Types Morphology Epidemiology Virulence Factors Diseases Prevention/ Treatment

Eukaryotes: therefore a problem when trying to treat

Monomorphic or dimorphic (Monomorphic form is in yeast
form, Dimorphic becomes yeast when parasitic)
filamentous: moulds: most common at room temperature
and free living. Unicellular: Yeasts
4 classifications based
site of body affected::
1. Superficial (Black
and white piedra, tinea
Fungus: general
versicolor, tinea nigra)
2. Cutaneous: (most
tineas)
3. Submucotaneous
4. Systemic (invade
from lung foci:
histoplasmosis,
blastomycosis,
coccidioidomycoses)
Superficial: live on outermost, non-living layer of
Tinea (pityriasis) versicolor
skin. No immune reaction.
Superficial Mycoses Tinea nigra Found in soil
Black piedra
White piedra
Mistakenly termed
Cutaneous Mycoses Affects deeper layers of skin, hair, nails. Most tineas
"dermatophytes"
Fluoresce under Clinical diseases are termed
Among most common of human disease
Wood's Lamp (+) "tineas".
Evokes inflammatory immune response
Affecs dermis, subcutaneous tissue (fascia,
Submucotaneous muscle and bone)
Mycoses Most commonly due to tissue trauma
 Mycotic agents are
fungi that are inherently
Invade internal organ M/C'ly from lung foci of
virulent and can cause Histoplasmosis
infection
disease in healthy
humans.
Strict pathogens or M/C'ly develop mild acute/asymptomatic lung
opportunistic infections, but can also develop into chronic or Blastomycosis
pathogens. sub-clinical (latent) disease.
Monomorphic
(cryptococcus
neoformans) or
Coccidioidomycoses
dimorphic (change
shape in infection:
thermal dimorphism)
Found in "Histo belt". Grows in soil rich in
Systemic mycoses Histoplasma 2 phases: Saprobic phase (in this phase when in Histoplasmosis (acute and
nitrogen (agricultural belt where there is lots of
environment/ culture), found in nitrogen-rich soil (eg. chronic), ocular histoplasmosis
capsulatum fertilizer use). Also found in areas of lots of
Agricultural areas) syndrome.
bird/bat excrement (caves).
Fragments are inhaled, phagocytosed by
In parasitic phase, they are found in the macrophages of
macrophages, replication within macrophages,
MPS (mononucleocyte phagocytic system)
carried by lymphatics throughout body.
Blastomyces Endemic areas overlap those of
dermatides Histoplasmosis.
Rarely cultured from soil (unknown reservoir)
Dust clouds at construction sites. Spread by
inhalation of conidia. Replicate in
macrophages, carried by lympatics OR
BLOOD.
Dimorphic: at 37C (tissue), multinucleated spherule Endemic in soils of hot, dry, semi-arid areas,
Coccidiodes immitis
"sporangia". spread via dusty storms.
Body fights viruses through:
Basic viral structure: Most commonly acquired by inhallation. Interferon, NK cells, T cells,
Antibodies.
Spread to secondary site via blood (viremia) or
Virion: whole virus particle lymphatics (during incubation period). Could
have prodrome in this period.
Capsid: Protein coat
Nucleocapsid
VAPs (viral attachment particles)
Envelope: contains VAPs
Viruses: general
Hemagglutinins: cause clotting
Enveloped viruses are less hardy than naked capsid
viruses.
Enveloped: Fragile, must be wet, acid-labile, spreads
btwn cells without lysing them, pathogenesis d/t
hypersensitivity/inflammt'n
Naked Capsid: Robust, survive some drying, Acid-
resistant, spread by lysing cells, pathogenesis d/t cell
lysis.

HSV TRANSMISSION = 4 M's

Group of viruses with common virion morphology AND Even prodrome can be infectious.
MIXING, MATCHING of MUCOUS
mode of replication Wear gloves when examining.
MEMBRANES
Structure = ENVELOPED so must be MOIST to be
infectious
Replication:
ENTRY = envelope fuses with host cell plasma
membrane
OUTCOMES (for each HSV type):
1) LYTIC Infections
Herpes Veridae 2) LATENT Infections
Family 3) PERSISTENT Infections
4) IMMORTALIZING Infections
Infects and replicates by MUCOEPITHELIAL cells and
establishes lytic, persistent and latent infections. TRANSMISSION: Infects above the waist.
HSV-1 Infection process: EARLY on in life. ORAL contact.
SKIN BREAK > Localized primary infection in mucosa > Autoinnoculation possible to eye or mouth
VASCULAR lesions > RETROGRADE transport (latent TRANSMISSION: Below the waist. Later on in
HSV-2 infection) > STRESS trigger (emotional, fever, direct life.
sunlight, menstruation/hormones, immunosuppression) * Horizontal & Vertical (in utero).
infects SAME spot/dermatome each time
 LIKE HSV:
Cause blister like lesions (like HSV) but different sizes,
stages, deeper, more painful and can cause scarring)
Establishes LATENT infections
Very contagious from 48 hours before
symptoms until all lesions are completely dry.
Peak occurrence of chicken pox is under 5yrs
old, but Shingles is over 65 yrs old

