General Pathology: Test #3

PATHOLOGY STUDY SHEET TEST 3

Environmental and Nutritional Pathology
Laboratory Microbiology
Viral Infections
Bacterial Infections
Mycotic Infections
Parasitic Infections

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ENVIRONMENTAL PATHOLOGY

RADIATION:

MECHANISMS OF INJURY:

DIRECT INJURY: Radiation directly producing single or double-stranded chromosomal breaks in DNA.
INDIRECT INJURY: Ionizing radiation ------> radiolysis of water ------> free oxygen radicals ------> interact with DNA to produce mutations.

EFFECTS

LATE EFFECTS OF RADIATION:

Small arterial thickening (hyaline, collagenous), which may result in local ischemia.
Mutation to fetuses exposed in utero
Bone marrow hypoplasia
Radiation dermatitis
Radiation pneumonitis
Induction of cancer:

Leukemias and lymphomas
Breast cancer
Thyroid
Lung
Osteosarcoma

WHOLE BODY ACUTE RADIATION SYNDROME: Consisting of three distinct sub-syndromes

HEMATOPOIETIC: 300 rads, pancytopenia develops after two weeks

Anemia, bleeding, infection

GI: 1000 rads, destruction of GI epithelium

Diarrhea, dehydration, enteric sepsis

CNS: 2000 rads, damage and death secondary to endothelial injury and cerebral edema.

TYPES OF RADIATION:

ELECTROMAGNETIC (IONIZING) RADIATION: X-Rays and Gamma Ra0ys

Produce ionization with subsequent free radical formation, damaging tissues.

PARTICULATE RADIATION: Neutrons and charged particles (alpha, beta, protons, deuterons)
ULTRAVIOLET:

Effects: Sunburn, photosensitivity reactions, cataracts, skin neoplasia.

MEASURES OF RADIATION:

Rad (r): Radiant energy, expressed in ergs, that is absorbed by a tissue.

The absorption of radiant energy is biologically more important than the total amount emitted.

Gray: 100 rads
Relative Biological Effectiveness (RBE): Term comparing the effectiveness of different forms of radiation in producing the same effect.
Roentgen (R): Measure of emmission of radiant energy (not absorption).
Roentgen-equivalent Man (rem): Describes the biological effects produces by 1 rad of high-energy biological radiation.

RADIOSENSITIVITY: Some cell-types (and tumors) are more radiosensitive than others

HIGH SENSITIVITY: Cell that tend to divide a lot

Lymphomas
Gonads / Seminoma

LOW SENSITIVITY: Cells that normally do not divide a lot

Osteosarcomas
Gliomas

RADIATION PNEUMONITIS:

Often a side-effect of chemotherapy for lung cancer.
There must be sufficient oxygen tension in the lung for it to occur. It won't occur in a COPD lung due to poor oxygenation.
MORPHOLOGY:

intra-alveolar hyaline membranes
Interstitial edema and chronic inflammation
Infiltration and proliferation of mononuclears and fibroblasts, many with large atypical nuclei.

TYPES OF INJURY:

ABRASION: Defect in skin caused by direct or tangential impact. Crushes or scrapes the epithelial surface.
AVULSION: Tearing away of skin and underlying tissue.
CONTUSION (BRUISE): Localized area of mechanical injury with focal hemorrhage.

HEMATOMA: Discrete hemorrhage within tissue, caused by mechanical injury.

INCISION: Opening of skin by a cutting instrument, leaving apposed edges as in surgeon's knife.
LACERATION: Discontinuity of the skin resulting from a tangential impact that splits and tears the epithelium.
PUNCTURE WOUND: Injury made by a pointed instrument.
CRUSH SYNDROME: Secondary body changes from muscle injury.

Muscle releases hemoglobin and myoglobin.
Hemoglobin in kidneys causes vasoconstrictive renal ischemia.

ELECTRICAL INJURY:

Effects:

Causes burn to skin due to high electrical resistance of skin.
Disruption of neural conductance can cause cardiac arrhythmias.

BATTERED CHILD SYNDROME:

Discrepancy between history and physical findings.
Wounds or injuries in different stages of healing.

BLAST INJURY: Positive pressure from one direction followed by sudden negative pressure from the other direction.

Results:

Thoracic collapse.
Multiple pulmonary hemorrhages

IMMERSION BLAST: Positive pressure from all directions followed by sudden negative pressure.

