Micro Chart #3-- Italics Only

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

Fungus: general

4 classifications based site of body affected:: 1. Superficial (Black and white piedra, tinea 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 skin. No immune reaction.

Cutaneous Mycoses

Submucotaneous Mycoses

Tinea (pityriasis) versicolor Tinea nigra Black piedra White piedra

Superficial Mycoses

Mistakenly termed "dermatophytes" Fluoresce under Wood's Lamp (+)

Affects deeper layers of skin, hair, nails.

Most tineas

Among most common of human disease

Clinical diseases are termed "tineas".

Evokes inflammatory immune response Affecs dermis, subcutaneous tissue (fascia, muscle and bone) Most commonly due to tissue trauma

Found in soil

Mycotic agents are fungi that are inherently virulent and can cause disease in healthy humans. Strict pathogens or opportunistic pathogens. Monomorphic (cryptococcus neoformans) or dimorphic (change shape in infection: thermal dimorphism) Systemic mycoses Histoplasma capsulatum

Blastomyces dermatides

Coccidiodes immitis

Invade internal organ M/C'ly from lung foci of infection

Histoplasmosis

M/C'ly develop mild acute/asymptomatic lung infections, but can also develop into chronic or sub-clinical (latent) disease.

Blastomycosis

Coccidioidomycoses

Found in "Histo belt". Grows in soil rich in nitrogen (agricultural belt where there is lots of fertilizer use). Also found in areas of lots of 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. Endemic areas overlap those of 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, "sporangia". spread via dusty storms. 2 phases: Saprobic phase (in this phase when in environment/ culture), found in nitrogen-rich soil (eg. Agricultural areas)

Basic viral structure:

Virion: whole virus particle

Most commonly acquired by inhallation.

Histoplasmosis (acute and chronic), ocular histoplasmosis syndrome.

Body fights viruses through: Interferon, NK cells, T cells, Antibodies.

Spread to secondary site via blood (viremia) or lymphatics (during incubation period). Could have prodrome in this period.

Capsid: Protein coat Nucleocapsid VAPs (viral attachment particles) Envelope: contains VAPs 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

Viruses: general

Naked Capsid: Robust, survive some drying, Acidresistant, spread by lysing cells, pathogenesis d/t cell lysis. Group of viruses with common virion morphology AND mode of replication 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 2) LATENT Infections 3) PERSISTENT Infections 4) IMMORTALIZING Infections

Herpes Veridae Family

HSV-1 HSV-2

Infects and replicates by MUCOEPITHELIAL cells and establishes lytic, persistent and latent infections. Infection process: SKIN BREAK > Localized primary infection in mucosa > VASCULAR lesions > RETROGRADE transport (latent infection) > STRESS trigger (emotional, fever, direct sunlight, menstruation/hormones, immunosuppression) * infects SAME spot/dermatome each time

HSV TRANSMISSION = 4 M's MIXING, MATCHING of MUCOUS MEMBRANES

TRANSMISSION: Infects above the waist. EARLY on in life. ORAL contact. Autoinnoculation possible to eye or mouth TRANSMISSION: Below the waist. Later on in life. Horizontal & Vertical (in utero).

Even prodrome can be infectious. Wear gloves when examining.

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 Zoster Virus (Herpes Virus 3)

Varicella: Healthy kids not treated relatively mild disease that gives life log immunity

Primary Infection = lymphatics 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: 1) cell-cell spread- syncytia 2) latent state 3) reactivation in immunosuppressed state

Cytomegalovirus

Lymphotropic latent in T cells

saliva remains infectious for months after clinical recovery. -immunity to EBV is “life-long”. Very mild in children. I

EBSTEINN-BARR VIRUS

HSV-6 Roseola infantum HIV-6A Other Herpes Virus HSV-7

Rapid onset of high fever for 4-5 days. Fever subsides and then get maculopapular rash (trunk and neck). Exanthum subitum Mononucleosis type illness (heterophile -). ORPHAN virus

Fetus is infected either: 1) placenta blood 2) ascending infection from cervix Confirm by isolating CMV from child’s urine in 1st week of life

healthy immune system, safe sex.