In nerves, CMI plays a big role in controlling infections

Active Herpes Zoster can cause Chicken Pox in
a susceptible child or adult but will NOT cause
UNLIKE HSV: Shingles.
Spread predominantly by the RESPIRATORY route (see
more lesions on thorax) and NO DETECTABLE
LESIONS at site of entry. Varicella: Healthy kids not treated -
Varicella Zoster Virus
relatively mild disease that gives
(Herpes Virus 3)
Primary Infection = lymphatics life log immunity
Secondary Viremia = concentrated in thoracic with
vesiculopapular rash.

VZV becomes latent in dorsal root or cranial root ganglia.

THEN reactivated in older adults in older adults and
immunocompromised, migrates to dermatome =
Shingles.

contains both mRNA and DNA unlike other viruses

Opportunistic pathogen
trasnmitted as STD, Transfusion/ transplantation, oral,
congenital

Similar to other Herpesviridae: Fetus is infected either: 1) placenta

Cytomegalovirus
1) cell-cell spread- syncytia blood 2) ascending infection from
healthy immune system, safe sex.
2) latent state cervix Confirm by isolating CMV from
3) reactivation in immunosuppressed state child’s urine in 1st week of life

Lymphotropic
latent in T cells .

Ultimate B lymphocyte pathogen – mitogenic

and immortalizing (keeps cell growing by
stopping apoptosis)
saliva remains infectious for months after clinical EBV Mono TX and control
-transmitted by saliva or contaminated
recovery. -Ginseng, Licorrice, Schisandra,
EBSTEINN-BARR glassware
-immunity to EBV is “life-long”. Very mild in children. Carsinosum (homeopathy).
VIRUS -cause neoplasms (but need cofactor)
I Control: impossible virus is
-very limited host range and tissue tropism
-lytic (lesions) or latent infections OR ubiquitous and is shed from saliva
immortalizing infection of healthy people.

Rapid onset of high fever for 4-5 days. Fever subsides

HSV-6 Roseola
and then get maculopapular rash (trunk and neck).
infantum
Exanthum subitum
HIV-6A Mononucleosis type illness (heterophile -).

Other Herpes Virus HSV-7 ORPHAN virus

Other Herpes Virus

Kaposi’s sarcoma (neoplasm of blood vessels –

HSV-8 weakened bv’s. Purple lesion) in AIDS patient (high
incidence after KI transplant)

Structure: Delicate outer envelope. Glycoprotein (gp) 120 Retroviridae: “retrovirus” because it uses
(Ag and receptor specificity high amount of antigenic reverse transcriptase. Four subfamilies: know
shift). Very limited host and species range. This gp-120 LENTIVIRINAE (slow replicating) causes
continuously changes so it is difficult to treat (no vaccine). AIDS

Tropism: gp120 à initially attaches to CD4

receptor on macrophages, later attaches to
CD4 receptor on Th cells and CXCR4 (fusin)
chemokine receptors (i.e. need these co-
receptors/chemokines to get HIV in for
development of AIDS)
Types: HIV-1(world) HIV-1: 70% men, 42% MSM (men sex with men). Developing
and HIV-2 (West countries: relative increase among heterosexuals. HIV-
Africa). 2: mostly west Africa
pathogenesis: Attachment to cell FUSION of
envelope. Makes dsDNA copy of itself.
HIV and HIV (+) does not mean you have
Reverse transcriptase is very ERROR prone
opportunistic fungal AIDS. CD4+:CD8+ tells status and
(structurally changing all the time).
infections Increased risk with anal sex – only one staging of AIDS.
INTEGRASE (to integrated into host
layer of colonic cells and cells might Lots we can naturopathically.
chromosome). ). Viral DNA transcribed by host
have certain co-receptors Prevention: safe sex – latex
DNA pol II, also transcribes its own
condoms only
enhancer/promoter region. Viral protease
cleaves to make infectious virions. Lytic
. infection. Synctitia (can spread between cells).

TRANSMISSION : Sexual (anal and vaginal). Oral sex less infectious than other STDs.
Peri-natal. Blood: IV drug users, needle stick injury, blood transfusions.
Risks are slight unless close intimate contact and/or transfer of semen, blood, vaginal
secretions. Problem: long, prodromal asymptomatic period (infectious before identifiable
symptoms).
Delicate outer membrane: can’t stick, wont get the infection!
Not likely by: casual contact, touching, kissing (even open mouth), coughing, sneezing,
inset bites, water, food, utensils, toilets, swimming pools, public baths

Opportunistic fungi,
Associated with: Cause Disease iff:
-Dimorphic but unlike other mycotic agents
defective T cell immunity only , immunocompromised, broad spectrum
only present in hyphae in body
Candida Spp hypoparathyroidism, hypoadrenals ,glucose ABCS, dietary imbalance , endocrine
-no yeast cells
imbalances changes, pH changes
-detect after treatment of KOH 10%
disruption of normal bacterial ecology -Diseases are not contagious