Diaphragmatic lacerations
Visceral rupture

FRACTURE:

Simple: Closed fracture
Comminuted: Bone is splintered or crushed.
Impacted: One bone fragment is firmly driven into another.
Incomplete: Continuity of the bone is not entirely destroyed.
Greenstick: One side of bone is broken while the other side is bent.
Stress: Fine hairline fracture without soft tissue injury.
Compound: Open fracture, open skin.
Pathologic: Due to weakening of bone by some pathologic process

Osteoporosis
Osteomalacia
Neoplasia
Osteomyelitis

GUNSHOT WOUND: The hole of entrance is usually smaller than the hole of exit.

CONTACT WOUND: The only case where the hole of entrance is actually larger than the hole of exit.

Contact Ring: Abrasive collar around entrance wound from the gunpowder.

CLOSE RANGE

CLOSE-RANGE (< 1 ft):

FOULING: Grey-black discoloration, caused by heat, smoke, and small grains of burning powder.
STIPPLING: Marks produced by discrete larger particles of unburned powder.

CLOSE-RANGE (1-3 ft):

STIPPLING only -- no fouling.

CLOSE-RANGE (> 3 ft):

No fouling or stippling.

HOLE OF EXIT: Irregularly lacerated edges with no fouling or stippling.

SOUND WAVE INJURY: To hair cells and other auditory components.

THERMAL INJURIES:

BURNS

Degrees

FIRST DEGREE: Involving superficial epidermis only.
SECOND DEGREE: Deep partial thickness, involving epidermis with some viable dermal appendages capable of regeneration.
THIRD DEGREE: Full Thickness, both epidermis and dermis, and requiring grafts to heal.

Primary Effects: Necrosis, inflammation, fluid loss.
Secondary Effects:

Superinfection: Staph Aureus + Pseudomonas aeruginosa -- most frequent cause of death from burns.
Shock
Acute gastroduodenal stress ulcer

INHALATION BURN: Respiratory hyperthermic injury.

Results:

Laryngeal and pulmonary edema
Adult Respiratory Distress Syndrome (ARDS)

ADULT RESPIRATORY DISTRESS SYNDROME (ARDS): Hyaline Membranes

Causes:

Trauma
Infection
Aspiration
Drugs: heroin, oxygen
Radiation

GENERALIZED HYPOTHERMIA: Decrease in body temp. below 35C (95F). Results:

Cooling of blood perfusing the brain.
Increased vagal discharge leading to cardiac arrhythmias.

FROSTBITE: Local freezing hypothermic injury with necrosis due to crystallization of water, vasoconstriction, endothelial damage, and thrombosis.
TRENCHFOOT: Non-freezing hypothermic injury to feet. No water-crystallization.

Necrosis due to vasoconstriction, endothelial damage, and thrombosis.

HEAT STROKE: Systemic hyperthermia.

Classic Heatstroke: Very young or elderly, and chronically ill, caused by drugs affected thermoregulation.
Exertional Heatstroke: Healthy adults, during vigorous exercise.
Effects: Hot dry skin, rhabdomyolysis, cessation of sweating, lactic acidosis, hypocalcemia, myoglobinuric renal failure.

HEMODYNAMIC INJURIES:

CARBOXYHEMOGLOBIN: Carbon monoxide bound to hemoglobin.

Results:

Cherry red tissues.
Hypoxic injury to brain, liver, renal tubules.

CYANIDE POISONING: In contrast to carboxyhemoglobin, cyanide will also show cherry red tissues because the blood is fully oxygenated.

Cyanide binds to Cytochrome Oxidase, thus inhibiting cellular respiratory, such that poisoned cells cannot use O₂.

ASPHYXIA: Lack of respired oxygen.

Causes:

Mechanical (strangulation)
Traumatic (Violent thoracic compression)
Drowning

HIGH ALTITUDE SYNDROME: Systemic hypoxia, resulting in loss of consciousness, circulatory / respiratory collapse, death, long-term compensatory polycythemia.
OXYGEN TOXICITY:

Respirator Lung:

Intra-alveolar fibrin
Hyaline membranes
Septal edema and fibrosis
alveolar cell hyperplasia

Retinal Fibroplasia: Retinopathy that occurs with premature infants given oxygen.