.

Ultimate B lymphocyte pathogen – mitogenic and immortalizing (keeps cell growing by stopping apoptosis) -transmitted by saliva or contaminated glassware -cause neoplasms (but need cofactor) -very limited host range and tissue tropism -lytic (lesions) or latent infections OR immortalizing infection

EBV Mono TX and control -Ginseng, Licorrice, Schisandra, Carsinosum (homeopathy). Control: impossible virus is ubiquitous and is shed from saliva of healthy people.

Other Herpes Virus

HSV-8

Kaposi’s sarcoma (neoplasm of blood vessels – 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 coreceptors/chemokines to get HIV in for development of AIDS)

Types: HIV-1(world) and HIV-2 (West Africa).

HIV-1: 70% men, 42% MSM (men sex with men). Developing countries: relative increase among heterosexuals. HIV2: mostly west Africa

HIV and opportunistic fungal infections

.

pathogenesis: Attachment to cell FUSION of envelope. Makes dsDNA copy of itself. Reverse transcriptase is very ERROR prone (structurally changing all the time). Increased risk with anal sex – only one INTEGRASE (to integrated into host layer of colonic cells and cells might chromosome). ). Viral DNA transcribed by host have certain co-receptors DNA pol II, also transcribes its own 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

Candida Spp

Aspergillus spp

Cryptococcus spp

Opportunistic fungi, -Dimorphic but unlike other mycotic agents only present in hyphae in body -no yeast cells -detect after treatment of KOH 10%

Associated with: defective T cell immunity only , hypoparathyroidism, hypoadrenals ,glucose imbalances disruption of normal bacterial ecology

Cause Disease iff: immunocompromised, broad spectrum ABCS, dietary imbalance , endocrine changes, pH changes -Diseases are not contagious

Extremely common, no yeast-like form--only a mold form Strict pathogen (unlike Candida), -Aspergillosus flavus produces aflatoxin hepatocellular carcinoma (HCC) NO dimorphism in pathogenesis , encapsulated yeast , Acidic mucopolysaccharide capsule Virulence factors: -Ubiquitous capsule (anti-phagocytic) -pigeon droppings (desiccated alkaline rich, N2 rich, hypertonic

HIV (+) does not mean you have AIDS. CD4+:CD8+ tells status and staging of AIDS. Lots we can naturopathically. Prevention: safe sex – latex condoms only

Pneumocystis jirovecii (carinii)

has features like protozoans

Included with fungi only because of molecular traits , Opportunistic infection, found in rodents, Transmission thru respiratory droplets (increased risk if immuno suppressed)

Moribillovirus: measles Similarities in family: Enveloped, form syncytia, replicate virus - "rubeola", animal in cell cytoplasm, transmitted via respiratory droplets disease. Paramyxovirus: parainfluenzae and mumps viruses

mumps related to parainfluenza virus 2. one serotype (like measles)

Paramyxoviridae family

Pneumovirus: respiratory syncitial virus "RSV"

Oxygen ABCs

immunity from reinfection adult infectin is more severe than children. VERY infections (less than mostly in school age 5-14 yr old. Increae risk of measles or Chicken pox). Spread by spread with crowding and in winter direct contactor respiratory secretions Life long resiistance to infection (like measles)

ubiquitous, almost everyone in NA is infected smaller nuceocapsid more fragile ( to freezing) than other by age 4. epidemics EVERY winter in cold paramyxoviruses. Pathology due to direxct invasion of temperate climate ( hot humid summerns in respiratory epithelium (syncythia) Hong Kong)

Mumps

Tx:sympomatic only no viral agents. Prevention: control almost imposs due to virus ubiquitous and infectxion is subacute

