skin test rxn
IV. LABORATORY DIAGNOSIS

@ 3 Approaches to lab diagnosis of fungal diseases:
1. direct microscopic examination = specimen used are sputum, lung biopsy material, & skin
scrapings depends on the finding characteristic asexual spores, hyphae, or yeasts in the
light microscope
= the specimen is either treated with 10% KOH to dissolve tissue material, leaving the
alkali-resistant fungi intact
= stained w/ special fungal stains
= diagnostically important findings made by direct examination are:
A. the spherules of Coccidioides immitis
B. the wide capsule of Cryptococcus neoformans seen in India Ink preparation of
spinal fluid
2. culture of the organism = fungi are frequently cultured on Sabourauds agar
3. serologic tests = test for the presence of Abs in the patients serum or spinal fluid are useful in
diagnosing the systemic mycoses; but less so in diagnosing other fungal infections
= a significant rise in the Ab titer must be observed to confirm a diagnosis
= complement fixation test is most frequenly used
= in cryptococcal meningitis, the presence of the polysaccharise capsular Ags of
Cryptococcus neoformans in the spinal fluid can be detect by the latex agglutinatiojn test
V. ANTIFUNGAL THERAPY
@ Amphotericin B = most important antifungal drug; used in the treatment of a variety of
disseminated fungal diseases
MYCOSES
MYCOSES = are diseases of fungal etiology

= medical mycoses can be divided into 4 categories:
1. cutaneous
2. subcutaneous
3. systemic
4. opportunistic
@ CLASSIFICATION / CATEGORIES:
I. SUPERFICIAL OR CUTANEOUS MYCOSES are fungal infection that infects only superficial
keratinized structures (the hair, skin & nails ) w/o invasion of the tissue
A. Dermatomycoses or Dermatophytoses = are caused by fungi (Dermatophytes); most common
fungal infections of humans & are usually referred to as TINEA or ringworm
= are chronic infections favored by heat & humidity
= characterized by pruritic papules & vesicles, broken hairs, & thickened, broken nails
Examples: Tinea corporis ringworm of the body
Tinea capitis ringworm of the scalp & hair
Tinea unguimm ringworm of the nails
Tinea pedis ringworm of the feet (Athletes foot)
Tinea barbae ringworm of the beard
Tinea cruris ringworm of the groin
= only three fungi are associated with Dermatomycoses: (spread from infected persons by
direct contact)
1. Epidermophyton affecting skin & nails
2. Microsporum affecting skin & hair; spread from animals such as dogs & cats
- this indicates that to prevent reinfection, the animal must be treated
also
3. Trichophyton affecting skin, hair, & nails
= Lab Dx:
1. scrapings of skin or nail placed in 10% KOH on a glass slide show hyphae under
microscopy
2. culture on Sabourauds agar at rm temp develop typical hyphae & conidia
= Treatment: antifungal creams (undecylenic acid, miconazole, tolnaftate, etc) or oral
griseofulvin
= Prevention:: centers on keeping skin dry & cool
B. Tinea versicolor or Pityriasis versicolor = skin disease characterized by brownish scaly, itchy
areas caused by Malassezia furfur (New name: Pityrosporum orbicular)
= lesions are usually noticed as hypopigmented areas esp on tanned skin in the
summer; lesions contain both budding yeast cells & hyphae
= usually the infection is asymptomatic
= occurs more frequently in hot, humid weather
= Lab Dx: KOH wet mount, culture is usually done
= Treatment: topical miconazole (but the lesions have a tendency to recur & a
permanent cure is difficult to achieve)
C. Tinea nigra = manifested as light brown to blackish spot due to the melaninlike pigment in the
hyphae; located on the palmar & plantar surfaces caused by Cladosporium or Exophiala
werneckii
= causative agent is found in the soil & transmitted during injury
= Lab Dx: microscopic examination & culture of skin scrapings
= Treatment: topical keratolytic agent ex salicylic acid
D. Piedra = fungal infection of the hair characterized by nodules on the distal shaft
Two Types: a. Black piedra caused by Piedraia tortai
b. White piedra caused by Trichospores beigelii
CHARACTERISTICS OF THE MORE COMMON ISOLATED DERMATOPHYTES
DERMATOPHYTES COLONIAL GROWTH MICROSCOPIC

MORPHOLOGY RATE MORPHOLOGY
A. Epidermophyton center of colony 1 week Macroconidia large, smooth-walled

floccosum tends to be folded multiseptate, clavate & borne sin-
gly or in clusters of 2 or 3 (banana
clusters), or no microconidia
B. Microsporum
1. M. audouinii velvety aerial mycelium 2 weeks sterile hyphae,terminal chlamydos-
cause of epide- that is colorless to lt gray pores, macroconidia rarely seen-
mic Tinea to tan; reverse tan to bizarre shaped if seen; microconi-
capitis; infected salmon pink dia reare or absent
hair fluoresce
yellow green
using Woods
light
2. M. canis granular or cottony w/ 1 week thick-walled spindle shaped, multi-

infected hair feathery periphery, cen- septate, rough-walled macroconi-
fluoresce bright ter of colony are white to dia some w/ curved tips; microco-
yellow green buff w/ lemon yellow or nidia rare
yellow orange fringe at the
periphery; reverse side is
bright yellow or orange or
reddish brown with age
3. M. gypseus cinnamon colored, 1 week rough-thin walled, elliptical multi-

no fluorescence powdery colony; septate macroconidia w/ ??????
observed reverse light tan surface
C. Trichophyton
1. T. mentagro- cottony to granular, 7-10 days many round to globose microconi-
phytes white to cream colored dia most commonly in grapelike
to yellow; reverse side clusters or laterally along hyphae
buff to reddish brown spiral hyphae may be seen; macro-
conidia if seen are thin-walled,
smooth,club-shaped & multiseptate
2. T. tonsurans white, tan to yellow or 7-14 days microconidia are teardrop or club-
rust, suidelike to powdery, shaped w/ flat bottoms marcoconi-
wrinkled w/ heaped or dia rare & balloon forms found
sunken center reverse when present
side yellow to tan to
rust red
3. T. rubrum flat or heaped up colony, 2 weeks delicate hyphae w/ tear-shaped

white to reddish w/ a microconidia produced laterally a-
cottony or velvety sur- long filaments, marcroconidia
face; reverse side wine usually absent, when present are
red or cherry red smooth, thin walled & pencil
shaped
4. T. violaceum portwine to deep violet 2-3 weeks no conidia as a rule hyphae tor-
colony, may be heaped tuous and tangled
or flat w/ waxy glabrous
surface
5. T. schoenleinii irregularly heaped 2-3 weeks many antler type hyphae (FAVIC
causing FAVUS smooth white to cream CHANDELIER)
severe infection colored w/ radiating
of scalp & hair grooves
6. T. verrucosum glabrous to velvety 2-3 weeks microconidia rare large & teardrop
white rare strains pro- when seen; macroconidia extreme-
duce yellow brown ly rare, but form char rat tail
color, rugal folds w/ types when seen, many chlamydo-
tendency to sunk into spores seen
agar surface
II. SUBCUTANEOUS MYCOSES = are caused by fungi that grow in soil & on vegetation & are
introduced into subcutaneous tissue through trauma
A. Sporotrichosis = also known as rose gardeners disease caused by Sporothrix schenckii w/c is
dimorphic fungus that lives on vegetation:
** Mycelial Phase: Colony-w/in 7 days moist, white leathery colonies appearance,
radiating furrow develop & w/ age the colony takes on a wrinkled appearance;
the white growth darkens & may become brown to black
** Yeast Phase: small, oval to cigar-shaped budding yeast cells (seen in tissue spn)
= Lab Dx:
@ microsopic: hyphae are delicate, septate, exhibit branchings & bear one-celled
pyriform shaped conidia borne bouquetlike
@ in culture: hyphae occur bearing oval conidia in clusters at the tip of slender
conidiophores (resembling a daisy)
= when introduced into the skin, typically by a thorn; it causes a local pustule or ulcer
w/ nodules alon the draining lymphatics
= little systemic illness; lesions may be chronic
= Treatment: oral potassium iodide or ketoconazole
= Prevention: protecting skin when touching plants, moss, & wood
B. Chromoblastomycosis or Chromomycosis = a slowly progressive granulomatous infection that is
caused by several soil fungi
= introduced into the skin through trauma; wartlike lesions w/ crusting abscesses extend
along the lymphatics
= the disease occurs mainly in the tropics & is found on bare feet & legs
= Lab Dx: dark brown, round fungal cells are seen in leukocytes or giant cells
= Treatment: oral flucytosine or thiabendazole, plus local surgery
Etiologic Agents Diagnostic Features
1. Cladosporium carrionii = long chains of elliptical conidia borne from erect, tall branching
conidiophores
2. Phialophora verrucosa = tubelike or flank-shaped phialides each w/ a distinct collarette
3. Fonsecae compacta = conical heads w/ sympodial arrangement of conidia
Fonsecae pedrosoi
Colonies: All are slow growing & produce heaped up & slightly folded, darkly
pigmented colonies w/ a grayish velvety appearance. The reverse side is jet
black.
C. Mycetoma (Maduromycosis) = most common cause of Pseudallescheria boydii (sexual form);