DRUGS / DRUG-INTERACTIONS:

ADVERSE DRUG REACTION:

CLINDAMYCIN: Antibiotic treatment can result in overgrowth of Clostridium Difficile, leading to Pseudomembranous Colitis.
SALICYLISM: Salicylate poisoning

Respiratory Alkalosis followed by metabolic acidosis.
Erosive gastritis
Inhibition of platelets
Interstitial nephritis, renal-papillary necrosis
Reye's Syndrome

SLE-LIKE SYNDROME: Procainamide, Hydralazine.

Clinically looks like SLE, but due to autoimmune reaction to the drug.
Goes away after discontinuation of medication.

ANTINEOPLASTIC AGENTS: Alkylating agents, antimetabolites

Consequences:

bone marrow suppression
immunosuppression
initiation of cancer

IMMUNOSUPPRESSIVE AGENTS:

Examples: Corticosteroids, Cyclosporine, Azathioprine.

BIOTRANSFORMATION: Metabolism of drugs to active (or toxic) form by liver enzymes.

Ethylene Glycol is transformed to Oxalic Acid, which is then toxic to:

Kidneys
CNS
Cardiorespiratory

Methyl Alcohol--> Formaldehyde ------> Formic Acid, which may cause

Blindness (due to retinal receptor cell degeneration)
Brain swelling.

ILLICIT DRUGS:

HEROIN:

Produces true addiction.
OVERDOSE: respiratory depression, ARDS, pulmonary edema.
Infections occur with prolonged use (needles)

COCAINE:

Produces tolerance and withdrawal
OVERDOSE: Cardiac arrhythmia may result in sudden death

AMPHETAMINES:

OVERDOSE: Seizures and cardiac arrhythmias.

PHENCYCLIDINE (PCP)

OVERDOSE: Deep coma or seizures

LYSERGIC ACID (LSD)

OVERDOSE: Large overdose causes coma, convulsions, respiratory arrest.

FINGERNAIL POLISH / GLUES:

Active Ingredients: Benzene, CCl₄, Acetone, Toluene

FETAL ALCOHOL SYNDROME:

Growth retardation
Characteristic facial features (epicanthal folds)
CNS dysfunction

FETAL TOBACCO SYNDROME:

Low birth weight: 200 grams lighter (light for gestational age)
Increased perinatal mortality, due to:

Increased risk of abruptio placentae
placenta previa
uterine bleeding
Premature Rupture of Membranes (PROM)

INDUSTRIAL POLLUTANTS:

AIR POLLUTION:
ASBESTOS: Causes Pneumoconiosis, or Pulmonary Interstitial Fibrosis.

Other effects: Pleural fibrous plaques, malignant mesothelioma, lung carcinoma (particularly in smokers).

CAUSTIC AGENT: Corrosive agent such as concentrated NaOH.

Produces gastroesophageal and respiratory necrosis when ingested. Immediately damages the mucosa it contacts.

MERCURIALISM:

MINAMATA DISEASE: Organic compounds of Mercury (Hg) can produce CNS damage.
Inorganic Mercury causes:

Renal tubular necrosis, membranous glomerulonephritis
Gingivitis

PLUMBISM: Lead poisoning

Sources: Paint, gasoline combustion
Effects:

CNS: Peripheral neuropathy, encephalopathy
Kidneys: Renal Tubular Acidosis leading to Fanconi's Syndrome
Hematopoietic:

Anemia with decreased erythropoiesis
Hemolysis
Basophilic Stippling of red cells.

RADON: Indoor gas linked to lung cancer, but it isn't proven.

NATURAL ENVIRONMENTAL POISONS:

AMINATA PHALLOIDES: Toxic mushroom

Consequences:

Gastroenteritis
Hepatic hemorrhagic necrosis
Renal tubular necrosis
CNS changes

ARTHROPOD BITE

Most common insects in US: Brown recluse spiders, black widow spiders, ticks, scorpions.
Effects:

Direct toxic effects
allergic anaphylaxis (bees)
Transmission of infectious disease

REPTILE BITE: Rarely fatal

Pit vipers (snakes), have four venom factors:

Neurotoxic
Spreading
Digestive
Hemorrhagic

Coral Snake: Primarily hemolytic
Gila Monster: Local tissue destruction.