Tx: zinc lozengges every 2-4 hours. Max 60 mg. too high will lower immune system. Engestol VERY congagious, tranmitted by hands RSV, #1 cause of severe lower (heel product decreases sore fomites and respiratory secretions.no repiratory infection in young throat for flu virus) also systemic spread/veremia . No long children ( day care and nurseries) homeopathic eupatorium . term immunity (unlike measles or #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 severe respiratory distress in infants and young children, also causes croup Types 4: mild URI in children and adults

replicate faster than measles or mumps. Contagious before sx are present

only partial immunity from reinfection. Get milder form ( unlike measels)

#1 cause of RSV. 2nd main cause of severe respiratatory distress in infants and young children. Laryngeotrachebronchitis ( croup)

homeopathic: spongia. Tx symptoms only with nebulized hot or cold stream, no Anti viral therapy or vacines. Mistle toe good anti viral

transmission p to p in respiratory droplets Haemophillus influenza bacteria (epiglottitis)

Toga virus genus rubivirus

enveloped ss RNA genome, unlike other toga virus: respiratory tropism and no detectable cytopathology (no lysis), only 1 serotype. Causes heterologous interference interference with replication of super infecting piconavirus NAKED capsid virus = very RESISTANT to drying, acid/base, salt, ect.

FAMILY PAROVIRUS

spread by repiratory secretions or transplacental

TRANSMISSION = Respiratory droplets or close contact or blood products

Rubella (german measles) Always symptomatic but range less contagious than measles or from mild childhhood dz. German mumps or varicella. Life long immunity measles to severe congential just get sick defects. Increased risk of harmful dz if pregnant Erythema Infectiosum (5th DZ), Aplastic Crisis and Arthritis.

no anti viral treatment, mild dz with life long immunity. Vacination as MMR. Reduce risk of materal infection, live cold adapted vacine do NOT give to pregnant mothers DDX bwt: HSV6 B (roseola enphantu ??) Tx not usually required (mild and self-limiting).

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

HAV

NAKED = extremely STABLE capsid - except for CHOLORINE. Slow replication Pathology due to immune mediated hepatocyte damage Not associated with HEP C Rarely get immune complex related rash and polyarthritis, rarely fatal (fulminant hepatitis)

TRANSMISSION = Person to Person , FecalOral, Sewage Contaminated food/water * often traceable source bc can live in water for many months

Avoid uncooked shellfish Chlorine treatment of water. VACCINE

NO CHRONIC CARRIER

ENVELOPED - unusally stable for an enveloped virus Hepatitis Family HBV

HepDNA Virus CAN cause HEPATOCELLULAR CARCINOMA NOT as resistant as HAV Chronic, symptomatic or asymptomatic hepatitis See GROUND GLASS hepatocytes in chronic phase m'cly regeneration of LV parenchyma after infection is resolved.

HCV

ENVELOPED FLAVIVIRUS (like west nile virus) Inactivated by DETERGENTS M'C cause of NON-ALCOHOLIC LIVER DZ in USA Only get partial immunity after recovery

HDV

Delta Agent = viral parasite ie. NEEDS HBV as HELPER virus

HEV

Severe in PREGNANT women

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.

TRANSMISSION = 1) percutaneous, 2) close personal contact (highest risk is babies born to HBV+ mothers NOT transplacental, 2) Blood or Blood Products {(serum hepatitis) - needles, std, perinatal, blood} CHRONIC CARRIER

Prevention = - Screening blood donors/products - Avoid intimate contact with HBV carrier (safe sex, no needle sharing) - UNIVERSAL Blood/Fluid Precautions - wash with 10% bleach VACCINE

TRANSMISSION = parenteral (blood transfusion, drug users, piercings, tatoos) rarely sexual or perinatal Close link with HIV

TRANSMISSION = Fecal-oral (m'c in developing nations)