Extremely common, no yeast-like form--only a

mold form
Strict pathogen (unlike Candida),
Aspergillus spp
-Aspergillosus flavus produces aflatoxin
hepatocellular carcinoma (HCC)

NO dimorphism in pathogenesis ,
encapsulated yeast ,
Acidic mucopolysaccharide capsule Virulence factors:
Cryptococcus spp
-Ubiquitous capsule (anti-phagocytic)
-pigeon droppings (desiccated alkaline rich, N2
rich, hypertonic
 Included with fungi only because of molecular
Oxygen
Pneumocystis traits , Opportunistic infection, found in
has features like protozoans ABCs
jirovecii (carinii) rodents, Transmission thru respiratory droplets
(increased risk if immuno suppressed)
Moribillovirus: measles
Similarities in family: Enveloped, form syncytia, replicate
virus - "rubeola", animal immunity from reinfection
in cell cytoplasm, transmitted via respiratory droplets
disease.
adult infectin is more severe than
children. VERY infections (less than Tx:sympomatic only no viral
Paramyxovirus:
mumps related to parainfluenza virus 2. one serotype mostly in school age 5-14 yr old. Increae risk of measles or Chicken pox). Spread by agents. Prevention: control almost
parainfluenzae and Mumps
(like measles) spread with crowding and in winter direct contactor respiratory secretions imposs due to virus ubiquitous and
mumps viruses
Life long resiistance to infection (like infectxion is subacute
measles)
Paramyxoviridae
family Tx: zinc lozengges every 2-4
hours. Max 60 mg. too high will
lower immune system. Engestol
VERY congagious, tranmitted by hands
ubiquitous, almost everyone in NA is infected RSV, #1 cause of severe lower (heel product decreases sore
Pneumovirus: smaller nuceocapsid more fragile ( to freezing) than other fomites and respiratory secretions.no
by age 4. epidemics EVERY winter in cold repiratory infection in young throat for flu virus) also
respiratory syncitial paramyxoviruses. Pathology due to direxct invasion of systemic spread/veremia . No long
temperate climate ( hot humid summerns in children ( day care and nurseries) homeopathic eupatorium .
virus "RSV" respiratory epithelium (syncythia) term immunity (unlike measles or
Hong Kong) #2 cause of parainfluenza Amost impossible and too
mumps)
ubiquitous to control. Good
vacines n/a. better prevention via
gloves, masks etc

Parainfluenza Family 4 serotypes

Types 1-3: 2nd M/C of #1 cause of RSV. 2nd main cause homeopathic: spongia. Tx
severe respiratory of severe respiratatory distress in symptoms only with nebulized hot
replicate faster than measles or mumps. only partial immunity from reinfection.
distress in infants and infants and young children. or cold stream, no Anti viral
Contagious before sx are present Get milder form ( unlike measels)
young children, also Laryngeotrachebronchitis therapy or vacines. Mistle toe good
causes croup ( croup) anti viral
Types 4: mild URI in transmission p to p in respiratory
children and adults droplets
Haemophillus influenza bacteria
(epiglottitis)
no anti viral treatment, mild dz with
Rubella (german measles)
enveloped ss RNA genome, unlike other toga virus: life long immunity. Vacination as
Always symptomatic but range
respiratory tropism and no detectable cytopathology (no less contagious than measles or MMR. Reduce risk of materal
Toga virus genus spread by repiratory secretions or from mild childhhood dz. German
lysis), only 1 serotype. Causes heterologous mumps or varicella. Life long immunity infection, live cold adapted vacine
rubivirus transplacental measles to severe congential
interference interference with replication of super just get sick do NOT give to pregnant mothers
defects. Increased risk of
infecting piconavirus DDX bwt: HSV6 B (roseola
harmful dz if pregnant
enphantu ??)
NAKED capsid virus = very RESISTANT to drying, TRANSMISSION = Respiratory droplets or Erythema Infectiosum (5th DZ), Tx not usually required (mild and
acid/base, salt, ect. close contact or blood products Aplastic Crisis and Arthritis. self-limiting).
FAMILY PAROVIRUS
FAMILY PAROVIRUS Assembly & replication - virus binds P antigen on RBCs,
erythrocyte progenitor cells, vascular endothelium and
fetal myocytes (anemia causing)
7 Types = grouped
because they all cause
LIVER damage
(jaundice)
HAV (infectious
hepatitis), HBV (serum
hepatitis), HCV, HDV,
HEV
NAKED = extremely STABLE capsid - except for
CHOLORINE. TRANSMISSION = Person to Person , Fecal-
Slow replication Oral, Sewage Contaminated food/water * often Avoid uncooked shellfish
Pathology due to immune mediated hepatocyte damage traceable source bc can live in water for many Chlorine treatment of water.
HAV
Not associated with HEP C months
Rarely get immune complex related rash and VACCINE
polyarthritis, rarely fatal (fulminant hepatitis) NO CHRONIC CARRIER