GENERAL NUTRITION / NUTRITION DISORDERS:

CACHEXIA: General muscle wasting, as seen in Marasmus.
EMACIATION: Excessive leanness. A wasted condition of the body.
DIABETES TYPE II: Adult onset hyperglycemia, reflects down-regulation of insulin receptors.

80% of patients are obese.

ALCOHOLISM:

Selected chronic complications:

Mallory-Weiss tear of Esophagus
Acute rhabdomyolysis
Testicular atrophy
GERD
PUD
Wernicke / Korsakoff
Nutritional deficits

DIVERTICULOSIS: Herniation of mucosa and submucosa through muscular layers of the colon. Occurs with chronic low fiber diets.
GOITER: Iodine deficiency leading to hypothyroidism, increased TSH, and hyperplasia of Thyroid gland.
KWASHIORKOR: Protein malnutrition with adequate carbohydrate.

Growth failure
Hair changes
Fatty liver
Ascites
Skin depigmentation.

MARASMUS: Malnutrition

Muscle wasting

MEGALOBLASTIC ANEMIA: Most commonly caused by impaired DNA synthesis, as a result of Vitamin-B12 or Folate deficiency.

Large nucleated progenitors of RBC's (immature) stuck in bone marrow. Large oval erythrocytes in the periphery.

OBESITY: 20% or more above mean body fat

Diabetes Type II is most important complication
Atherosclerosis, MI
Gallstones
Gout
Varicose Veins
Oligomenorrhea

WATER-SOLUBLE VITAMINS:

VITAMIN B1 -- THIAMINE:

Function: Thiamine Pyrophosphate (TPP) -- it is phosphorylated twice by ATP to get to its active form. Functions in active aldehyde transfers.
DEFICIENCY:

WERNICKE'S ENCEPHALOPATHY

Classic Triad of Symptoms:

Ophthalmoplegia -- paralysis of eye muscles
Ataxia -- lost muscular coordination
Mental Confusion

BERIBERI: Nutritional deficiency of polyneuropathy, edema, and high output cardiac failure.

WET BERIBERI: Referring to symptoms of edema and high output cardiac failure
DRY BERIBERI: Referring to polyneuropathy.

VITAMIN B2 -- RIBOFLAVIN:

ACTIVE FORMS

FMN: Add one phosphate to the terminal OH-Group.
FAD: Add one phosphate to terminal OH-group, plus an AMP

DEFICIENCY:

Dermatitis, Glossitis
Anemia
Chaelosis

VITAMIN-C: ASCORBIC ACID

SPECIFIC REACTIONS: Covalent Hydroxylation Reactions

Formation of hydroxylysine and hydroxyproline in collagens
Anti-Oxidant

DEFICIENCY: SCURVY

ROSARY: Prominence of costochondral junction in children, seen in scurvy and rickets.
Hemorrhagic Diathesis: Predisposition to disease in joints, skin, sublingual
Tooth loss, gingivitis
Inability to limit infections, poor wound healing
poor growth

VITAMIN B6 -- PYRIDOXINE:

FUNCTION: Forms stable, yet transient Schiff-Base Complexes with amines.
Deficiency:

CNS disturbance: excitability, convulsions.
Hypochromic microcytic anemia.

NIACIN:

DEFICIENCY: PELLAGRA, characterized by the 3 D's: Dermatitis, Diarrhea, Dementia

May also find glossitis
Degeneration of the posterior and lateral columns of the spinal cord.

VITAMIN B12 -- COBALAMIN

DEFICIENCY:

Leads to PERNICIOUS (MEGALOBLASTIC) ANEMIA, usually from Type-A Gastritis against Parietal Cells (intrinsic factor) in stomach.

Can be caused by lack of intrinsic factor in the intestine (that is what absorbs Vitamin B12 in intestine)

Subacute Combined Degeneration: Demyelination of ascending and descending tracts of the spinal cord.
Glossitis of tongue.

FOLATE:

FUNCTION: One-Carbon transfers, in the form of Tetrahydrofolate.
DEFICIENCY: PERNICIOUS (MEGALOBLASTIC) ANEMIA -- abnormal DNA structure due to insufficient nucleotide synthesis leads to chromosomal abnormalities in the RBC's.

Has been linked to neural tube defects. Adequate amounts must be taken during pregnancy.
Homocystinemia is elevated homocysteine, which can result from no folate.