Universal blood screening, reduce risk behaviours Vaccine difficult due to HIGH VIRAL HETEROGENEITY

Microbe

System Skin (superficial)

Condition

Malassezia furfur (long name we don't need to know) don’t need name don't need name don't need name

Tinea (pityriasis) versicolor

Skin (superficial)

Tinea nigra

Skin (superficial) Skin (superficial) Skin (cutaneous)

Black Piedra White Piedra Tineas

Histoplasma capsulatum

Systemic

Acute histoplasmosis

Histoplasma capsulatum

Eye

Ocular histoplasmosis syndrome

Histoplasma capsulatum

Systemic

Progressive histoplasmosis (chronic)

Blastomyces dermatides

Systemic

Acute blastomycosis

Blastomyces dermatides

Systemic

Chronic blastomycosis

Coccidiodes immitis

Systemic

Signs and Symptoms Non-itchy, hypopigmented lesions on upper torso, arms, abdomen Well demarcated lesions on palms and soles

Dark pigmented yeast cells

Dark, hard nodules along infected hair shaft Soft, pasty white growth on hair shaft Named for part of body they affect Primary histopasmosis: acute, self-limiting influenzaelike illness. Complications: mediastinal fibrosis, ocular NO histoplasmosis syndrome. Serious retinal condition. Leading cuase of blindness in 20-40 year olds. Get "histo spots" bilaterally. MC'ly no NO visual loss

CXR: residual calcified lesions in lung, LN: "coin lesions"

Disseminated via lymphatics. Increased risk if cellmediated immunity is impaired. Can look like TB! Fever, NO night sweats, weight loss with destructive (caseating) necrosis, lung lesions. Bronchopneumonia, drenching sweats.

LESIONS: "Dews drops on a rose petal" Secondary infections are less severe, more loca;lized and shorter in duration than primary infection.

Oral Herpes (Herpes Simplex/Herpes Gingivastomatitis)

HSV HSV

Eyes Extremities

Ocular Herpes/Herpes Keratitis Herpetic Whitlow

HSV-2

Systemic

Meningitis

HSV-1

CNS

Encephalitis

HSV-1 and HSV-2

Genitourinary

Genital Herpes

HSV-1 and HSV-2

Genitourinary

Genital Herpes - Female

HSV-1 and HSV-2 HSV

Genitourinary Systemic

Genital Herpes - Male Neonatal HSV

NO

TB or cancer-like!!! May present with skin lesions: slowly exanding ulcerative or verrucous lesions on face and NO mucocutaneous borders of nose and mouth.

Most commonly asymptomatic. 40% mild, febrile to moderately severe respiratory disease (much higher than histo). In disseminated form of disease (<<1%), erythema nodosum with arthralgia.

Oral Cavity

DDX and Lab DX "Spaghetti and meatballs" organism after KOH prep. Wood's lamp (+). Use this to DDX from vitiligo

Coccidiodomycosis

Herpes (HSV)

Contagious?

Corneal Ulcers Infectious lesions on fingers and wrists. Sudden onset of nuchal rigidity, blinding headache, nausea and photphobia Seizures, space occupying lesions (SOL) - cause destruction of temporal lobe. STD - 3 to 5 days after contact. Signs/SX = regional lymphadenopathy and painful shallow ulcers on genitals RECURRENT with prodrome of burning & tingling. Pruritis, vaginal or cervical mucoid discharge. Pain with intercourse. Slight increased risk of cervical cancer in adulthood. Dysuria and/ro dyspaerunia Acquired in utero or during vaginal birth. Often fatal.

NO

Microscopy: 10% KOH prep with silver or Giemsa stain. Serological: skin tests (like TB test), but there are too many false positives. Cultures: slow growing (1-2 weeks) and spores are infectious. CXR: no residual calcified lesions, unlike histoplasmosis. Skin test and serology: too many false positives. Microscopy: biopsy/histology of KOH-prepped tissue sample. Culture (?). Skin test antigens (like TB): Use 2-4 weeks after symptoms. Antigens are Coccidiodin and Spherulin. CXR: Egg-shell lesions. Tissue biopsy: spherules. Culture: CAUTION: Infectious. Leading cause of lab-acquired infections.