asexual form is Scodosporium apiospernum
= soil organisms (Petriellidium, Madurella) enter through wounds on the feet, hands, or
back & cause abscesses, w/ pus discharged through sinuses; the pus contains compact
colored granules
= Lab Dx:
** Colonies: white fluffy colony that changes in several weeks to a brownish gray
mycelium. Reverse is black
** Microscopic: elliptical single-celled conidia borne singly from the tips of
conidiospores
= Treatment: no effective drug against the fungal form; surgical excision is
recommended
D. Rhinosperidiosis = caused by Rhinosporidium seeberi
E. Lobomycosis = caused by Loboa loboi
III. DEEP OR SYSTEMIC MYCOSES caused by soil fungi & infection is acquired through inhalation;
of the spores of dimorphic fungi
- fungi causing deep mycoses are DIMORPHIC
- they have 2 phases of growth:
A. Yeast phase, tissue phase or parasitic form = takes place at 37C; w/in the lungs
B. Mycelial phase or saprophytic form = take place at room temperature; in the soil
- most lung infections are asymptomatic & self-limited; however, some persons develop
disseminated disease in which the organisms grow in other organs, cause destructive
lesions, & may result in death
- infected persons do not communicate these disease to others
A. Coccidioides
@ Disease: Coccidioides immitis causes coccidioidomycosis
@ Properties:
C. immitis is a dimorphic fungus that exists as a mold in soil & as a sperule in tissue
@ Transmission & Epidemiology:
the fungus is endemic in the arid regions of southwestern USA & Latin America
in soil, it forms hyphae w/ alternating arthrospores & empty cells
arthrospores are very light & are carried by the wind thus they can be inhaled & infect the
lungs
@ Pathogenesis
in the lungs, arthrospores form spherules that are large, thick & are filled w/ endospores
upon the rupture of the wall, endospores are released & differentiate to form new
spherules
the organism can spread by direct extension or via the bloodstream
dissemination indicates some defect in cell-mediated immunity; most persons who
develop a positive skin test to infection develop immunity to spread & to reinfection
@ Clinical Findings:
some infected persons have an influenzalike illness w/ fever & cough; 50% have changes
in the lungs as seen in x-rays, 10% develop erythema nodosum or arthralgias==this
syndrome is called valley fever or desert rheumatism
the incidence of dissemination in Filipinos & blacks is 10 times higher than the usual 1%;
as well as pregnant women in the 3rd trimester have increased dissemination
(EN) erythema nodosum manifests as red, tender nodules on extensor surfaces such as the
shins; it is delayed (cell-mediated) hypersensitivity response to fungal Ags & thus is an
indicator of a good prognosis
@ Laboratory Diagnosis:
in tissue specimens, spherules are seen microscopically
cultures on Sabourauds agar show hyphae w/ arthrospores (CAUTION: cultures are
highly infectious; precautions against inhaling arthrospores must be taken)
in infected persons, skin tests w/ fungal extracts (coccidioidin or spherulin) cause at least
a 5-mm in duration 48 hours after injection (delayed hypersensitivity reaction)
skin tests become positive w/in 2-4 weeks of infection & remain so for years but are often
negative (anergy) in patients w/ disseminated disease
@ Treatment & Prevention:
no treatment is needed in asymptomatic or mild primary infection
amphotericin B = used for persisting lung lesions or disseminated disease
ketoconazole = also effective in lung disease
no means of prevention except avoiding travel to endemic areas
B. Histoplasma
@ Disease: Histoplasma capsulatum causes histoplasmosis
@ Properties:
is dimorphic fungus that exists as a mold in soil & as yeast in tissue
forms 2 types of asexual spores:
1. tuberculate macroconidia = w/ typical thick walls & fingerlike projections that are
important in laboratory identification
2. microconidia = are smaller, thin, smooth-walled spores that, if inhaled, transmit the
infection
grows in soil, particularly if the soil is heavily contaminated w/ bird droppings
@ Pathogenesis & Clinical Findings:
inhaled spores are engulfed by macrophages & develop into yeast forms
in tissues, H. capsulatum occurs as an oval budding yeast inside macrophages
the organisms spread widely throughout the body, but most infections remain
asymptomatic bec the small granulomatous foci heal by calcification
w/ intense exposure, pneumonia may become clinically manifest
in tissue biopsies or bone marrow aspirates, oval yeast cells w/in macrophages are seen
microscopically
cultures on sabourauds agar show typical structures (ex. tuberculate macroconidia)
skin test w/ fungal extract (histoplasmin) becomes positive (induration) w/in 2-3 wks of
infection & remains so for years
2 serologic tests are most useful:
1. complement fixation (CF) = 1:32 Ab titer w/ yeast phase Ags is diagnostic
= CF titers fall when the disease becomes inactive & rise in
disseminated disease
2. immunodiffusion (ID) = detects precipitating Abs (precipitins) by forming 2 bands,
M and H, in an agar-gel diffusion assay
= more specific but less sensitive than the CF test
no therapy is needed in asymptomatic or mild primary infection
oral ketoconazole = w/ progressive lung lesions
amphotericin B = treatment of choice in disseminated disease
oral itraconazole = used to treat pulmonary & disseminated disease
C. Blastomyces
@ Disease: Blastomyces dermatitidis causes blastomycosis
@ Properties:
dimorphic fungus that exists as a mold in soil & as a yeast in tissue
the yeast is round w/ doubly refractive wall & a single broad-based bud
endemic in North & Central America & Africa
grows in moist soil rich in organic material, forming hyphae & small pear-shaped conidia
inhalation of the conidia causes human infection
infection occurs mainly via the respiratory tract
asymptomatic & mild cases are rare
dissemination may result in ulcerated granulomas of skin, bone, or other sites
in tissue biopsies, thick-walled yeast cells w/ single broad-based buds are seen
microscopically
culture = hyphae w/ small pear-shaped conidia are visible
ketoconazole = drug of choice in persons w/ lesions
oral itraconazole = used to treat pulmonary or disseminated disease
surgical excision may be helpful
no means of prevention
D. Paracoccidioides
@ Disease: Paracoccidioides brasiliensis causes paracoccidioidomycosis
@ Properties:
dimorphic fungus that exists as a mold in soil & as a yeast in tissue
the yeast is thick-walled w/ multiple buds, in contrast to B. dermatitidis, w/c has a single
bud
fungus grows in the soil & is endemic in rural Latin America
disease occurs only in that region
spores are inhaled & early lesions occur in the lungs
asymptomatic infection is common
oral mucous membrane lesions, lymph node enlargement & sometimes dissemination to
many organs develops
in pus or tissue, yeast cells w/ multiple buds are seen microscopically
culture = may grow typical organism (2-4 weeks)
serologic tests: (a significant titer means an active disease is present)
1. immunodiffusion
2. complement fixation
IV. OPPORTUNISTIC MYCOSES

- opportunistic fungi fail to induce disease in most normal persons but may do so in those
impaired host defenses
A. Candida
** other species:
1. Candida albicans = most common species to cause disseminanted disease
2. Candida tropicalis
3. Candida parapsilosis
4. Candida krusei
5. Torulopsis glabrata
( #s 2 & 3 are important pathogens also)
@ Diseases:
Candida albicans (the most important candica) causes the ff:
1. thrush 3. chronic mucocutaneous candidiasis
2. vaginitis
@ Properties:
yeast = is oval w/ single bud
a normal flora of mucous membranes of the upper respiratory, gastrointestinal, & female
genital tracts
in tissue = may appear as budding yeast or an elongated budding pseudophyphae
@ Transmission:
not transmitted (since its a member of the NF)
when local or systemic host defenses are impaired, disease may result
thrush = overgrowth of the organism in the mouth produces white patches
vulvovaginitis = itchy & discharge is favored by high pH, diabetes, or use of antibiotics
skin invasion = in warm & moist areas
fingers & nails become involved when repeatedly immersed in water (persons employed
as dishwashers in restaurants & institutions are commonly affected)
thickening & loss of nails can occur
chronic mucocutaneous candidiasis = occur in immunosuppressed persons
intravenous drugs predisposes to disseminated candidiasis
in exudates & tissues = budding yeasts & pseudohyphae are seen microscopically
culture = GERM TUBE form in serum at 37C (this serves to distinguish C albicans
from other Candida species)
skin test w/ Candida Ags = (+) in normal adults
= used as an indicator of competent cellular immunity
clotrimazole or nystatin = oral or topical antifungal drugs
= treats local infections (ex. thrush)
ketoconazole = for mucocutaneous candidiasis
amphotericin B w/ or w/o flucytosine or ketoconazole = disseminated candidiasis
treatment should be supplemented by reduction of predisposing factors (ex. thrush can be
prevented by oral clotrimazole or nystatin)
no vaccine
B. Cryptococcus
@ Disease: Cryptococcus neoformans causes cryptococcosis (esp cryptococcal meningitis)
@ Properties:
not dimorphic
yeast are oval, budding & surrounded by a wide polyssacharide capsule
@ Transmission:
yeast occur widely in nature & grows abundantly in soil containing bird droppings (esp
pigeon)
human infection results from inhalation of the organism
lung infection = often asymptomatic / may produce pneumonia
occurs mainly in immunocompromised persons (in whom the organism disseminates to
the CNS-meningitis)
in spinal fluid mixed w/ INDIA INK = the yeast cell is seen microscopically surrounded
by a wide unstained capsule
culture = CSF the specimen
serologic test = in infected spinal fluid, CAPSULAR Ag occurs in high titer
combination of amphotericin B & flucytosin
fluconazole = used in AIDS patients for long-term suppression
no means of prevention
C. Aspergillus
@ Disease: Aspergillus fumigatus cause aspergillosis
@ Properties:
exists ONLY AS MOLDS
not dimorphic
have septate hyphae that form V-shaped (dichotomous) branches
walls are more or less parallel & its conidia form radiating chains in contrast to those of
Mucor & Rhizopus, w/c are enclosed w/in a sporangium
@ Transmission:
widely distributed
grow on decaying vegetation, producing chains of conidia
transmission is by AIRBORNE CONIDIA
organism colonizes & later invades abraded skin, wounds, burns, the cornea, the external
ear, or paranasal sinuses
in immunocompromised persons = invade the lungs & other organs producing
hemoptysis & granulomas
grows in pulmonary cavities = produce FUNGUS BALL (seen in x-ray)
cause allergic asthma
grows on cereals or nuts & produces aflatoxins that may be carcinogenic & acutely toxic
biopsy specimens show septate, branching hyphae invading tissue
culture shows the characteristic radiating chains of conidia (but + culture doesnt show
disease coz colonization is common)
serological test = high levels of IgE (esp in asthma)
= high titers of galactomannan Ag in serum
amphotericin B = for invasive aspergillosis but results are poor
fungus ball = can be surgically removed (from the pulmonary cavity or sinuses)
no specific means of prevention
D. Mucor & Rhizopus
- are saprophytic molds that are widely found
@ Disease:
mucormycosis (zygomycosis, phycomycosis)
invade tissues of immunocompromised hosts
proliferate in the walls of blood vessels esp of the paranasal sinuses, lungs, or gut &
result in tissue necrosis
biopsy specimen = organisms are seen microscopically as NONSEPTATE HYPHAE w/
broad, irregular walls & branches that form more or less at right angles
culture = shows colonies w/ spores contained w/in a sporangium
if diagnosis is made early, treatment of the disorder, plus administration of amphotericin
B & surgical removal of necrotic infected tissue has resulted in some emissions cures
BASIC VIROLOGY
General Characteristics:
1. Viruses are particles composed of an internal core containing either DNA or RNA ( but not both)
covered by a protective protein coat. Some viruses have an outer lipoprotein membrane, called an
envelope, external to the coat.
2. Viruses are obligate intracellular parasites = because they can reproduce only within cells since
they cannot generate energy or synthesize proteins
3. Viruses replicate in a manner different from that of a cells = they dont undergo binary fission
Comparison of viruses and cells:
Property Viruses Cells

Type of nucleic acid DNA or RNA but not both DNA and RNA
Proteins Few Many
Lipoprotein membrane Envelope present in some viruses Cell membrane present in all cells
Ribosomes Absent Present
Mitochondria Absent Present in eukaryotic cells
Enzymes None or few Many
Multiplication by binary fission No Yes (most cells)
VIRAL STRUCTURE
peplos
SIZE & SHAPE = ranges from 20-300 nm in diameter
= shapes are referred to in colloquial terms (ex. spheres, rods, bullets, or bricks)
= in reality, they are complex structures of geometric symmetry
= the shape is determined by the arrangement of the repeating sub-units that form the protein
coat CAPSID of the virus
VIRION = the complete infectious viral particle
NUCLEIC ACID CORE = constitute the genetic material or viral genome w/c can either be DNA or RNA
= located internally & can be either single- or double-stranded DNA or single- or double-stranded
RNA
= nucleic acid could either be linear or circular
= the DNA is always a single molecule which the RNA can exist either as a single molecule or in
several pieces
= viruses are haploid (they contain only one copy of their genes); except for retroviruses w/c are
diploid
CAPSID = protein coat or sheath that surrounds the nucleic acid core
= made up of subunits called capsomers
= functions;
1. protect the viral genome/genetic material from destructive agents in the external environment
2. introduce the viral genome into the host cell / mediate the attachment of the virus to specific
receptors on the host cell surface
CAPSOMER = protein sub-units of the capsid

= each is consist of one or several proteins
= the arrangement of capsomers gives the virus structure its geometric symmetry
= 2 forms of symmetry:
1. icosahedral capsomers are arranged in 20 triangles
2. helical capsomers are arranged in a hollow coil
SPIKES = protein projections that extends from the capsid w/c attach to host cell receptors during the entry
of the virus into the cell
PEPLOS = a lipoprotein projections that extends from the capsid

= ex. Hemagglutinin & neuraminidase spikes
PEPLOMERS = lipoprotein sub-units of the peplos

ENVELOPE = is a lipoprotein membrane composed of lipid derived from the host cell membrane &
protein that is virus-specific
= confers instability on the virus
= enveloped viruses are more sensitive to heat, detergents, & lipid solvents such as alcohol &
ether than are nonenveloped viruses, w/c are composed only of nucleic acid & capsid proteins
= the surface proteins of the virus, whether they are the capsid proteins or the envelope
glycoproteins are the principal antigens against w/c the host mounts its immune response to
viruses; they are also the determinants of type specificity
Atypical Viruslike Agents