ENVELOPED - unusally stable for an enveloped virus

Prevention =
HepDNA Virus - Screening blood donors/products
Hepatitis Family TRANSMISSION = 1) percutaneous, 2) close
CAN cause HEPATOCELLULAR CARCINOMA - Avoid intimate contact with HBV
personal contact (highest risk is babies born to
NOT as resistant as HAV carrier (safe sex, no needle
HBV+ mothers NOT transplacental, 2) Blood or
Chronic, symptomatic or asymptomatic hepatitis sharing)
HBV Blood Products {(serum hepatitis) - needles,
- UNIVERSAL Blood/Fluid
std, perinatal, blood}
See GROUND GLASS hepatocytes in chronic phase Precautions - wash with 10%
bleach
CHRONIC CARRIER
m'cly regeneration of LV parenchyma after infection is
resolved. VACCINE

ENVELOPED
TRANSMISSION = parenteral (blood Universal blood screening, reduce
FLAVIVIRUS (like west nile virus)
transfusion, drug users, piercings, tatoos) - risk behaviours
Inactivated by DETERGENTS
HCV rarely sexual or perinatal
M'C cause of NON-ALCOHOLIC LIVER DZ in USA
Vaccine difficult due to HIGH
Only get partial immunity after recovery
Close link with HIV VIRAL HETEROGENEITY
Delta Agent = viral parasite ie. NEEDS HBV as HELPER
HDV
virus
TRANSMISSION = Fecal-oral (m'c in
HEV Severe in PREGNANT women
developing nations)
NOTE - Leisheid ran
out of time with
Hepatitis lecture so said
that we only have to
know a couple of points
for Hep D and Hep E.
These points are
include in this
document.
 Microbe System Condition Signs and Symptoms Contagious? DDX and Lab DX
"Spaghetti and meatballs" organism
Non-itchy, hypopigmented lesions on upper torso, arms, after KOH prep. Wood's lamp (+).
Malassezia furfur Skin (superficial) Tinea (pityriasis) versicolor abdomen Use this to DDX from vitiligo
(long name we don't need to
Skin (superficial) Tinea nigra Well demarcated lesions on palms and soles Dark pigmented yeast cells
know)
don’t need name Skin (superficial) Black Piedra Dark, hard nodules along infected hair shaft
don't need name Skin (superficial) White Piedra Soft, pasty white growth on hair shaft
don't need name Skin (cutaneous) Tineas Named for part of body they affect
Primary histopasmosis: acute, self-limiting influenzae-
CXR: residual calcified lesions in
Histoplasma capsulatum Systemic Acute histoplasmosis like illness. Complications: mediastinal fibrosis, ocular NO
lung, LN: "coin lesions"
histoplasmosis syndrome.
Serious retinal condition. Leading cuase of blindness in
Histoplasma capsulatum Eye Ocular histoplasmosis syndrome 20-40 year olds. Get "histo spots" bilaterally. MC'ly no NO
visual loss
Microscopy: 10% KOH prep with
Disseminated via lymphatics. Increased risk if cell- silver or Giemsa stain. Serological:
mediated immunity is impaired. Can look like TB! Fever, skin tests (like TB test), but there are
Histoplasma capsulatum Systemic Progressive histoplasmosis (chronic) NO
night sweats, weight loss with destructive (caseating) too many false positives. Cultures:
necrosis, lung lesions. slow growing (1-2 weeks) and
spores are infectious.
CXR: no residual calcified lesions,
Blastomyces dermatides Systemic Acute blastomycosis Bronchopneumonia, drenching sweats. NO
unlike histoplasmosis.
Skin test and serology: too many
TB or cancer-like!!! May present with skin lesions: slowly
false positives. Microscopy:
Blastomyces dermatides Systemic Chronic blastomycosis exanding ulcerative or verrucous lesions on face and NO
biopsy/histology of KOH-prepped
mucocutaneous borders of nose and mouth.
tissue sample. Culture (?).
Skin test antigens (like TB): Use 2-4
weeks after symptoms. Antigens
Most commonly asymptomatic. 40% mild, febrile to
are Coccidiodin and Spherulin.
moderately severe respiratory disease (much higher
Coccidiodes immitis Systemic Coccidiodomycosis NO CXR: Egg-shell lesions. Tissue
than histo). In disseminated form of disease (<<1%),
biopsy: spherules. Culture:
erythema nodosum with arthralgia.
CAUTION: Infectious. Leading
cause of lab-acquired infections.
Yes: infectious from
Oral Herpes LESIONS: "Dews drops on a rose petal" prodrome even to
Herpes (HSV) Oral Cavity (Herpes Simplex/Herpes Secondary infections are less severe, more loca;lized crusted lesions (wear
Gingivastomatitis) and shorter in duration than primary infection. gloves when
examining)
Lab Tests in general for HSV:
HSV Eyes Ocular Herpes/Herpes Keratitis Corneal Ulcers Yes
HSV Extremities Herpetic Whitlow Infectious lesions on fingers and wrists. Yes TZANCK SMEAR - look for
Sudden onset of nuchal rigidity, blinding headache, SYNCTIA. This test is not specific
HSV-2 Systemic Meningitis Yes
nausea and photphobia for HSV, also tests for VZV and HIV
Seizures, space occupying lesions (SOL) - cause
HSV-1 CNS Encephalitis Yes
destruction of temporal lobe. COWDRY TYPE A INCLUSION
STD - 3 to 5 days after contact. BODIES - positive with HSV and
Signs/SX = regional lymphadenopathy and painful VZV
HSV-1 and HSV-2 Genitourinary Genital Herpes Yes
shallow ulcers on genitals
RECURRENT with prodrome of burning & tingling. CHARACTERISTIC CPEs
Pruritis, vaginal or cervical mucoid discharge. Pain with
HSV-1 and HSV-2 Genitourinary Genital Herpes - Female intercourse. Slight increased risk of cervical cancer in
adulthood.
HSV-1 and HSV-2 Genitourinary Genital Herpes - Male Dysuria and/ro dyspaerunia
HSV Systemic Neonatal HSV Acquired in utero or during vaginal birth. Often fatal.