Yes: infectious from prodrome even to crusted lesions (wear gloves when examining) Lab Tests in general for HSV: Yes Yes TZANCK SMEAR - look for SYNCTIA. This test is not specific Yes for HSV, also tests for VZV and HIV Yes Yes

COWDRY TYPE A INCLUSION BODIES - positive with HSV and VZV CHARACTERISTIC CPEs

One of 5 childhood EXANTHEMS (others = rubella, roseola, 5th disease, measles/rubeola)

Varicella (VZV/HSV-3)

Systemic

Chicken Pox

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; prolonged low grade fever extreme irritability/malaise. Scarring MUCH MORE HARMFUL TO ADULTS COMPLICATIONS: Secondary bacterial infection, Reye's Syndrome, CNS Syndrome. Can occur after: Chicken POX, Enterovirus, EBV, Influenza B, Aflatoxin, Pesticide

Varicella (VZV/HSV-3)

Systemic

Reye's Syndrome

ASA associated = do NOT give aspirin to a child with chicken pox.

Lab Tests in general for VZV TZANCK SMEAR - giant multinucleate cells = SYNCTIA. This test is not specific for VZV, also tests for HSV. 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.

Recurrence of LATENT VZV infection due to stress, immunocompromised)

COWDRY TYPE A INCLUSION BODIES = "drop-like masses of acidophilic material surrounded by a clear halo within the nucleus"

Prodrome - severe pain in localized nerve area

Herpes Zoster

Systemic

Shingles

3-5 days later - gradual development of small red macules, closely spaced, most common in thoracic area 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

Herpes Zoster

Eyes

Ramsey Hunt Syndrome (Herpes Zoster Oticus)

Herpes Zoster

Cytomegalovirus syndromes

Herpes Zoster Opthalmicus

congenital cns skin other

cytomegalic inclusion disease microencephaly / hearing loss

Inflamed Cranial Nerves 5 (facial paralysis) and 3 (corneal ulcers and blindness) Painful lesions along Cranial Nerves 8 (severe otalgia, hearing loss, vertigo) and CN 5

M/C viral agent of congenital disease in U.S

rash hepatosplenomegaly toxoplasmosis, other, rubella virus, CMV, herpes simplex/histoplasmosis •TORCH syndrome

Clinical signs and symptoms too vague to be that useful and often ASYMPTOMATIC Conditions!27:27 -Tissue biopsy: Conditions!G43 eye nucleus -cell culture: characterisitic CPE in diploid FIBROBLAST cells (best Dx). Conditions!H26

peri-natal child/adult

immunocompromised

Cause: infected cervix, colostrums or milk. Two outcomes: (1) no clinical disease (2) clinical disease if immunocomprimised heterophile (-) and “mono-like” infection (mono is heterophile +). Very common cause of failure of KI transplants.

Mononucleosis

Immunity

Chronic EBV disease

Nasopharyngeal carcinoma

African Burkitt’s Lymphoma

Hairy Oral Leukoplakia

HIV

Immune

HIV Acute retroviral syndrome

Conditions!H26

pizza pie retina” CMV retinitis. Scotoma absence or abnormal area in visual field kissing disease” – heterophile (+) ONLY one that is heterophile (+) Sx’s: high fever, malaise, pharyngitis, tonsils with exudates, lymphadenopathy, hepatosplenomegaly, fatigue. Looks like Strep throat. Rare progression: spleen rupture (avoid contact sports), hepatitis

EB V

Clinical signs and symptoms too vague to be that useful and often ASYMPTOMATIC Conditions!27:27 -Tissue biopsy: Conditions!G43 eye nucleus -cell culture: characterisitic CPE in diploid FIBROBLAST cells (best Dx).