There are 4 exceptions to the typical virus as described above:
1. Defective viruses
= are composed of viral nucleic acid & proteins but cannot replicate w/o a helper virus, w/c
provides the missing function
= the ratio of defective to infectious virus particles can be as high as 100:1
= aid in recovery from an infection by limiting the ability of the infectious particles to grow
2. Pseudovirions
= contain host cell DNA instead of viral DNA w/in the capsid
= can infect cells but they dont replicate
3. Viroids
= consist solely of a single molecule of circular RNA w/o a protein coat or envelope
= cause several plant diseases but are not implicated in any human disease
4. Prions
= are infectious protein particles that are composed solely of protein, they contain no nucleic acid
(DNA or RNA)
= are much more resistant to inactivation by ultraviolet light, heat, & acid than are viruses
= resistant also to formaldehyde & nucleases but are inactivated by hypochlorite, NaOH, &
autoclaving
= hypochlorite is used to sterilize surgical instruments & other medical supplies that cannot be
autoclaved
REPLICATION
Viral Growth Curve

= the first event, the virus disappears (as represented by the solid line dropping to the X axis)
= although the virus particle is no longer present, the viral nucleic acid continues to function &
beings to accumulate w/in the cells (as indicated by the dotted line)
= the time during w/c no virus is found inside the cell is known as eclipse period
= the eclipse period ends with the appearance of virus (solid line)
= the latent period, in contrast, is defined as the time from the onset o infection to the appearance
of virus extracellularly
= the infection begins with one virus particle & ends w/ several hundred virus particles having
been produced
Stages of the viral growth cycle

Attachment & penetration by parental virion
EARLY EVENTS
Uncoating of the viral genome

Early viral mRNA synthesis

Early viral protein synthesis

Viral genome replication MIDDLE EVENTS

Late viral mRNA synthesis

Late viral protein synthesis

Progeny virion assembly
LATE EVENTS
Virion release from cell
= the infecting parental virus particle attaches to the cell membrane & then penetrates the host cell
= the viral genome is uncoated by removing the capsid protein, & the genome is free to function
= early mRNA & proteins are synthesized
= the early proteins are enzymes used to replicate the viral genome
= late mRNA & proteins are then synthesized
= these late proteins are the structural, capsid proteins
= the progeny virion are assembled from the replicated genetic material & newly made capsid proteins are
then released from the cell
Lysogeny
= the typical replicative cycle described above occurs most of the time when viruses infect cells
= lysogenic cycle, is an alternative pathway use by some viruses in w/c the viral DNA becomes integrated
into the host cell chromosome & no progeny virus particles are produced at that time
= important medical function: is the synthesis of several exotoxins in bacteria
(ex. diphtheria & botulinum toxins, coded for by the genes of the integrated bacteriophage (prophage)
= lysogenic conversion the term applied to the new properties that a bacterium acquires as a result of
expression of the integrated prophage genes
= Fig 29-4: several aspects of infections by tumor viruses & herpesviruses are similar to the events in the
lysogenic cycle of lambda phage; infection by lambda phage in E. coli begins w/ injection of the
linear, double-stranded DNA genome through the phage tail into the cell; the linear DNA
circularizes (circularization is important bec it is the circular form that integrates into the host cell
DNA); and then viral DNA integrates into the cell DNA; the integration occurs by the matching
of a specific attachment site on the lambda DNA to a homologous site on the E. coli DNA & the
integration (breakage & rejoining) of the 2 DNAs mediated by a phage-encoded recombination
enzyme; the integrated viral DNA is called a prophage
GENETICS & GENE THERAPY
@ The study of viral genetics falls into 2 general areas:

1. mutation & their effect on replication & pathogenesis
2. the interaction of 2 genetically distinct viruses that infect the same cell
@ Viruses serve as vectors in gene therapy & in recombinant vaccines (2 areas that hold great promise for
the treatment of genetic diseases & the prevention of infectious diseases)
Mutations
= mutation is a change in the base sequence of DNA or RNA that usually results in insertion of a
different amino acid into a protein & the appearance of an altered phenotype
= important practical use of mutation is in the production of vaccines containing live, attenuated
virus; these attenuated mutants have lost their pathogenicity but have retained their antigenicity,
so that they induce immunity w/o causing diseases
Interactions
When 2 genetically distinct viruses infect a cell, 3 different phenomena can ensue:
1. Recombination = is the exchange of genes between 2 chromosomes that is based on crossing
over w/in regions of significant base sequence homology
2. Complementation = can occur when one of the 2 viruses that infects the cell has a mutation
that results in a nonfunctional protein
= the nonmutated virus complements the mutated one by making a functional protein
that serves for both viruses
= complementation is an important method by which a helper virus permits replication
of
a defective virus
= Fig 30-1: If either virus A or virus B infects a cell, no virus is produced because each
has a mutated gene. If both virus A & virus B infect a cell, the protein produce
of gene Y of virus A will complement virus B, the protein produce of gene A of
virus B will complement virus A.
3. Phenotypic mixing = the genome of virus type A can be coated w/ the surface proteins of
virus type B
= this phenotypically mixed virus can infect cells as determined by its type B protein
coat but the Progeny virus from this infection has a type A coat, it is encoded solely by
its type A genetic material
= Fig 30-2: A retrovirus (A) & a rhabdovirus (B) infect the same cell; the progeny
viruses include phenotypically mixed particles (2, 3, 4, & 5) & normal progeny virions (1
& 6).
Gene Therapy & Recombinant Vaccines

Viruses are being used as genetic vectors in 2 ways:
1. to deliver new, functional genes to patients w/ genetic diseases (gene therapy)
= retroviruses are currently being used as vectors of the gene encoding adenine deaminase (ADA) in
patienhts w/ immunodeficiencies resulting from a defective ADA gene
2. to produce new viral vaccines that contain recombinant viruses carrying the genes of several different
viruses, thereby inducing immunity to several diseases w/ one immunization
= recombinant viral vaccines contain viruses that have been genetically engineered to carry the genes
of other viruses
= ex. the gene for the surface antigen of hepatitis B virus has been introduced into vaccinia virus & is
expressed in infected cells
CLASSIFICATION OF MEDICALLY IMPORTANT VIRUSES
= the classification of viruses is based on chemical & morphologic criteria

= 2 major components of the virus used in classification are:
1. the nucleic acid (its molecular weight & structure)
2. the capsid (its size & symmetry & whether it is enveloped)
I. Based on Tissues predilection

1. Pneumotrophic viruses viruses affecting the respiratory tract
Ex. Influenza virus, Adenovirus, Rhinovirus
2. Dermothrophic viruses those affecting the skin
Ex. Verruca virus (causing wart)
3. Neurotrophic viruses those affecting the nervous system
Ex. Rabies virus, Poliovirus
4. Viscerotrophic viruses those affecting the visceral organs
Ex. Hepatitis virus, yellow fever virus
II. Based on Nucleic Acid Type
Table 31-1 Classification of DNA viruses
Virus Family Envelope Capsid Particl DNA DNA Medically important Viruses
present symmetry e size MW structure
(nm) (x 10)
Parvovirus No Icosahedral 22 2 SS, linear B19 virus
Papovavirus No Icosahedral 55 3-5 DS, circular, Papillomavirus
supercoiled
Adenovirus No Icosahedral 75 23 DS, linear Adenovirus
Hepadnavirus Yes Icosahedral 42 1.5 DS, Hepatitis B virus
incomplete
circular
Herpesvirus Yes Icosahedral 100 100-150 DS, linear Herpes simplex virus,
Varicella-zoster virus,
cytomegalovirus. Epstein-Barr
virus
Poxvirus Yes Complex 250 x 125-185 DS, linear Smallpox virus, vaccine virus
400
A. DNA Containing Viruses
1. Parvoviruses = very tiny naked icosahedral viruses w/c multiply in the nucleus of infected cells; they
are only single stranded DNA virus
Ex. Adeno-associated virus (AAV) = multiply only in the simultaneously infected w/
Adenoviruses
2. Papovaviruses = naked icosahedral tumor inducing viruses

= 2 genera:
i. Genus Papillomavirus
Ex. Human papilloma virus causing varrucae vulgaris or warts
ii. Genus Polyomavirus
Ex. BK virus isolated from urine of renal transplant patients
JC virus isolated from brain of patients w/ progressive
multifocal leucoencephalopathy (PML)
3. Adenoviruses = naked icosahedral double stranded DNA viruses

Ex. i. Human adenoviruses agents of respiratory disease of the cold variety
ii. Enteric adenoviruses causing enteritis-associated enteric infections
4. Hepadnavirus
Ex. Hepatitis B virus is the human pathogen in this family
5. Herpesvirus = enveloped icosahedral viruses; they are highly cytopathic in cultured cells & frequently
establish latent infections in sensory ganglia for indefinite periods of time & then reactive
Ex: i. Herpes simplex virus type I commonly termed as the oral strain, producing
infections above the waist; stomatitis, fever blisters, upper respiratory
infections, severe & generally fatal encephalitis
ii ii. Herpes simplex virus type II commonly termed as the genital strain causing
iii genital infections
iii. Varicella-zoster virus man is the only known natural host
- the name of the virus reflects 2 diesases:
a. Varicella or chicken pox the result of the primary infection
b. Zoster or shingles the result of the reactivation of varicella virus
present in latent from in the sensory ganglia
iv. B virus causing fatal encephalitis in humans
v. Cytomegalovirus most common cause of congenital infections in humans; can
iv also cause jaundice, brain damage & death
vi. EB virus or Epstein-Barr virus causative agent of infectious Mononucleosis or
v Kissings Disease; also associated w/ Burkitts lymphoma &
vi nasopharyngeal carcinomag
6. Poxviruses = largest & most complex of all viruses

= characteristically brick-shaped
= multiply in the cytoplasm
Ex. i. Variola major causing small pox
ii. Variola minor causing alastrim
iii. Cowpox causing vesicular eruptions of the skin in humans
iv. Erf virus a poxvirus of sheep that can also affect humans, producing nodules on
vii hands
v. Molluseum contagiosum affecting only humans causing benign epidermal
viii tumors
vi. Yaba Monkey tumor virus affecting monkeys & humans causing benign
ix subcutaneous tumors
7. Iridoviruses = icosahedral cytoplasmic deoxyviruses w/c are mostly insect viruses
Table 31-2. Classification of RNA viruses

Virus family Envelop Capsid Particle RNA RNA structure Medically
e symmetry size (nm) MW Important Viruses
present (x10)
Picornavirus No Icosahedsral 28 2.5 SS,linear, Poliovirus,
nonsegmented, rhinovirus,
positive polarity hepatitis A virus
Calicivirus No Icosahedral 38 2.7 SS, linear, Norwalk virus,
nonsegmented, Hepatitis E virus
positive polarity
Reovirus No Icosahedral 75 15 DS linear, 10 Reovirus,
segments rotavirus
Flavivirus Yes Icosahedral 45 4 SS linear, Yellow fever
nonsegmented, virus, dengue
positive polarity virus
Togavirus Yes Icosahedral 60 4 SS linear, Rubella virus
nonsegmented,
positive polarity
Retrovirus Yes Icosahedral 100 7 SS linear, 2 HIV, human T-cell
segments, positive leukemia virus
polarity
Orthomyxov Yes Helical 80-120 4 SS linear, 8 Influenza virus
irus segments, negative
polarity
Yes Helical 150 6 SS linear, Measles virus,
Paramyxovir nonsegmented, mumps virus
us negative polarity
Rhabdovirus Yes Helical 75 x 180 4 SS linear, Rabies virus
nonsegmented,
negative polarity
Filovirus Yes Helical 80 4 SS linear, Ebola virus,
nonsegmented, Marburg virus
negative polarity
Coronavirus Yes Helical 100 5 SS linear, Coronavirus
nonsegmented,
positive polarity
Arenavirus Yes Helical 80-130 5 SS circular, 2 Lymphocytic
segments with with choriomeningitis
cohesive ends, virus
negative polarity
Bunyavirus Yes Helical 100 5 SS circular, 3 California
segments with encephalitis virus
cohesive ends,
negative polarity
B. RNA Containing Viruses