One of 5 childhood EXANTHEMS (others = rubella,

roseola, 5th disease, measles/rubeola)

Mild systemic signs: maculopapular rash ("dew drop on

a rose petal");
intense pruritis;
spread from back/chest to scalp (rarely on soles/palms)
and can spread to mouth, conjunctiva, vagina
SUCCESSIVE CROP OF LESIONS;
Varicella (VZV/HSV-3) Systemic Chicken Pox
prolonged low grade fever
extreme irritability/malaise.

Scarring

MUCH MORE HARMFUL TO ADULTS

COMPLICATIONS: Secondary bacterial infection, Lab Tests in general for VZV

Reye's Syndrome, CNS Syndrome.
TZANCK SMEAR - giant
Can occur after: Chicken POX, Enterovirus, EBV, multinucleate cells = SYNCTIA. This
Influenza B, Aflatoxin, Pesticide test is not specific for VZV, also
Varicella (VZV/HSV-3) Systemic Reye's Syndrome tests for HSV.
ASA associated = do NOT give aspirin to a child with
chicken pox. COWDRY TYPE A INCLUSION
BODIES = "drop-like masses of
acidophilic material surrounded by a
clear halo within the nucleus"
 test is not specific for VZV, also
tests for HSV.

COWDRY TYPE A INCLUSION

BODIES = "drop-like masses of
Recurrence of LATENT VZV infection due to stress, acidophilic material surrounded by a
immunocompromised) clear halo within the nucleus"

Prodrome - severe pain in localized nerve area

3-5 days later - gradual development of small red

macules, closely spaced, most common in thoracic area
Herpes Zoster Systemic Shingles
or trigeminal nerve area - UNILATERAL

Post Herpetic Neuralgia - if over 65 yrs old when

shingles develop = get long term (months to years)
severe recurring, burning or itching pain, hyperesthesia

UNLIKE HSV - lesions are various sizes

Inflamed Cranial Nerves 5 (facial paralysis) and 3

Herpes Zoster Eyes Herpes Zoster Opthalmicus
(corneal ulcers and blindness)
Ramsey Hunt Syndrome Painful lesions along Cranial Nerves 8 (severe otalgia,
Herpes Zoster
(Herpes Zoster Oticus) hearing loss, vertigo) and CN 5

Cytomegalovirus syndromes congenital cytomegalic inclusion disease M/C viral agent of congenital disease in U.S
cns microencephaly / hearing loss

skin rash
other hepatosplenomegaly Clinical signs and symptoms too
toxoplasmosis, other, rubella virus, CMV, herpes vague to be that useful and often
simplex/histoplasmosis ASYMPTOMATIC
•TORCH syndrome Conditions!27:27
-Tissue biopsy: Conditions!G43 eye
nucleus -cell culture:
characterisitic CPE in diploid
FIBROBLAST cells (best Dx).

Conditions!H26
 Clinical signs and symptoms too
vague to be that useful and often
ASYMPTOMATIC
Conditions!27:27
Cause: infected cervix, colostrums or milk. Two -Tissue biopsy: Conditions!G43 eye
peri-natal outcomes: (1) no clinical disease (2) clinical disease if nucleus -cell culture:
immunocomprimised characterisitic CPE in diploid
FIBROBLAST cells (best Dx).
child/adult
heterophile (-) and “mono-like” infection (mono is
heterophile +). Very common cause of failure of KI Conditions!H26
transplants.

immunocompromised pizza pie retina” CMV retinitis.