TRIAD of: fever, pharyngitis, lymphadenopathy for 1-4 weeks. DOWNEY cells. MONOSPOT test (+) HETEROPHILE Abs – polyclonal activation of B cells produces wide repertoire of Abs that recognize “Paul Bunnell” Ags on horse, sheep, cow red blood cells but not guinea pig.

1. overactive immune system: infectious mono 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). EBV induced lymphoproliferative disease (leukemia like) Epithelial cell tumor. Cofactor = ingested nitrosamines (preserved fish). Tumor cells are from lymphocytes and contain EBV DNA. Malaria is a co-carcinogen (co-infection). Osteolytic lesions in jaw, necrosis, gray-white. Opportunistic infection in HIV/AIDS. Vertically ribbed 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). Sits “under radar” of immune system and decreases immune system. Suppresion: Direct (cytoxicity of CD4+) OR Indirect (induce apoptosis, decreased suppressive factors). Only in 5%. Mono-like syndrome (heterophile negative – do spot test!) Mucocutaneous sores. PGL – persistent generalized lymphadenopathy. Mouth ulcers, oral candidiasis

Initial screen: indirect ELISA for gp120 or gp41. New – Ora Quick Rapid HIV-1 Ab test.

Western Blot (to confirm): for gp120, p24, p31 proteins

HIV

Mild Stage

HIV

AIDS

HIV

Secondary infections

HIV

Dementia

HIV

Malignancy

Candida Spp

Oral candidiasis : “Thrush

Candida Spp

Vaginal candidiasis “Yeast infection

Candida Spp

Chronic mucocutaneous candidiasis (CMC)

Candida Spp

Disseminated candidiasis

Candida Spp

Candida endopthalmitis

Aspergillus spp

Aspergillus secondary colonization

Aspergillus spp

Paranasal granuloma

Aspergillus spp

Apergillosus systemic disease

Cryptococcus spp

Cryptococcosis

Cryptococcus spp

Cryptococcosis meningitis

Pneumocystis jirovecii (carinii)

pneumonia

Hairy oral leukoplakia, extensive oral thrush, Kaposi’s sarcoma, Pneumocystis pneumonia (caused by P. carinii), CMV retinitis.

Measles (Rubeola)

Morbillovirus

Sub-acute sclerosing panencephalitis (complication of measles)

Lab Dx: Active viral replication (recent infection or late stage). Direct ELISA for p24 (viral load or reverse transcriptase in blood via PCR). Syncytia (from culture).

Sub-acute encephalopathy. Slow, progressive deterioration of mental abilities (can mimic Alsheimer’s disease). Kaposi’s sarcoma Focal white patches on oral mucosa, palate and tongue that bleed when scraped off , red flag for AIDS iff thrush in adults NOT receiving corticosteroid therapy or broad spectrum ABCS Common female disease--change in vaginal flora or STD, signs and symptoms: erythema (“beefy red”)/ inflammation vagina/ vulva thick white or curd-like discharge intense pruritus, Heterogeneous group of treatment resistant superficial Candida infections of skin, nails and oropharynx Spread to many organs eg. eye, *****must be immunocompromised n/a

A chronic clinical situation, minimal distress, hemoptysis fungus ball on CXR that moves with dependency

Microscopy tissue scrapings treated with 10% KOH -Culture -confirm + microscopy--grow on Sabourad agar -Germ tube test fmust be examined after 2-3 hours unique to Candida spp -Serology high titer of fungal glycoprotein Abs in recent or active infection or Candida specific mannan

Culture: on Saboraud agar -Tissue biopsy: 10% KOH prep of sputum fungus ball on CXR that moves with dependency

Chronic sinusitus due to Aspergillus colonization of paranasal sinuses rapidly fatal if not treated