1. Picornaviruses = naked icosahedral viruses; the name picorna is derived from pico (small)
a. Genus Enteroviruses very tiny viruses found in the intestines of man & other animals;
stable at ph 3
Ex. i. Poliovirus causing poliomeylitis
ii. Coxsackievirus A & B causing aseptic meningitis; these 2 groups are
x differentiate on the basis of selective tissue damage:
xi > Coxsackievirus A produce extensive myositis of the skeletal muscles
xii w/ flaccid paralysis
> Coxsackievirus B produce focal muscle lesions, necrosis of the fat pads
& spastic paralysis
iii. ECHO virus (enteric Cytopathogenic Human Orphan) causing paralysis,
xiii diarrhea, aseptic meningitis
iv. Human enterovirus 72 or Hepatitis A virus causing infections hepatitis or
xiv Hepatitis A
b. Genus Cardiovirus
Ex. Encephalomyocarditis virus (EMC) causing mild febrile illness
c. Genus Rhinovirus
Ex. Human rhinovirus causing common colds, bronchitis, bronchopneumonia
d. Genus Aphthovirus
Ex. Foot & mouth disease virus
2. Calicivirus = naked icosahedral viruses

Ex. 2 human pathogens: i. Norwalk virus causing gastroenteritis
ii. Hepatitis E virus
3. Reoviruses = REO stands for respiratory-enteric orphan (so called because they were originally
found in the respiratory & enteric tracts & were not associated w/ any human disase); naked
nucleocapsid possess 2 capsid shells & double-stranded DNA
Genus Orthorevirus Mammalian reviruses
Genus Orbivirus Colorado Tick fever causing encephalitis in man
Genus Cypovirus
Genus Phytoreovirus & Genus Fijivirus plant viruses
Genus Rotavirus Human rotavirus causing diarrhea in infants
4. Flaviviruses = include yellow fever virus, dengue virus, & St. Louis & Japanese encephalitis viruses
5. Togaviruses = enveloped icosahedral viruses include many of the viruses previously known as
arboviruses (arthropod borne); they multiply in bloodsucking insects as well as vertebrates;
rarely producing disease in either
** Genus alphavirus (mosquito-borne) causing encephalitis in man
- Eastern, Western & Venezuelan Equine Encephalitis causing encephalitis in man
- Chikungunya causing myositis & arthritis
- ONyong-Nyong causing fever, arthralgia, rash
Genus Flavivirus
- yellow fever virus causing hemorrhagic fever, hepatitis, etc.
- Dengue virus causing fever, arthralgia, rash
- Japanese encephalitis -- causing fatal encephalitis
** Genus Rubivirus causing German measles (Rubella virus) & severe deformities of
fetuses in the 1st trimester of pregnancy
Genus Pestivirus
- Hog cholera virus
** are human pathogens
6. Retroviruses = (RNA tumor viruses) envelope particles containing a coiled nucleocapsid w/an
icosahedral core shell; all members possess the unique enzyme known as reverse transcriptase
thats why its named retro
= 3 medically important groups:
a. Oncovirus group w/c contains the sarcoma & leukemia viruses
Ex. human T-cell leukemia (HTLV)
b. Lentivirus group slow virus group w/c includes human immunodeficiency virus
(HIV)
c. Spumaviruses comprises the foamy virus
= in cell cultures (esp kidney), it causes the formation of multinucleated vacuolated giant cells
that have a highly characteristic appearance
7. Orthomyxoviruses = the term myxo refers to the affinity of these viruses for mucins, & ortho is
added to distinguish them from the paramyxoviruses
= possess 2 glycoprotein spikes: a. hemagglutinin
b. neuraminidase
Ex. Influenze virus main human pathogen; causing acute respiratory disease
8. Paramyxoviruses = they differ from orthomyxoviruses in that their genomes are not segmented & their
hemagglutinin & neuraminidase are located on the same glycoprotein spike
= sometimes referred to as hemadsorption viruses because their presence were recognized by the
hemadsorption of guinea pig red cells to tissue culture sheet
= important human pathogens: measles, mumps, parainfluenza & respiratory syncytial viruses
(RSV)
9. Rhabdoviruses = are bullet-shaped enveloped viruses w/ a helical nucleocapsid & a single-stranded,

linear, nonsegmented, negative-polarity RNA
= the term rhabdo refers to the bullet shape
Ex. rabies virus is the only important human pathogen
- causing rabies (acute infectious disease of CNS that is almost always fatal)
10. Filoviruses = highly pleomorphic; the term filo refers to the long filaments (long filaments that are
80 nm in diameter but can be thousands of nanometers long)
= 2 human pathogens: a. Ebola virus causing acute hemorrhagic fever
b. Marburg virus causing fatal hemorrhagic fever
11. Coronaviruses = the term corona refers to their characteristic large club-shaped spikes protruding
from the envelope w/c gives them a crown like appearance
= cause respiratory tract infections in human (ex. common cold)
Ex. Human infectious bronchitis virus causing acute upper respiratory diseases
12. Arenaviruses = the term arena (a Latin word) w/c means sandy that refers to granules on the virion
surface that are nonfunctional ribosomes
= 2 human pathogens: a. lymphocytic choriomeningitis virus
b. Lassa fever virus
13. Bunyaviruses = the term bunya refers to the prototype

= Bunyamwera virus, w/c is named for the place in Africa where it was isolated
Ex. viruses cause encephalitis & various fevers such as Korean hemorrhagic fever
PATHOGENESIS
The ability of viruses to cause disease can be viewed on 2 distinct levels:

1. the changes that occur within individual cells &
2. the process that takes place in the infected patient
The Infected Cell

@ 4 main effects of virus infection on the cell:
1. death
= inhibition of host cell protein synthesis frequently occurs first & is the most important
= inhibition of DNA & RNA synthesis may be a secondary effect
= NOTE: synthesis of cellular proteins is inhibited but viral protein synthesis still occurs
= infected cells contain inclusion bodies (w/c are discrete areas containing viral proteins or viral
particles) best example: Negri bodies (are eosinophilic cytoplasmic inclusions found in
rabies virus-infected brain neurons)
2. fusion of cells to form multinucleated cells

= multinucleated giant cells are characteristically form after infection w/ herpesviruses &
paramyxoviruses
= fusion occurs as a result of cell membrane changes w/c are probably due to the insertion of viral
proteins into the membrane
= CYTOPATHIC EFFECT (CPE) hallmark of viral infection of the cell
- refers to the change in appearance of the infected cell
- is the basis for the plaque assay, an important method for
quantifying the amount of virus in a sample
3. malignant transformation
= is characterized by unrestrained growth, prolonged survival, & morphologic changes
4. no apparent morphologic or functional change

= infection of the cell accompanied by virus production can occur w/o morphologic or gross
functional changes
= this highlights the wide variation in the nature of the interaction between the virus & the cell,
ranging from rapid destruction of the cell to a symbiotic relationship in w/c the cell survives &
multiplies despite the replication of the virus
The Infected Patient
@ Pathogenesis in the infected patient involves:
1. transmission of the virus & its entry into the host
= viruses are transmitted to the individual by many different routes:
a. person-to-person = by transfer of respiratory secretions, saliva, blood, or semen & by
fecal contamination of water or food
b. transplacental = between mother & offspring in utero across the placenta at the time of
delivery or during breast feeding
c. animal-to-human transmission = either directly from a bite of a reservoir host as in rabies
or indirectly through the bite of an insect vector, such as mosquito, w/c transfer the virus
frorn an animal reservoir to the person
d. activation of a latent, nonreplicating virus to form an active, replicating virus can occur
within the individual, w/ no transmission from an external source
2. replication of the virus & damage to cells

3. spread of the virus to other cells & organs
= viral infections are either:
a. localized to the portal of entry
- best example is the common cold, w/c involves only the upper respiratory tract; influenza
is localized primarily to the upper & lower respiratory tracts
b. spread systematically
- ex. is poliomyelitis (Fig 32-1: after poliovirus is ingested, it infects the cells of the small
intestine & then spreads to the mesenteric lymph nodes, where it multiplies again; it then
enters the bloodstream & is transmitted to the CNS, where damage to the anterior horn
cells occurs, resulting in the characteristic muscle paralysis; it is during this obligatory
viremia that circulating IgG Abs induced by the polio vaccine can prevent the virus from
infecting the CNS; viral replication in the gastrointestinal tract results in the presence of
poliovirus in the feces, thus perpetuating its transmission to others)
4. the immune response, both as a host defense & as a contributing cause of certain diseases
= viral diseases are the result of cell killing by virus-induced inhibition of macromolecular
synthesis; but there are certain diseases in w/c cell killing by immunologic attack plays an
important role in pathogenesis
= Ex. (LCM) lymphocytic choriomeningitis virus is inoculated into the brain of an adult mouse
[w/c also happens in man]; virus replication occurs & death follows; however, when LCM virus
is inoculated into the brain of an immunosuppressed adult mouse or newborn mouse, the animal
remains well despite extensive virus replication; when immune lymphocytes are inoculated into
these infected, healthy mice, death ensues
= similar case happens in hepatitis B virus infection, in w/c immune complexes play a role in
producing the chronic hepatitis & arthritis characteristic of this disease
5. persistence of the virus in some instances

= the mechanisms that may play a role in the persistence of viruses include:
a. integration of a DNA provirus into host cell DNA
b. immune tolerance bec neutralizing Abs are not formed
c. formation of virus-Ab complexes which remains infectious
d. location w/in an immunologically sheltered sanctuary (ex. brain)
e. rapid antigenic variation
f. spread from cell to cell w/o an extracellular phase so that virus is not exposed to Ab
g. immunosuppression as in AIDS
= 3 types of clinically important persistent viral infections :

a. chronic-carrier infections some patients who have been infected w/ certain viruses continue to
produce significant amounts of the virus for long periods
- the carrier state can either be asymptomatic or becomes symptomatic
- Ex. hepatitis B virus carriers, neonatal rubella virus & CMV ( in which
carriers can produce virus for years)
b. latent infections the patient recovers from the initial infection & virus production stops;
subsequently, the symptoms may recur, accompanied by the production of virus
- Ex. herpes simplex virus infections
c. slow virus infections the term slow virus refers to the prolonged period between the initial
infection & the onset of disease, w/c is measured in years
HOST DEFENSES
@ Host defenses against viruses fall into 2 major categories:
1. NONSPECIFIC DEFENSES = most important are the interferons w/c are an early, first-line defense
a. interferons are a heterogenous groups of glycoproteins (molecular wt 20,000-40,000)
produced by human & other animal cells after viral infection or after exposure to other
inducers
- they inhibit the growth of viruses by blocking the translation of viral proteins
- are divided into 3 groups based on the cell of origin
i. leukocyte
ii. fibroblast known as alpha, beta, & gamma interferons
iii. lymphocyte * alpha & beta = are induced by viruses
* gamma = induced by antigens
- Fig. 33-1: induction & action of interferon:
(A) virus infection induces the synthesis of interferon, w/c then leaves the infected cell
(B) interferon binds to the surface receptor of an uninfected cell & induces the synthesis of 3
new enzymes (antiviral proteins)
(C) antiviral proteins block the translation of viral mRNA
b. phagocytosis fixed macophages of the reticuloendothelial system & alveolar macrophages are
the important cell types in limiting virus infection; unlike PMN leukocytes are the
predominant cellular defense in bacterial infections
c. fever inhibits viral replication in 2 ways:

i. higher body temperature may directly inactivate the virus particles (esp enveloped
virus w/c are more heat-sensitive than non-enveloped viruses)
ii. replication of some viruses is reduced at higher temperatures
d. mucocillary clearance such mechanism of the respiratory tract may protect the host
- if damage (ex. from smoking), results in an increased frequency of viral respiratory
tract infections esp influenza
e. factors that modify host defenses:

i. age = is a significant variable in the outcome of viral infections
= viral infections are more severe in neonates & in the elderly than in older
children & young adults
ii. increased corticosteroids levels = corticosteroids can cause a variety of pertinent
effects such as lysis of lymphocytes, decreased recruitment of monocytes,
inhibition of interferon production & stabilization of lysosomes
2. SPECIFIC DEFENSES
@ Acquired immunity = the most important type of defense
a. Active immunity = actively acquired by exposure to the virus
= can be elicited by contracting the actual disease by having an inapparent infection or by
being vaccinated
= important in the prevention of disease w/c is chiefly due to the presence of
immunoglobulins
IgA confers protection against viruses that enter through the respiratory & gastrointestinal
mucosa
IgM & IgG protect against viruses that enter or are spread through the blood
- the lifelong protection against systemic viral infections (ex. childhood diseases:
measles, mumps, rubella, & chickenpos (varicella) is a function of anamnestic (2ndary)
response of IgG
= protection by active immunity can be affected by the phenomenon of original antigenic
sin (the term refers to the observation that when a person is exposed to a virus that cross-reacts
w/ another virus to which that individual was previously exposed, more Ab may be produce
against the original virus than against the current one; it appears that the immunologic memory
cells can respond to the original antigenic exposure to a greater extent than to the subsequent one
ex case of influenza virus & severe hemorrhagic dengue fever virus)
= 2 MAIN MECHANISMS HOW Ab INHIBIT VIRUSES:

i. neutralization neutralizing the infectivity of the virus by Ab binding to the proteins on the
outer surface of the virus
- 2 effects:
> it can prevent the interaction of the virus w/ cell receptors
> stabilize the virus so that uncoating does not occur (Ab-coated virus is more rapidly
phagocytized than normal virus, a process similar to the opsonizing effect of Ab on
bacteria)
ii. lysis of virus-infected cells in the presence of Ab & complement
= not all virus infections induce Abs; tolerance to viral Ags can occur when the virus infection
develops in a fetus or newborn infant (ex is what happens in lymphocytic choriomeningitis [LCM]
infection in mice
b. Passive immunity = passively acquired by the transfer of immune serum

= the term passive refers to the administration of preformed antibodies
= the 3 most frequently used high-titer preparations are used after exposure to :
i. hepatitis B virus
ii. rabies virus
iii. varicella-zoster virus
= low-titer immune globulin is used to prevent hepatitis A in people traveling to areas where this
infection is hyperendemic
LABORATORY DIAGNOSIS
3 Approaches to the diagnosis of viral diseases by the use of clinical specimens:
1. Identification of the virus in cell culture

= growth of viruses requires cell cultures bec viruses replicate only in living cells not on cell-free
media like most bacteria do
= virus growth frequently produces a characteristic cytopathic effect (CPE) that provide a
preliminary diagnosis
= if the virus does not produce a CPE, its presence can de detected by several other techniques:
a. hemadsorption attachment of rbc to the surface of virus-infected cells
- limited to viruses w/ a hemagglutinin protein on their envelope such as mumps,
parainfluenza, & influenza viruses
b. interference w/ the formation of a CPE by a 2nd virus
c. decrease in acid production by infected, dying cells used to detect certain enteroviruses
= a definitive identification of the virus grown in cell culture is made by using known Ab in the ff
tests: > complement fixation
> hemagglutination inhibition
> neutralization
> fluorescent Ab
> radioimmunoassay
> enzymes-linked immunosorbent assay
> immunoelectron microscopy
2. microscopic identification directly in the specimen

= specimens such as biopsy material or skin lesions
= 3 different procedures can be used:
a. light microscopy reveals characteristic inclusion bodies or multinucleated giant cells
b UV microscopy used for fluorescent-Ab staining of the virus in infected cells
c. electron microscopy detects virus particles w/c can be characterized by their size &
morphology
3. serologic procedures to detect a rise in Ab titer or the presence of IgM Ab
ANTIVIRAL DRUGS
the number of antiviral drugs is very small compared to drugs against bacterial infections
(the major reason for the difference is the difficulty in obtaining selective toxicity against
virus & their replication is involved w/ the normal synthetic processes of the cell)
limitation:
= are relatively ineffective (bec many cycles of viral replication occur during the incubation
period when the patient is well; by the time the patient has a recognizable systemic viral
disease, the virus has spread throughout the body & it is too late to interdict it)
= emergence of drug-resistant viral mutants
Potential sites for antiviral chemotherapy
Site of Action Effective drugs

Early events (entry or uncoating of the Amantadine
virus)
Nucleic acid synthesis by viral DNA & Acyclovir, ganciclovir, vidarabine, vidarabine
RNA polymerase Idoxuridine, trifluridine, azidothymidine, dideoxyinosine,
dideoxycytidine, ribavirin
Other virus-specific enzymes
Protein synthesis directed by viral mRNA
Cleavage of precursor polypeptides
Assembly of the particle, including the
matrix protein
Release of the particle by budding
@ Inhibition of early events:
A. amantadine = used to prevent influenza A infections

= it inhibits uncoating of the virus: absorption & penetration occur normally, but
transcription by the virion RNA polymerase does not
@ Inhibition of viral nucleic acid synthesis:
** Inhibitors of Herpesviruses:
A. acyclovir = is active primarily against herpes simplex virus types 1 & 2 & varicella-zoster
virus
= is due to the virus-encoded thymidine kinase, w/c phosphorylates acyclovir much more
effectively than does the cellular thymidine kinase
= bec only herpes simplex virus & varicella-zoster virus encode a kinase that efficiently
phosphorylates the drug; no activity against cytomegalovirus
B. ganciclovir = active against cytomegalovirus esp retinitis in AIDS & other infections caused
by this virus
C. vidarabine = effective against herpes simplex virus type 1 infections such as encephalitis &
dermatitis but is less effective & much more toxic than acyclovir
= on entering the cell, the drug is phosphorylated by cellular kinases to the triphosphate,
w/c inhibits the herpesvirus-encoded DNA polymerase more effectively than the cellular
DNA polymerase
D. idoxuridine = is clinically useful in the topical treatment of herpes simplex virus

keratoconjunctivitis
= it causes the formation of faulty progeny DNA & mRNA
E. trifluridine = mechanism of action is similar as idoxuridine
** Inhibitors of retroviruses: [the selective toxicity of the ff drugs is based on their ability to
inhibit DNA synthesis by the reverse transcriptase of human immunodeficiency virus
(HIV)]
F. azidothymidine = also inhibits growth of virus in cell culture; is currently the drug of choice in
patients w/ AIDS
G. dideoxyinosine = causes chain termination during DNA synthesis by the reserves transcriptase
of HIV & is used to treat patients who are intolerant of or resistant to AZT
H. dideoxycytidine = same as dideoxyinosine
** Inhibitors of other viruses:
I. ribavirin = inhibits the synthesis of guanine nucleotides, w/c are essential for both DNA &
RNA viruses
= used clinically to treat pneumonitis caused by respiratory syncytial virus in infants &
to treat severe influenza B infections
@ Inhibition of viral protein synthesis:
A. interferon = effective in the treatment of some patients w/ chronic hepatitis B & C infections
B. methisazone = specifically inhibits the protein synthesis of poxviruses, such as smallpox &
vaccinia viruses
= by blocking the translation of late mRNA
VIRAL VACCINES
@ 2 types of vaccines:
1. live virus -in general, live vaccines are preferred to vaccines containing killed virus bec their
protection is GREATER & LONGER-LASTING
- w/ live vaccines, the virus multiplies in the host, producing a prolonged antigenic
stimulus, & both IgA & IgG are elicited when the vaccine is administered by the natural
route of infection
- booster doses are also recommended esp w/ measles & polio vaccines
- 3 concerns about the use of live vaccines:
a. they are composed of attenuated viral mutants, w/c can revert to virulence either
during vaccine production or in the immunized person
b. live vaccine can be excreted by the immunized person
c. a 2nd virus could contaminated the vaccine if it was present in the cell cultures used to
prepare the vaccine.
2. killed virus - usually given intramuscularly, do not stimulate a major IgA response
- Disadvantages:
> produce a shorter duration of protection
> less protective
> induce fewer IgA Abs
- Advantages:
> they cannot revert to virulence
> are more heat-stable = so can be used more easily in tropical climates
@ Current viral vaccines (1993)
USAGE VACCINE LIVE / KILLED VIRUS

Common Measles Live
Mumps Live
Rubella Live
Polio Both
Influenza Killed
Hepatitis B Killed
Rabies Killed
Special situations Yellow fever Live
Japanese encephatlitis Killed
Adenovirus Live
Smallpox Live
@ Characteristics of live and killed viral vaccines
Characteristic Live Vaccine Killed Vaccine

Duration of immunity Longer Shorter
Effectiveness of protection Greater Lower
Immunoglobulins produced IgA and IgG IgG
Reversion to virulence Possible No
Stability to rm temp Low High
Excretion of virus & transmission to nonimmune Possible No
contacts
Features of viruses that infect the respiratory tract
Virus Disease Lifelong Vaccine Viral

Immunity to Available Latency
Disease
RNA viruses
Influenza A virus influenza no + -
Parainfluenza virus croup no - -
Respiratory bronchiolitis incomplete - -
syncytial virus
(RSV)
Rubella virus rubella yes + -
Measles virus measles yes + -
Mumps virus parotitis, yes + -
meningitis
Rhinovirus common cold no - -
Coronavirus common cold no - -
Coxasackievirus Herpangina, no - -
pleurodynia
DNA viruses
Herpes simplex gingivostomatitis no - +
virus type 1
Epstein-Barr virus infectious yes - +
mononucleosis
Varicella-zoster chickenpox, yes - +
virus shingles
Adenovirus pharyngitis no +2 +
2. Mumps Virus
Disease Mumps
Important Properties (refer to the table above)

= humans are the natural host
Transmission & Epidemiology

transmitted via respiratory droplets
occurs worldwide w/ peak incidence in the winter
Pathogenesis & Immunity

the virus infects the upper respiratory tract & then spreads through the blood to infect the
parotid glands, testes, ovaries, pancreas, & in some cases meninges
lifelong immunity occurs in persons who have had the disease
mumps occur only once
maternal Ab passes the placenta & provides protection during the 1st 6 mons of life
Clinical Findings
after an incubation period of 18-21 days, a prodromal stage of fever, malaise, & anorexia is
followed by tender swelling of the parotid glands, either unilateral or bilateral
there is a characteristic increase in parotid pain when drinking citrus juices
disease is benign & resolves spontaneously w/in a week
2 complications are of significance:
1. orchitis in postpubertal males, w/c if bilateral, can result in sterility
= unilateral orchitis does not lead to sterility
2. meningitis = benign & self-limited & w/o sequelae
= mumps virus, coxsackievirus & echovirus are the 3 most frequent causes of
viral (aseptic) meningitis
Laboratory Diagnosis
viral isolation through cell culture from saliva, spinal fluid, or urine
hemagglutination inhibition & CF = 4-fold rise in Ab titier is diagnostic
mumps skin test = used to detect previous infection
Treatment
no antiviral therapy
Prevention
immunization (live, attenuated vaccine)
= effective & long-lasting (at least 10 yrs)
= given to children at 15 mons of age, usually in combination w/ measles & rubella
vaccines
= bec its live, it should not be given to immunocompromised persons or pregnant
women
immune globulin is not useful for prevention
3. Respiratory Syncytial Virus (RSV)
Disease pneumonia & bronchiolitis in infants
Important properties (refer to the table above)