Scotoma absence or abnormal area in visual field
TRIAD of: fever, pharyngitis,
lymphadenopathy for 1-4 weeks.
kissing disease” – heterophile (+) ONLY one that is
DOWNEY cells.
heterophile (+)
MONOSPOT test (+)
Sx’s: high fever, malaise, pharyngitis, tonsils with
HETEROPHILE Abs – polyclonal
exudates, lymphadenopathy, hepatosplenomegaly,
EB V activation of B cells produces wide
fatigue. Looks like Strep throat.
repertoire of Abs that recognize
Rare progression: spleen rupture (avoid contact sports),
“Paul Bunnell” Ags on horse, sheep,
hepatitis
cow red blood cells but not guinea
pig.
Mononucleosis

1. overactive immune system: infectious mono

Immunity 2. lack immune response: lymphoma (Burkitt’s m/c).
Lymphadenopathy and atypical lymphocytes –
DOWNEY CELLS
Cyclic recurrent disease (of mono). Symptoms greater
than six months (normal is less than 4 months).
Chronic EBV disease
EBV induced lymphoproliferative disease (leukemia like)

Epithelial cell tumor.

Nasopharyngeal carcinoma Cofactor = ingested nitrosamines (preserved fish).

Tumor cells are from lymphocytes and contain EBV

DNA.
African Burkitt’s Lymphoma Malaria is a co-carcinogen (co-infection). Osteolytic
lesions in jaw, necrosis, gray-white.

Opportunistic infection in HIV/AIDS. Vertically ribbed

Hairy Oral Leukoplakia keratinized plaques on lateral borders of tongue (DDx:
candidiasis and histoplasmosis)
Inactivate keys elements of immune system (inactivate
CD4+ T cell). Hypervariable regions (gp120). Latent
infection (unique promoter/enhancer regions – LTRs).
HIV Immune Sits “under radar” of immune system and decreases
immune system. Suppresion: Direct (cytoxicity of Initial screen: indirect ELISA for gp120
CD4+) OR Indirect (induce apoptosis, decreased or gp41. New – Ora Quick Rapid HIV-1
suppressive factors). Ab test.
Only in 5%. Mono-like syndrome (heterophile negative –
do spot test!) Mucocutaneous sores. PGL – persistent
HIV
generalized lymphadenopathy. Mouth ulcers, oral Western Blot (to confirm): for gp120,
Acute retroviral syndrome candidiasis p24, p31 proteins
 Markers: P24 – high at start and then
goes down, then high at AIDS. Anti-
Weight loss (“slim disease”), night sweats, fatigue, HIV-1 Ab: low, then high for most of
HIV Mild Stage disease, then drops at AIDS. CD4 T cell
opportunistic infections
– gradually goes down (AIDS = below
200-400 ug/ml)
1. Presence of anti-HIV gp120 Abs. 2. decreased CD4+
HIV AIDS T cell count. 3. Wasting syndrome 4. Presence of
opportunistic infections because CD4+ is diminished)
Lab Dx:
Active viral replication (recent
Hairy oral leukoplakia, extensive oral thrush, Kaposi’s infection or late stage). Direct ELISA
HIV Secondary infections sarcoma, Pneumocystis pneumonia (caused by P. for p24 (viral load or reverse
carinii), CMV retinitis. transcriptase in blood via PCR).
Syncytia (from culture).

Sub-acute encephalopathy. Slow, progressive

HIV Dementia deterioration of mental abilities (can mimic Alsheimer’s
disease).
HIV Malignancy Kaposi’s sarcoma

Focal white patches on oral mucosa, palate and tongue Microscopy

that bleed when scraped off , red flag for AIDS iff tissue scrapings treated with 10%
Candida Spp Oral candidiasis : “Thrush KOH
thrush in adults NOT receiving corticosteroid therapy or
broad spectrum ABCS -Culture
Common female disease--change in vaginal flora or -confirm + microscopy--grow on
STD, signs and symptoms: Sabourad agar
Candida Spp Vaginal candidiasis “Yeast infection erythema (“beefy red”)/ inflammation vagina/ vulva -Germ tube test
thick white or curd-like discharge fmust be examined after 2-3 hours
intense pruritus, unique to Candida spp
Chronic mucocutaneous candidiasis Heterogeneous group of treatment resistant superficial -Serology
Candida Spp
(CMC) Candida infections of skin, nails and oropharynx high titer of fungal glycoprotein Abs
Spread to many organs in recent or active infection or
Candida Spp Disseminated candidiasis eg. eye, Candida specific mannan
*****must be immunocompromised
Candida Spp Candida endopthalmitis n/a

Culture:
Mycotoxicoses hypersensitivity
on Saboraud agar
pneumonitis
Aspergillus spp allergic bronchopulmonary aspergillosis associated with asthma (10-20%)
-Tissue biopsy:
10% KOH prep of sputum

Aspergillus spp
Aspergillus spp
Aspergillus spp
A chronic clinical situation, minimal distress, hemoptysis fungus ball on CXR that moves with
Aspergillus secondary colonization
fungus ball on CXR that moves with dependency dependency
Chronic sinusitus due to Aspergillus colonization of
Paranasal granuloma
paranasal sinuses
rapidly fatal if not treated
Apergillosus systemic disease