Busse-Buschke disease or torulis M/C’ly self-limiting mild pulmonary infection M/C in males M/C cause of fungal meningitis, insidious onset , immunocompromised also get skin lesions or osteolytic bone lesions, 50% mortality

Cryptoccocus neoformans diagnosis Microscopy: examine CSF after treating with 10% KOH and India ink, -Serology look for capsular Ags unlike other systemic mycoses that look for Abs

non-specific

PCP CXR plasma cell infiltrates from hilum with “ground glass appearance" Microscopy typical octonucleate cysts

Extrapulmonary--in AIDS

Morbillovirus

Markers: P24 – high at start and then goes down, then high at AIDS. AntiHIV-1 Ab: low, then high for most of disease, then drops at AIDS. CD4 T cell – gradually goes down (AIDS = below 200-400 ug/ml)

1. Presence of anti-HIV gp120 Abs. 2. decreased CD4+ T cell count. 3. Wasting syndrome 4. Presence of opportunistic infections because CD4+ is diminished)

Mycotoxicoses hypersensitivity pneumonitis allergic bronchopulmonary aspergillosis associated with asthma (10-20%)

Aspergillus spp

Pneumocystis jirovecii (carinii)

Weight loss (“slim disease”), night sweats, fatigue, opportunistic infections

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 (cough coryza, conjunctivitis). Complete resistance to Very contagious: 85% re-infection. Big contrast in disease severity with proper infection rate nutrition, access to health care, etc. Signs and 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.

Diagnosis: M/C clinical only, pathognomonic. 4X increase in measles-specific IgMs suggest recent infection.

parainfluenza virus

haemophilllus influenza

repiratory

respiratory

mild cold like URI (pharyngitis, coryza fever, wheezing) to bronchitis and pneumonia. Milder disease in older severe respiratory distress and croupin in children and adults. Subglottal swelling, erythema and infants.Laryngeotrachebronchitis AKA edema of tracheal walls, sounds worse than the look. CROUP 2-6 day incubation: seal bark horse brassy cough. inspiratory stridor. tachycardia, tachypnea, suprasternal retraction. Self limiting in 48 hrs. boys 1-6

epiglottitis

paramyxiviridae genus Paramyxovirus ( related to parainfluenza virus 2

URT, CNS, glandular, testes, ovaries, pancreas

mumps

paramyxiviridae genus Paramyxovirus

URT,

RSV (respiratory syncitial virus)

Toga virus genus rubivus

Parovirus

respiratory, skin, lymphatics

skin

Rubella

Erythema Infectiosum

Parovirus B19

systemic

Hyrops Fetalis

Parovirus B19

systemic

Aplastic Crisis

Parovirus B19

systemic (joints)

Picornavirus

systemic

Hepatitis A

swelling of epiglottis, look worse than they appeartoxic appearance. Major repiratory distess and dyspnea NO COUGH. Dysphagia with drooling.irritability, fever, dysphonia (hot potato voice). 2-5 y olds. Medical Emergency (don't do throat swab as childs thoat could spasm)

ubiqutous and spreads rapidly in hospitals and nurseries

DDX: laryngitis ( hoarseness, burnng retrosternal pain with breathing). Lab DX: Xray: steeple sign. CPE in primary monkey Ki cells: presence of Syncytia and haemadsorb guinea pig RBC's

ubiqutous and spreads rapidly in hospitals and nurseries

Lab DX: Xray: Thumb sign

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 and edema. SX: mostly asymptomatic (unlike measles), sudden onset of malaise, anorexia for 2days, then fever very infections but (38.3-40 C), ear ache, bilateral parotitis. Self limiting in less than measles or 2 weeks. Sequelae: Orchitis: unilateral testicular chicken pox swelling if bilaterally = sterility. Oophoritis: unexplained abdominal pain. Pancreatitis (rare but linked to juvenile DM. Meningitis: H/A, stiff neck, drowsiness, unsteadiness when walking. #1 cause of aseptic meningitis in non immunized. arthritis (rare)

test samples from saliva ( 5 days after onset). Urine ( 2 weeks after onset), also CFS. Serology. 4X increase in mumps specifc IgM in blood, elevated amylase (affects pancreas). Hemadsoption (guinea pig RBC syncytia from due to presence of viral hemagglutin