= the fusion protein causes cells to fuse, forming syncytia, w/c give rise to the name of the virus
= humans & chimpanzees are the natural host
Transmission &Epidemiology
transmitted via respiratory droplets & by direct contact of contaminated hands w/ the nose or
mouth
cause outbreaks every winter & in hospitalized infants (the latter outbreaks can be controlled
by hand washing & use of gloves, w/c interrupt transmission by hospital personnel

in infants RSV infection is more severe & often involves the lower respiratory tract
adults mild uppter respitory infections
localized infection, viremia does not occur
maternal Ab passed to the infant may react w/ the virus & damage the respiratory tract cells
trials w/ a killed vaccine resulted in more sever disease
immunity is incomplete so may have multiple infections due to RSV
Clinical Findings
infants = lower respiratory tract disease (bronchiolitis & pneumonia predominates)
older children & adults = upper respiratory infections resemble the common cold
isolation in cell culture
immunofluorescence on smears of respiratory epithelium
at least a 4-fold rise in Ab titer is diagnostic
Treatment
aerosolized ribavirin is recommended for severely ill hospitalized infants
Prevention
no vaccine
nosocomial outbreaks can be limited by hand washing and use of gloves
4. Parainfluenza Viruses
Disease
croup & pneumonia in children
disease resembling the common cold in adults
Important Properties (refer to the table above)

worldwide primarily in the winter months

cause upper & lower respiratory tract disease w/o viremia
parainfluenza 1 & 2 are major causes of croup & pharyngitis
Clinical Findings
known as the main cause of croup (acute laryngotracheobronchitis) in children under 5 yrs of
age; also cause a variety of respiratory disease such as common cold, pharyngitis, bronchitis
& pneumonia
croup is characterized by a harsh cough & hoarseness
viral isolation in cell culture
4-fold or greater rise in Ab titer
Treatment & Prevention
no antiviral therapy nor vaccine available
III. TOGAVIRUSES
1. Rubella Virus
Diseases rubella (German measles) & congenital rubella syndrome
Important Properties
composed of one piece of single-stranded RNA
icosahedral nucleocapsid
lipoprotein envelope
has positive-strand RNA (unlike paramyxoviruses) & has no virion polymerase
surface spikes contain hemagglutinin
human are the natural host

occurs worldwide; epidemics occur every 6-9 years

initial replication of the virus occurs in the nasopharynx & local lymph nodes; then spreads
via the blood to the internal organs & skin
natural infection leads to lifelong immunity
2nd cases of rubella do not occur; similar rashes are caused by other viruses, such as
coxsackieviruses & echoviruses
Ab crosses the placenta & protects the newborn
Clinical Findings
A. Rubella = is a milder, shorter disease than measles
= after an incubation period of 14-21 days, a brief prodromal period w/ fever & malaise is
followed by a maculopapular rash w/c starts on the face & progresses downward to involve the
extremities & typically lasts for 3 days
= posterior auricular lymphadenopathy is characteristic
B. Congenital Rubella Syndrome

= when a pregnant woman is infected during the 1st trimester esp the 1st month, significant
congenital malformations can occur as a result of maternal viremia & fetal infection
= increased rate of abnormalities during the early weeks of pregnancy is attributed to the very
sensitive organ devt that occurs at that time
= malfunctions include the ff:
heart (patent ductus arteriosus)
eyes (cataracts)
brain (deafness & mental retardation)
= children infected in utero can CONTINUE TO EXCRETE rubella virus for months following
birth public hazard bec virus can be transmitted to pregnant women
= congenitally infected infants have significant IgM titers & persistent IgG titers long after
maternal Ab has disappeared
cell culture = produces cytopathic effect (CPE)
hemagglutination test or ELISA = 4-fold or greater rise in Ab titer between the acute-phase
& convalescent-phase sera
in pregnant woman exposed to rubella virus, the presence of IgM Ab indicates recent
infection
1:8 or greater titer of IgG Ab indicates immunity & consequent protection of the fetus
Treatment no antiviral therapy
Prevention
live, attenuated vaccine = effective & long-lasting ( at least 10 yrs)
= given to children at 15 months of age, usually in combination w/ measles & mumps
= given also to unimmunized young adult women if they are not pregnant & will use
contraception for the next 3 months
= not give to immunocompromised patients
immune globulin administration does not prevent fetal infection in pregnant women exposed
to rubella virus
to protect pregnant women from exposure to rubella virus, many hospital require their
personnel to demonstrate immunity, either by serologic testing or by proof of immunization
2. other Togaviruses
other medically important togaviruses are descrigbed on arboviruses
IV. RHABDOVIRUSES
@ Rabies virus
Disease rabies
single-stranded RNA enclosed w/in a bullet-shaped capsid surrouded by a lipoprotein
envelope
genome has a negative polarity
rabies virus has a broad host range = it can infect all mammals
street virus = virus isolated directly from infected animals
fixed virus = virus continuously passaged in rabbit brains; the fixed virus was used in the
original Pasteur type of the vaccine

transmitted by the bite of a rabid animal except rodents & rabbit, mostly dogs
bats are remarkable for their ability to transmit the virus while remaining healthy

the virus multiplies locally at the bite site & then infects the sensory neurons & moves by
axonal transport to the CNS; multiplies in the CNS & then travel down the peripheral nerves
to the salivary glands & other organs; from the salivary glands, it enters the saliva to be
transmitted by the bite
no viremic stage
infected neurons contain an eosinophilic cytoplasmic inclusion called NEGRI BODY
no record of immunity bec few have survived rabies
Clinical Findings
the incubation period varies according to the location of the bite from as short as 2 wks to 16
wks or longer
it is shorter when bites are sustained on the head rather than on the leg, bec virus has a shorter
distance to travel to reach the CNS
w/in a few days, signs such as confusion, lethargy & increased salivation develop
most notable is the painful spasm of the throat muscles on swallowing hydrophobia ( an
aversion to swallowing water bec it is so painful)
w/in several days, the disease progresses to seizures, paralysis, & coma & some death
1. animal
= rapid diagnosis: examination of brain tissue using either fluorescent Ab to rabies virus or
histologic staining of Negri bodies in the cytoplasm of hippocampal neurons
= viral isolation: cell culture (but takes too long)
2. humans
= isolation of virus by cell culture
= rise in titer of Ab to the virus
= negri bodies can be demonstrated in corneal scrapings & in autopsy specimens of the brain
Treatment
no antiviral therapy only supportive treatment is available
Prevention
2 approaches to prevention of rabies in humans:
1. preexposure = immunization w/ rabies vaccine should be given to individuals in high-risk
groups such as veterinarians, zoo keepers, & travelers to hyperendemic areas
= rabies vaccine (HDCV) contains inactivated fixed virus grown in human diploid
cells, but duck embryo vaccine or nerve tissue vaccines are also available
2. postexposure = involves the use of bothe the vaccine & human rabies immune globulin
(RIG), obtained from hyperimmunized persons) + immediate cleaning of the wound
= tetanus immunization should also be considered
the decision to give postexposure immunization depends on a variety of factors:

1. the type of animal (all wild-animal attacks demand immunization)
2. whether an attack by a domestic animal was provoked
3. the severity of the bite & its location
4. whether rabies is endemic in the area
5. the advice of local public health officials should be sought
if the decision is to immunize, both HDCH & RIG are recommended

** HDCV = five doses are given
** RIG = given only ones
captured animal should be observed for 10 days &sacrificed if symptoms develop
the vaccine for cats & dogs immunization consists of live, attenuated rabies grown in chick
embryos
vaccination must be repeated at intervals
RNA NONENVELOPED VIRUSES
I. PICORNAVIRUSES
= small (20-30 nm) nonenveloped, composed of an icosahedral nucleocapsid & a single-stranded
RNA genome
= the genome RNA has positive polarity
= replication in the cytoplasm of cells
= are activated by lipid solvents (like ether) bec they dont have envelope
= this family includes 2 medically important groups:
A. enteroviruses
= infect primarily the enteric tract
= replicate optimally at 37C
= stable in acid conditions (pH 3-5); thus they are able to survive exposure to
gastric acid
B. rhinoviruses
= found in the nose & throat (hence their name)
= grow better at 33C
= are acid labile (thats why restricted to the nose & throat only)
Features of viruses commonly infecting the intestinal tract
Virus Nucleic Acid Disease Lifelong Vaccine Antiviral

Immunity to Available Therapy
Disease
Poliovirus RNA Poliomyelitis Yes (type- + -
specific)
Echoviruses RNA Meningitis, etc. No - -
Coxsackievirus RNA Meningitis, No - -
carditis, etc.
Hepatitis A virus RNA Hepatitis Yes - -
(enterovirus 72)
Rotavirus RNA Diarrhea No - -
Norwalk virus RNA Diarrhea Unknown - -
Adenovirus DNA Diarrhea Unknown - -
A. Enteroviruses
1. Poliovirus
Disease poliomyelitis
have 3 serologic (antigenic) types based on different antigenic determinants on the outer
capsid proteins, thus protection from disease requires the presence of Ab against each of the 3
types

transmitted by the fecal-oral route
replicates in the oropharynx & intestinal tract
humans are the only natural hosts
poliomyelitis occurs worldwide esp in areas where hygience & sanitation are poor & children
are exposed at an early age & experience mostly asymptomatic infections

after replicating in the oropharynx & small intestine, the virus spreads through the
bloodstream to the CNS
in CNS, poliovirus replicates in the motor neurons causing death of these cells & results in
paralysis of the muscles innervated by those neurons
infection provides lifelong type-specific immunity (consists both intestinal IgA & humoral
IgG to the specific serotype)
Clinical Findings:
incubation period is usually 10-14 days
the range of responses to poliovirus infection includes:
a. inapparent, asymptomatic infection
b. abortive poliomyelitis = most common clinical form (mild, febrile illness)
= most patients recover spontaneously
c. nonparalytic poliomyelitis = manifests as an aseptic meningitis w/ fever, headache & a stiff
neck; resolves spontaneously
d. paralytic poliomyelitis = flaccid paralysis is the predominant finding; permanent motor
nerve damage; painful muscle spasm
isolation of virus = from the throat, stool or spinal fluid
= virus causes a cytopathic effect (CPE) w/c can be identified by neutralization
method using a specific antisera
by rise in Ab titer
Treatment
no antiviral therapy
treatment is limited to symptomatic relief & respiratory support
physiotherapy for the affected muscles
Prevention
immunization of both killed (Salk) & the live, attenuated (Sabin) vaccines
both vaccines induce humoral Abs w/c neutralize virus entering the blood & prevent CNS
infection & disease
live vaccine = is currently preferred
= advantages: i. Interrupsts fecal-oral transmission
ii. given orally unlike the killed vaccine w/c must be injected
= disadvantages:
i. reversion of the attenuated virus to virulence will occur
ii. cause disease in immunodeficient persons
iii. infection of the gastrointestinal tract by other enteroviruses can limit replication
of vaccine virus & reduce protection
iv. must be kept refrigerated to prevent heat inactivation of the live virus
killed vaccine = used in 2 special instances:
i.. initial vaccination of unimmunized adults (bec the risk of disease from the live
vaccine is higher in adults than in children)
ii. vaccination of immunodeficient individuals
passive immunization w/ immune serum globulin is available for protection of unimmunized
individuals known to have been exposed & newborns
2. Coxsackieviruses
= named for the town of Coxsackie, NY, where they were first isolated
Disease
Group A viruses = herpangina & hand-foot-&-mouth disease
Group B viruses = pleurodynia, myocarditis, & pericarditis
size & structure of the virion & the nature of the genome RNA are similar to those poliovirus

are transmitted by fecal-oral route
respiratory aerosols also play a role
occurs worldwide primarily in the summer & fall