Busse-Buschke disease or torulis Cryptoccocus neoformans diagnosis

Cryptococcus spp Cryptococcosis M/C’ly self-limiting mild pulmonary infection Microscopy:
M/C in males examine CSF after treating with 10%
M/C cause of fungal meningitis, KOH and India ink,
insidious onset , -Serology
Cryptococcus spp Cryptococcosis meningitis immunocompromised also get skin lesions or look for capsular Ags
osteolytic bone lesions, unlike other systemic mycoses that
50% mortality look for Abs

non-specific PCP CXR plasma cell infiltrates

Pneumocystis jirovecii (carinii) pneumonia
Extrapulmonary--in AIDS
Pneumocystis jirovecii (carinii)
Morbillovirus Measles (Rubeola)
Sub-acute sclerosing panencephalitis
Morbillovirus
(complication of measles)
from hilum with “ground glass
appearance" Microscopy
typical octonucleate cysts
Is still one of the most common causes of death in
children 1-5 years of age in developing countries.
WHY? (Nutritional status plays a huge role). Nearly all
people infected become unwell and develop disease.
Very characteristic, pathognomonic clinical presentation
Diagnosis: M/C clinical only,
(cough coryza, conjunctivitis). Complete resistance to
Very contagious: 85% pathognomonic. 4X increase in
re-infection. Big contrast in disease severity with proper
infection rate measles-specific IgMs suggest
nutrition, access to health care, etc. Signs and
recent infection.
Symptoms: Cough coryza, conjunctivities, photophobia.
2 days later: Koplik's spots "grains of salt surrounded by
a red halo". 1-2 days later: rash, maculopapular
descending rash. Treatment and prevention: MMR
vaccine.
Characterized by changes in personality, behaviour,
memory, movement.
 mild cold like URI (pharyngitis, coryza fever, wheezing)
DDX: laryngitis ( hoarseness,
to bronchitis and pneumonia. Milder disease in older
ubiqutous and burnng retrosternal pain with
severe respiratory distress and croupin in children and adults. Subglottal swelling, erythema and
spreads rapidly in breathing). Lab DX: Xray: steeple
parainfluenza virus repiratory infants.Laryngeotrachebronchitis AKA edema of tracheal walls, sounds worse than the look.
hospitals and sign. CPE in primary monkey Ki
CROUP 2-6 day incubation: seal bark horse brassy cough.
nurseries cells: presence of Syncytia and
inspiratory stridor. tachycardia, tachypnea, suprasternal
haemadsorb guinea pig RBC's
retraction. Self limiting in 48 hrs. boys 1-6

swelling of epiglottis, look worse than they appear-

toxic appearance. Major repiratory distess and dyspnea ubiqutous and
NO COUGH. Dysphagia with drooling.irritability, fever, spreads rapidly in
haemophilllus influenza respiratory epiglottitis Lab DX: Xray: Thumb sign
dysphonia (hot potato voice). 2-5 y olds. Medical hospitals and
Emergency (don't do throat swab as childs thoat nurseries
could spasm)
infects respiratory tract epitheial cells, parotid gland via
viremia or Stenson's duct (on oral cheek near 2nd
molar). Parotitis ( infected cells lining ducts of glands
degenerate. Causes inflmation , lymphocyte infiltration test samples from saliva ( 5 days
and edema. SX: mostly asymptomatic (unlike measles), after onset). Urine ( 2 weeks after
sudden onset of malaise, anorexia for 2days, then fever onset), also CFS. Serology. 4X
paramyxiviridae genus very infections but
(38.3-40 C), ear ache, bilateral parotitis. Self limiting in increase in mumps specifc IgM in
Paramyxovirus ( related to URT, CNS, glandular, testes, ovaries, pancreas mumps less than measles or
2 weeks. Sequelae: Orchitis: unilateral testicular blood, elevated amylase (affects
parainfluenza virus 2 chicken pox
swelling if bilaterally = sterility. Oophoritis: pancreas). Hemadsoption (guinea
unexplained abdominal pain. Pancreatitis (rare but pig RBC syncytia from due to
linked to juvenile DM. Meningitis: H/A, stiff neck, presence of viral hemagglutin
drowsiness, unsteadiness when walking. #1 cause
of aseptic meningitis in non immunized. arthritis
(rare)
4-5 day incubation. Infection localized to upper or
lower respiratory tracts. Ranges from common cold to serology 4X increase in anti RSV
paramyxiviridae genus
URT, RSV (respiratory syncitial virus) pneumonia and bronchiolitis. URI with marked very titre indicates actdive dz..direct
Paramyxovirus
rhinorrhea.Bronchiolitis in infants. OM also common, ELIZA or immune florecence, CXR
risk of asthma attack