4-5 day incubation. Infection localized to upper or lower respiratory tracts. Ranges from common cold to pneumonia and bronchiolitis. URI with marked very rhinorrhea.Bronchiolitis in infants. OM also common, risk of asthma attack

serology 4X increase in anti RSV titre indicates actdive dz..direct ELIZA or immune florecence, CXR

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 severity even if immunosuppressed. In adults, more months of life severe than in children. Also polyarthritis of fingers, Congenital rubella: mstly females ankles wrists and knees,. Lasts a few increased risk (70%)if 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

difficult to Dx clinically, urine viral ag, serology: RIA, or ELIZA. Congenital: highly specifc anti rubella IgM, NO CULTURE no characteristic CPE

50% are ASYMPTOMATIC If symptomatic = SLAPPED CHEEK rash on cheeks spreading to trunk and limbs (lacey reticulate appearance) 2 Phases: 1) Infectious 2) Immune reaction = RECURRENT RASH that is worse with sunlight, exercise, hot water and stress If mother infected during 2nd and 3rd trimester = HYDROPS FETALIS (massive edema) Increased risk if SCA or Thalassemia ie. Chronic Symmetrical, transient polyarthritis. Presents just like RUBELLA arthritis Often asymptomatic (only 1-2% get jaundice) One month incubation - abrupt onset of icteric symptoms - progressively worse for 4-6 days and then symptoms DECREASE = jaundice appears (67%) Rarely progresses to fulminant hepatitis.

Rash or arthralgia stages are NOT infectious (immune complex related)

Serology: IgM 2-7 days after rash, but IgG comes later and persisit for life

Ingested SHELLFISH

Food ingested = source of infection Serology: ACUTE or RECENT AntiHAV by ELISA or RIA

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

Hepadnavirus

systemic

Hepatitis B

ACUTE HBV: only apparent clinically in 25% of patients; Infectious up to 45 non-specific symptoms = hepatomegaly with RUG days before onset of tenderness and Jaundice symptoms SERUM SICKNESS CHRONIC HBV: Detected through LAB DX (increased LV enzymes on CBC) If co-infected with HDV can lead to FULMINANT HEPATITIS

HBV (hepadnavirus) AFLOTOXIN B (peanuts)

Liver

Hepatocellular Carcinoma

Flavivirus

systemic

Hepatitis C

Delta Agent (virus like) Calcivirus

systemic systemic

Hepatitis D Hepatitis E

SEROLOGY: (1) RECENT INFXN = ANTI-HBc IgM or use PCR for HBV DNA; HBsAG, HBcAG, HBcAG; (2) CHRONIC HBV = HBcAG and HbsAg; (3) CHRONIC CARRIER = HBsAg, HBcAb, HBV DNA(+)

80% of primary hepatocellular carcinoma is due to HBV infection = 1st vaccine preventable cancer Most common if HBV and HCV coinfection. 1/3 asymptomatic - m'c sx = weight loss, fatigue, anorexia (non-specific) 6-8 WEEK incubation Perdispose to cirrhosis (especially if alcoholics and smoker) RARELY progress to Fulminant Hepatitis - BUT cause 30% of all cased of fulminant hepatitis 40% of Fulminant Hepatitis cases

INDIRECT elisa: ANTI-HCV Ab

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

Sample Question

Sample Question

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 C) epithelial cells with owl’s eye inclusion bodies in urine sample D) immunofluorescence of tearinfected 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 B) Evaluation for HIV viremia C) Monospot screen test for EBV infection D) Rapid plasma reagin screen test for syphilis