Group A viruses = have a predilection for skin & mucous membranes
Group B viruses = in various organs such as the heart, pleura, pancreas & liver
both groups affect the meninges & motor neurons to cause paralysis
immunity following infection is provided by type-specific IgG Ab
Clinical Findings
A. Groups A = herpangina: char by fever, sore throat & tender vesicles in the oropharynx
Hand-foot-and-mouth disease: char by vesicular rash on the hands & feet
B. Group B = pleurodynia/epidemic myalgia/devils grip/Bornholm disease
= myocarditis & have a similar role in juvenile diabetes in humans
C. Caused by both groups = aseptic meningitis, mild paresis & transient paralysis
Laboratory Diagnosis:
cell culture or suckling mice
rise in titer of neutralizing Abs
Treatmetn & Prevention

no antiviral drug therapy nor vaccine available
3. Echoviruses
the prefix ECHO is an acronym for Enteric Cytopathic Human Orphan
called orphans bec they were not initially associated w/ any disease
cause a variety of diseases: aseptic meningitis, upper respiratory infection, febrile illness w/
& w/o rash, etc.
structure is similar to other enteroviruses
transmitted by fecal-oral route & occur worldwide
one of the leading cause of aseptic (viral) meningitis
diagnosis: cell culture but serologic tests are of little value
no antiviral therapy or vaccine available
4. Other Enteroviruses
Enterovirus 70 = main cause of acute hemorrhagic conjunctivitis
= complete recovery occurs & no therapy
Enterovirus 71 = one of the leading causes of viral CNS disease
Enterovirus 72 = is hepatitis A virus
B. Rhinoviruses
Disease main cause of the common cold
replicate better at 33C than at 37
acid labile

2 modes of transmission:
1. direct = from person to person via aerosols of respiratory droplets
2. indirect = respiratory droplets are deposited on the hands or on a surface such as a table
then transported by fingers to the nose or eyes
occurs worldwide & causing disease in the fall & winter
higher prevalence in children than adults

the portal of entry is the upper respiratory tract & the infection is limited to that region
probably bec they grow poorly at 37C
immunity is serotype-specific & is a function of nasal secretory Ab
Clinical Findings
after incubation period of 2-4 days, sneezing, nasal discharge, sore throat, cough & headache
are common & a chilly sensation occurs
illness lasts about 1 week
note that other viruses such coronaviruses, adenoviruses, influenza C virus &
coxsackieviruses also cause common cold syndrome
viral isolation from nasal secretion in cell culture
serologic tests are not done

no specific antiviral therapy is available
vaccines appear impractical bec of the large # of serotypes
paper tissues impregnated w/ disinfectants such as iodine, limit transmission when used to
remove rhinoviruses from fingers contaminated w/ respiratory secretions
high doses of Vit C have little ability to prevent rhinovirus-induced colds
II. REOVIRUSES
= REO is an acronym for Respiratory Enteric Orphan
= when the virus was discovered, it was isolated from the respiratory & enteric tracts& was not
associated w/ any disease
= Rotaviruses are the most important human pathogens in this family
@ Rotavirus
Disease most common cause of gastroenteritis in young children
segmented, double-stranded RNA genome w/ an icosahedral capsid w/o an envelope
the virion contains an RNA-dependent RNA polymerase (a virion polymerase is required bec
human cells do not have an RNA polymeralse that can synthesize mRNA from a double-
stranded RNA template

transmitted by the fecal-oral route
infection occurs worldwide

rotavirus replicates in the mucosal cells of the small intestine loss of salt, glucose & water
leads to diarrhea (nonbloody)
immunity is unclear
Clinical Findings
infection is characterized by nausea, vomiting & watery, nonbloody diarrhea
gastroenteritis is most serious in young children (concern is dehydration & electrolyte
imbalance)
minor symptoms in adults
radioimmunoassay or ELISA = using a stool
4-fold or greater rise in Ab titer
cell culture & immunoelectron microscopy = not routinely done

no antiviral therapy nor vaccine is available
prevention rests on sanitation
HUMAN IMMUNODEFICIENCY VIRUS (HIV)
Disease: Acquired immunodeficiency syndrome (AIDS)
Important Properties:
1. HIV is one of the human T cell lymphotrophic retroviruses
2. infects & kills helper (CD4) T lymphocytes = resulting in the loss of cell-mediated immunity & a
high probability & susceptibility to opportunistic infections
3. may infect other cells also like macrophages & monocytes, that have CD4 protein on their
surfaces
4. cause slow infections w/ long incubation periods
5. Fig. 45-1: Cross-section of HIV
= in the interior, 2 molecules of viral RNA are shown associated with reverse transcriptase;
surrounding those structures is an icosahedral nucleocapsid composed of p24 proteins; on the
exterior are the 2 envelope proteins, gp120 & gp41, w/c are embedded in the lipid bilayer derived
from the cell membrane
6. typical retroviral genes:
a. gag gene = encodes the internal core proteins, the most impt is p24, an Ag used in
serologic tests
b. pol gene = encodes several proteins including the virion reverse transcriptase, w/c
synthesizes DNA by using the genome RNA as a template
c. env gene = encodes gp160, a precursor glycoprotein that is cleaved to form the 2
envelope (surface) glycoproteins, gp120 & gp41
d. tat gene = means transactivation of transcriptase, a regulatory gene w/c encodes a
protein that enhances viral gene transcription
= reduces the ability of cytotoxic T cells to kill HIV-infected cells
7. Important Ags of HIV:
a. gp120 & gp41 = are the type-specific envelope glycoproteins
= the gene that encodes gp120 mutates rapidly; Ab against gp120 neutralizes
the infectivity of HIV, but the rapid appearance of gp120 variants will make
production of an effective vaccine difficult
= the high mutation rate may be due to lack of an editing function in the reverse
transcriptase
b. p24 = the group-specific Ag
= Ab against p24 do not neutralize HIV infectivity but serve as impt serologic
markers of infection
8. infects human & certain primates BUT HIV is NOT AN ENDOGENOUS VIRUS of humans
9. viruses similar to HIV:
a. HIV-2 = proteins of HIV-2 are only about 40% identical to those of the original HIV isolates
b. Simian immunodeficiency virus (SIV) = isolated from monkeys w/ AIDS-like illness
= the proteins of SIV resemble those of HIV-2 more closely than they resemble those of
the original HIV isolates
c. HTLV-IV = infects T cells but does not kill them & is not associated w/ any disease
Summary of Replicative Cycle:

1. the initial step in entry of HIV into the cell is the binding of the virion gp120 envelope protein to
the CD4 protein on the cell surface
2. the virion gp41 protein then mediates fusion of the viral envelope w/ the cell membrane & the
virion enter the cell
3. after uncoating, the virion RNA-dependent DNA polymerase transcribes the genome RNA into
double-stranded DNA, w/c integrates into the host cell DNA
4. the virion assemble in the cytoplasm & are released from the cell by budding
5. much of the virus remains cell-associated & may be difficult to neutralize w/ Ab
Transmission & Epidemiology:

1. transmission of HIV occurs primarily by sexual contact & by transfer of infected blood (esp in
promiscuous homosexual men, intravenous drug abusers, & hemophiliacs; heterosexual
transmission is predominant in African countries; transmission from health care personnel to
patients is very rare)
2. perinatal transmission from infected mother to neonate also occurs, either transplacentally or via
breast milk
3. infection occurs by the transfer of either HIV-infected cells or free HIV (HIV that is not cell-
associated)
4. dose of HIV required to cause infection is much higher than that of HBV
5. since 1981, when AIDS was 1st reported, it is estimated worldwide that 8-10 million or more
people are infected
Pathogenesis & Immunity:

1. HIV infects helper T cells & kills them, resulting in suppression of cell-mediated immunity; this
predisposes the host to various opportunistic infections & certain cancer cells like Kaposis
sarcoma & lymphoma (but HIV are not found in these cancer cells so HIV does not directly cause
these tumors)
2. HIV acts as a superantigen, w/c indiscriminantly activates many helper T cells & leads to their
demise
3. persistently infected cells continue to produce HIV, w/c explains that a person infected w/ HIV is
considered to be infected for life
4. 90% of AIDS pxs have Abs against HIV (but these Abs neutralize the infectivity of the virus
poorly) = this indicates that immunity is incomplete & that infectious virus & Abs can coexist
5. abnormalities of B cells also occurs, aside from detrimental effects on T cells
Clinical Findings:
1. the clinical picture of HIV infection can be divided into 3 stages:
a. early, acute stage = 2-4 weeks after infection; Abs to HIV appear w/in 2 months after infxn
= fever, lethargy, sore throat, generalized lymphadenopathy, maculopapular rash,
leukopenia but # of CD4 cells is normal
b. middle, latent stage = a long latent period, measured in years
= px is asymptomatic & viremia is low or absent but a large amount of HIV is being
produced by the lymph node cells
= AIDS-related complex (ARC) syndrome can occur during this latent period
= frequent manifestation of the signs & symptoms of acute stage
c. late immunodeficiency stage =manifested by a decline in the # of CD4 cells to below 200/mm 3
& an increase in the frequency & severity of opportunistic infections
Fig. 45-3: Time course of HIV infection. Note that the level of virus in high early in the infxn,
drops to a low level for several years, & then rises during the immunodeficiency stage. The level
of CD4 lymphocytes remains more or less normal for many years but then falls. This results in
the immunodeficiency stage, w/c is characterized by opportunistic infections & malignancies
2. 2 most characteristic manifestation of AIDS

a. Pneumocystis pneumonia
b. Kaposis sarcoma
3. other opportunistic infections:
a. viral infxns = herpes simplex, herpes zoster, & CMV infxn & progressive multifocal
leukoencephalopathy
b. fungal infxns = thrush by Candida albicans, cryptococcal meningitis & histoplasmosis
c. protozoal infxns = toxoplasmosis & cryptosporidiosis
d. bacterial infxns = disseminated Mycobacterium avium-intracellulare & Mycobacterium
tuberculosis
4. neurologic problems = dementia & neuropathy
1. ELISA = detection of Abs; presumptive diagnosis of HIV infection
2. Western blot analysis = in cases of false-positives; the definitive diagnosis
3. isolation by culture = not available to all
= the polymerase chain reaction (PCR) is a very sensitive & specific technique used to
detect HIV DNA w/in infected cells
Treatment:
1. Azidothymidine (AZT, zidovudine, Retrovir) = is the treatment of choice
= prolongs survival & reduces the # of opportunistic infections but does not eliminated
the virus
2. Dideoxyinosine (ddI, didanosine, Videx) = is recommended for those who are intolerant of AZT
Prevention:
1. No vaccine for human is available
2. taking measures to avoid exposure to the virus (ex. using condoms, not sharing needles, &
discarding blood that is contaminated w/ HIV)
TUMOR VIRUSES
Overview:
= tumor viruses have no characteristic size, shape, or chemical composition
= the factor that unites all of them is their common ability to cause tumors.
Malignant Transformation of Cells
Features of malignant transformation

Feature Desrcription
Altered morphology Loss of differentiated shape
Rounded as a result of disaggregation of actin
filaments & decreased adhesion to surface
More refractile
Altered growth control Loss of contact inhibition of growth
Loss of contact inhibition of movement
Reduced requirement for serum growth factors
Increased ability to be cloned from a single cell
Increased ability to grow un suspension
Increased ability to continue growing
(immortalization)
Altered cellular properties Induction of DNA synthesis
Chromosomal changes
Appearance of new Ags
Increased agglutination by lectins
Altered biochemical properties Reduced level of cyclin AMP (cAMP)
Enhanced secretion of plasminogen activator
Increased anaerobic glycolysis
Loss of fibronectin
Changes in glycoproteins & glycolipids
Role of Tumor Viruses in Malignant Transformation

= although malignant transformation is a permanent change, revertants to normality do appear
= in the revertants studied, the viral genetic material remains integrated in cellular DNA but changes in the
quality & quantity of the virus-specific RNA occur.
Proviruses & Oncogenes

= are the 2 terms that expressed the 2 major concepts of the way viral tumor genesis occurs
1. In the provirus model, the genes enter the cell at the time of infection by the tumor virus
2. In the oncogenic model, the genes for malignancy are already present in all cells of the body by
virtue of being present in the initial sperm & egg; these oncogenes encode proteins that encourage
cell growth, ex. Fibroblast growth factor, in the oncogene model, carcinogens such as chemicals,
radiation, & tumor viruses activate cellular oncogenes to overproduce these growth factors; this
initiates inappropriate cell growth & malignant transformation.
Transformation of Tumor Viruses