Children 14 -21 day incubation. 3 day measles . Mild

URI, regional lymphadonopathy (esp sub occipital less contagious than
glands), one week later spead to skin ( rash -small measles or mumps or
erythematous nodles that spread from face to trunk/lims, varicella. Highly
gone in 3 days. Placenta joints, Ki. Dz has similar infectious for first difficult to Dx clinically, urine viral ag,
severity even if immunosuppressed. In adults, more months of life serology: RIA, or ELIZA. Congenital:
Toga virus genus rubivus respiratory, skin, lymphatics Rubella
severe than in children. Also polyarthritis of fingers, Congenital rubella: highly specifc anti rubella IgM, NO
mstly females ankles wrists and knees,. Lasts a few increased risk (70%)if CULTURE no characteristic CPE
days to a year. Rarely progrsses to post infection If in mother infected in 1st
first trimester virsu replicates in placenta :eratogenic tri. In 4th tri (20%) and
effects. Classic triad: eye cataracts, ears deafness, heart only risk of deafness.
ventral septal defects, ductus arterious.microencephaly

50% are ASYMPTOMATIC

If symptomatic = SLAPPED CHEEK rash on cheeks
spreading to trunk and limbs (lacey reticulate
appearance)
Parovirus skin Erythema Infectiosum
2 Phases: 1) Infectious 2) Immune reaction = Rash or arthralgia
Serology: IgM 2-7 days after rash,
RECURRENT RASH that is worse with sunlight, stages are NOT
but IgG comes later and persisit for
exercise, hot water and stress infectious (immune
life
complex related)
If mother infected during 2nd and 3rd trimester =
Parovirus B19 systemic Hyrops Fetalis
HYDROPS FETALIS (massive edema)
Parovirus B19 systemic Aplastic Crisis Increased risk if SCA or Thalassemia ie. Chronic
Symmetrical, transient polyarthritis. Presents just like
Parovirus B19 systemic (joints)
RUBELLA arthritis
Often asymptomatic (only 1-2% get jaundice)
One month incubation - abrupt onset of icteric symptoms
Food ingested = source of infection
- progressively worse for 4-6 days and then symptoms Ingested -
Picornavirus systemic Hepatitis A Serology: ACUTE or RECENT -
DECREASE = jaundice appears (67%) SHELLFISH
AntiHAV by ELISA or RIA
Rarely progresses to fulminant hepatitis.
 Longer incupation than HAV = up to 3 months and then
INSIDIOUS onset of symptoms

Most commonly mild symotoms with hypersenstivity

reactions due to HBsAG:Ab complexes

ACUTE HBV: only apparent clinically in 25% of patients;

Infectious up to 45
non-specific symptoms = hepatomegaly with RUG SEROLOGY:
Hepadnavirus systemic Hepatitis B days before onset of
tenderness and Jaundice (1) RECENT INFXN = ANTI-HBc
symptoms
SERUM SICKNESS IgM or use PCR for HBV DNA;
HBsAG, HBcAG, HBcAG;
CHRONIC HBV: Detected through LAB DX (increased (2) CHRONIC HBV = HBcAG and
LV enzymes on CBC) HbsAg;
(3) CHRONIC CARRIER = HBsAg,
If co-infected with HDV can lead to FULMINANT HBcAb, HBV DNA(+)
HEPATITIS

80% of primary hepatocellular carcinoma is due to HBV

infection = 1st vaccine preventable cancer
HBV (hepadnavirus) Most common if HBV and HCV coinfection.
Liver Hepatocellular Carcinoma
AFLOTOXIN B (peanuts)
1/3 asymptomatic - m'c sx = weight loss, fatigue,
anorexia (non-specific)
6-8 WEEK incubation
Perdispose to cirrhosis (especially if alcoholics and
Flavivirus systemic Hepatitis C smoker) INDIRECT elisa: ANTI-HCV Ab
RARELY progress to Fulminant Hepatitis - BUT cause
30% of all cased of fulminant hepatitis
Delta Agent (virus like) systemic Hepatitis D 40% of Fulminant Hepatitis cases
Calcivirus systemic Hepatitis E
 A 56-year-old man complains of
severe pain caused by a belt of
vesicular lesions across the left side of
his abdomen. What is the source of
his infection?
A) aerosolized droplets
SAMPLE QUEST; HIV B) contaminated food or water
C) endogenous activation of an earlier
infection
D) sexual activity

A 32-year-old man with AIDS

develops symptoms consistent with
the diagnosis of cytomegalovirus
(CMV) retinitis. Confirmation of the
diagnosis could be obtained by which
test result?
A) atypical lymphocytes in blood
sample
B) ELISA for antibody to CMV in
serum sample
Sample Question C) epithelial cells with owl’s eye
inclusion bodies in urine sample
D) immunofluorescence of tear-
infected tissue culture fibroblasts

A 23 year old man has been suffering

from a fever, pharyngitis, arthralgia,
and myalgia for approximately 1 week.
Throat examination shows white
exudate on enlarged tonsils. Which
analysis would be most useful for
confirming the diagnosis?
A) evaluation for antibody to CMV
Sample Question B) Evaluation for HIV viremia
C) Monospot screen test for EBV
infection
D) Rapid plasma reagin screen test
for syphilis