1. Vertical transmission
= occurs by three methods:
a. The viral genetic material is in the sperm & the egg
b. The virus is passed across the placenta
c. The virus is transmitted in the breast milk
2. Horizontal transmission
= when vertical transmission occurs exposure to the virus early in life can result in tolerance to viral Ags &
the immune system will not recognize the virus
= when horizontal transmission occurs, the immunocompetent animal produces Ab against the virus & the
frequency of cancer is slow.
Evidence for Human Tumor Viruses
1. Human T-cell Leukemia Virus (HTLV)

= both HTLV 1 & 2 are associated w/ leukemia & lymphomas
= is the cause of tropical spastic paraperesis
a. Human T-cell leuklemia virus-I (HTLV-I)

= its RNA & proteins are different from those of all other retroviruses
= is not an endogenous virus but an exogenously acquired virus
= infects CD4-positive T cells preferentially
= transmission occurs primarily by sexual contact & by exchange of contaminated blood
b. HTLV-II = has 6% genetic homology w/ HTLV-I

= is transmitted primarily by blood & semen & infects CD4-positive also
= polymerase chain rxn is required
2. Human Papillomavirus (HPV)

= papillomas (warts) are benign but can progress to form carcinomas esp in an
immunocompromised person
= primarily infects keratinizing or mucosal squamous epithelium
= carcinogenesis by HPV involves 2 proteins encoded by HPV genes E6 & E7 that
Interfere w/ the activity of the proteins encoded by 2 tumor suppressor genes, p53 & Rb
(retinoblastoma) found in normal cells.
= in most of these tumor cells, the viral DNA is integrated into the cellular DNA & the E6
& E7 proteins are produced.
3. Epstein-Barr virus (EBV)

= is a herpesvirus that was isolated from the cells of individual w/ Burkitts lymphoma
= associated also w/ nasopharyngeal carcinoma & thymic carcinoma & B cell lymphoma
= in Burkitts lymphoma cells, a cellular oncogene, c-myc, which is normally located on
chromosome 8, is translocated to chromosome 14 at the site of immunoglobulin heavy-
chain genes; this translocation brings the c-myc gene in juxtaposition to an active
promoter, & large amounts of c-myc RNA are synthesized.
4. Herpes Simplex Virus Type 2 (HSV-2)

= is included as a possible human tumor virus on the basis of 2 main lines of evidence:
a. Epidemiologic
b. Molecular
5. Hepatitis B Virus (HBV)
= HBV infection is significantly more common in patients w/ primary hepatocellular
carcinoma (hepatoma)
= chronic HBV infection commonly causes cirrhosis of the liver.
MINOR VIRAL PATHOGENS
Characteristics Representative Virus(es)

DNA enveloped viruses Herpes B virus, human herpesvirus 6, molluscum contagiosum virus,
cowpox virus, monkeypox virus
DNA nonenveloped viruses Parvovirus B19
RNA enveloped viruses Coronoviruses, Ebola virus, Hantaan virus, Japanese encephalitis virus,
Lassa fever virus, lymphocytic choroimeningitis virus, Marburg virus,
spumaviruses, Tacaribe complex of viruses
RNA nonenveloped viruses Astroviruses, encephalomyocarditis, Norwalk virus
@ These viruses are presented in alphabetical order:
1. Astroviruses = have a characteristic 5- or 5-pointed star-shaped morphology

= cause watery diarrhea esp in children
2. Coronaviruses = w/ club-shaped surface spikes that resemble a corona
= cause upper respiratory tract infection (colds) in adults
3. Ebola virus = is named for the river in Zaire that was the site of an outbreak of hemorrhagic
fever in 1976; member of the filovirus family
= disease begins w/ fever, headache, vomiting.& diarrhea; later bleeding into the GIT
occurs, followed by shock & disseminated intravascular coagulation
= mortality rate approaches 100%
4. Encephalomyocarditis virus = causes either encephalitis or mild febrile illness
= member of the picornavirus family
5. Hantaan virus = cause of Korean hemorrhagic fever (KHF); member of the bunyavirus family
= main reservoir: rodents, mice & voles
= transmission to humans: aerosols of various secretions or excretions; transmission
between humans does not occur
= ribavirin may be an effective treatment
6. Herpes B virus = cause a rare, fatal encephalitisin persons in close contact w/ monkeys & their
tissues (ex. zookeepers or cell culture technicians)
= diagnosis is made only by recovering the virus
= treatment: acyclovir
= prevention: * using protective clothing & masks to prevent exposure to the virus
* immune globulin containing Ab to herpes B virus should be given
after a monkey bite
7. Human Herpesvirus 6 = cause of exanthem subitum (roseola infantum), a common dse in infants,
characterized by high fever & transcient rash
= virus is lymphotropic & infects B cells primarily
8. Japanese Encephalitis virus = common cause of epidemic encephalitis
= member of flavivirus family
= transmitted to humans by certain species of Culex mosquitoes endemic to Asian rice
fields
= 2 main reservoir: birds & pigs
= dx: isolation of virus & detecting IgM Ab in serum or spinal fluid
= prevention: * consists of an inactivated vaccine & pesticides to control the
mosquito vector
* immunization for individuals living in endemic areas for several
months or longer
9. Lasse Fever virus = causes a severe, often fatal hemorrhagic fever characterized by multiple-organ
involvement
= member of the arenavirus family (arena means sand)
= most striking feature is the sandlike particles on their surface, w/c are ribosomes
= primary reservoirs: rodents Mastomys
= transmission: by contamination of food or water with animal urine
= dx: isolating the virus or by detecting a rise in Ab titer
= treatment: ribavirin, reduces the mortality rate if given early
= prevention: centers around proper infection control practices & rodent control
10. Lymphocytic Choriomeningitis virus = member of the arenavirus family
= a rare cause of aseptic meningitis & is indistinguishable from the other viral causes
= CSF show an increased # of cells, mostly lymphocytes, w/ an elevated protein level &
normal or low sugar level
= reservoir: mouse
= virus transmitted to humans via food or water contaminated by mouse urine or feces
= human are accidental dead-end hosts
= dx: isolating the virus from CSF & by detecting an increase in Ab titer
11. Marburg virus = similar to Ebola virus that both cause hemorrhagic fevers
= members of the filovirus family
= the common feature of the infected individuals was the exposure to African green
monkeys from Uganda
= dx: isolation of the virus & detecting a rise in Ab titer
= prevention: no vaccine available
2ndary cases among medical personnel have occurred, therefore,
stringent infection control practices must be instituted to
prevent nosocomial spread
12. Molluscum Contagiosum virus = one of the 2 causes of warts in the adult genital region, the other
being the human papillomavirus
= transmission: by direct skin contact, sexual intercourse (accounts for the genital
lesion)
= member of poxvirus family
= lesions are usually removed by surgery, electrocautery or cryotherapy
= even w/o treatment, the lesions will resolve spontaneously in a few years
13. Norwalk virus = one cause of gastroenteritis; member of calicivirus family
= transmission: virus is transmitted by the fecal-oral route & occurs worldwide;
(uncommon in children)
= temporary immunity: less than 2 years
= dx: either immunoelectron microscopy or radioimmunoassay can be used
= treatment & prevention: no antiviral therapy nor preventive measures other than hand
washing
14. Parvovirus B19 = is the 1st parvovirus to be confirmed as a cause of human disease
= common disease cause is erythema infectiosum (a self-limited dse of children that is
characterized by a slapped-cheeK rash
= preferentially infects immature red blood cell precursors & kills them
15. Poxviruses of Animal Origin = 4 poxviruses cause disease both in animals & man (poxlike
lesions): a. cowpox virus
b. pseudocowpox virus
c. orf virus = contagious pustular dermatitis in sheep & vesicular
lesions on the hands of sheepshearers
d. monkeypox = causes human dse that resembles smallpox
16. Spumaviruses = subfamily of retroviruses = cause a foamy appearance in culture cells (can
present problem in the production of viral vaccines if the contaminate the cell cultures
used to make the vaccine)
= no known human pathogens
17. Tacaribe Complex of viruses = contains 2 human pathogens: (both cause hemorrhagic fever-
characterized by fever & bleeding into the GIT, skin, other organs; the bleeding is due to
thrombocytopenia)
i. Junin virus in Argentina
ii. Machupo virus in Bolivia
= agricultural workers are at high risk; endemic in rodent population
= transmitted to humans by accidental contamination of food & water by rodent excreta
= dx: either by isolation of the virus or rise in Ab titer
= no antiviral therapy or vaccine is available

Basic Mycology Guide

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Basic Mycology Guide

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MYCOLOGY

I. STRUCTURES & GROWTH

Table 47-1 Comparison of fungi and bacteria

2 Fungal cell structures are important medically:

THALLUS = actively growing vegetative portion

SPORES structure set aside for reproduction

PHIALIDE a flask-shaped projection from the mycelium of certain fungi

III. FUNGAL TOXINS & ALLERGIES

2. allergies = to fungal spores

IV. LABORATORY DIAGNOSIS

MYCOSES = are diseases of fungal etiology

CHARACTERISTICS OF THE MORE COMMON ISOLATED DERMATOPHYTES

DERMATOPHYTES COLONIAL GROWTH MICROSCOPIC

A. Epidermophyton center of colony 1 week Macroconidia large, smooth-walled

2. M. canis granular or cottony w/ 1 week thick-walled spindle shaped, multi-

3. M. gypseus cinnamon colored, 1 week rough-thin walled, elliptical multi-

3. T. rubrum flat or heaped up colony, 2 weeks delicate hyphae w/ tear-shaped

Etiologic Agents Diagnostic Features

C. Mycetoma (Maduromycosis) = most common cause of Pseudallescheria boydii (sexual form);

D. Rhinosperidiosis = caused by Rhinosporidium seeberi

E. Lobomycosis = caused by Loboa loboi

IV. OPPORTUNISTIC MYCOSES

Comparison of viruses and cells:

Property Viruses Cells

CAPSOMER = protein sub-units of the capsid

PEPLOS = a lipoprotein projections that extends from the capsid

PEPLOMERS = lipoprotein sub-units of the peplos

Atypical Viruslike Agents

Viral Growth Curve

Stages of the viral growth cycle

GENETICS & GENE THERAPY

@ The study of viral genetics falls into 2 general areas:

Gene Therapy & Recombinant Vaccines

CLASSIFICATION OF MEDICALLY IMPORTANT VIRUSES

= the classification of viruses is based on chemical & morphologic criteria

I. Based on Tissues predilection

A. DNA Containing Viruses

2. Papovaviruses = naked icosahedral tumor inducing viruses

3. Adenoviruses = naked icosahedral double stranded DNA viruses

6. Poxviruses = largest & most complex of all viruses

7. Iridoviruses = icosahedral cytoplasmic deoxyviruses w/c are mostly insect viruses

Table 31-2. Classification of RNA viruses

B. RNA Containing Viruses

2. Calicivirus = naked icosahedral viruses

9. Rhabdoviruses = are bullet-shaped enveloped viruses w/ a helical nucleocapsid & a single-stranded,

13. Bunyaviruses = the term bunya refers to the prototype

The ability of viruses to cause disease can be viewed on 2 distinct levels:

The Infected Cell

2. fusion of cells to form multinucleated cells

4. no apparent morphologic or functional change

2. replication of the virus & damage to cells

5. persistence of the virus in some instances

= 3 types of clinically important persistent viral infections :

c. fever inhibits viral replication in 2 ways:

e. factors that modify host defenses:

= 2 MAIN MECHANISMS HOW Ab INHIBIT VIRUSES:

b. Passive immunity = passively acquired by the transfer of immune serum

3 Approaches to the diagnosis of viral diseases by the use of clinical specimens:

1. Identification of the virus in cell culture

2. microscopic identification directly in the specimen

3. serologic procedures to detect a rise in Ab titer or the presence of IgM Ab

Potential sites for antiviral chemotherapy

Site of Action Effective drugs