FAT-SOLUBLE VITAMINS

VITAMIN-A: RETINOL

FUNCTIONS:

Retinal (aldehyde) -- Visual Cycle.

VITAMIN-A TOXICITY: An excess of all-trans Vitamin-A in the diet ------> teratogenic birth defects.

beta-CAROTENE is NOT TOXIC!! -- only Vitamin-A is toxic. beta-Carotene is probably not toxic because the initial Dioxygenase (cutting) step is regulated.

DEFICIENCY:

FOLLICULAR HYPERKERATOSIS: Skin disorder resulting from squamous metaplasia, and occlusion of sebaceous glands.
KERATOMALACIA: Softening of the cornea, increasing vulnerability to ulcerative and bacterial infections, which may lead to blindness.
XEROPHTHALMIA: Dry eyes. Squamous metaplasia of conjunctiva and tear ducts, leading to dryness of cornea and conjunctiva.

Squamous metaplasia of other locales too.

NIGHT BLINDNESS

VITAMIN E: alpha-TOCOPHEROL

FUNCTION: Only one function -- as an anti-oxidant.

It will protect poly-unsaturated fats, cholesterol, and rods and cones, from radical oxidation.
Importantly, it is a fat-soluble anti-oxidant whereas Ascorbic Acid is water-soluble. So Vit. E gets into membranes.

DEFICIENCY: Rare, results:

Hemolytic anemia, thrombocytosis
Edema in premature infants

VITAMIN K: PHYLLOQUINONE

FUNCTION: The enzymes which use these calcium-chelating residues are CLOTTING FACTORS and enzymes involved in bone-mineralization and demineralization.
DEFICIENCY: Diminished clotting factor activity, leading to hemorrhagic diathesis.

VITAMIN D: CHOLECALCIFEROL (D3)

SYNTHESIS of 1,25-(OH)₂-D3, or 1,25-DIHYDROXYCHOLECALCIFEROL: Vitamin-D is not strictly a vitamin because we can synthesize it ourselves.

SKIN: Cholesterol ------> Cholecalciferol is a non-enzymatic cleavage catalyzed by UV-LIGHT.
LIVER: 25-Hydroxylase puts a hydroxyl group on the side chain.
KIDNEY: 1alpha-Hydroxylase puts a hydroxyl at the 1alpha position.

FUNCTION OF VITAMIN-D3: It is stimulated by Parathyroid Hormone, and it promotes the release of Calcium into the blood.

1alpha-Hydroxylase in the Kidney is tightly regulated. Parathyroid hormone will allow that reaction to occur, so Vitamin-D gets to its final form.
ACTION on INTESTINE: Vitamin-D promotes uptake of more calcium and phosphate in the intestine.
ACTION on LONG BONES: Will stimulate osteoclasts to break down hydroxyapatite and release calcium into blood.

DEFICIENCY:

OSTEOMALACIA: In adults, inadequate mineralization of newly formed bone matrix.
RICKETS: In children, inadequate mineralization of bone and also inadequate cartilaginous mineralization at the growth plate.

ROSARY: Prominence of the costochondral junction in children, may be seen with Rickets.

MINERALS:

FLUORINE: Deficiency results in dental caries.

Tooth enamel contains fluoroapatite

IRON:

DEFICIENCY: Microcytic Hypochromic Anemia, caused by lost blood usually.

KOILONYCHIA: Dystrophy of fingernails, in which they take a spoon shape.

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LABORATORY MICROBIOLOGY

DIRECT DETECTION METHODS:

General Process:

Collect the sample.
Extra the DNA from the sample.
Hybridize the DNA to an identifying probe.
Detect the signal.

SOUTHER BLOTTING: Hybridize radioactive probe and run a PAGE-gel to get DNA fingerprint of the organism or identify specific fragments.
IN SITU HYBRIDIZATION: In vivo, denature DNA directly in the tissue culture and hybridize a radioactive probe to it.

Is used to test which (or how many) cells in a tissue sample may contain a virus.

Pace 2 Test: Uses rRNA as the target, and is both sensitive and specific. This is a direct test for Chlamydia and Gonorrhea.

AMPLIFICATION METHODS: The sample must first be amplified before being identified.

POLYMERASE CHAIN REACTION (PCR):

Procedure:

Start with target DNA, denature with heat, and use a heat-stable polymerase to replicate it.
Then re-anneal (cool down), denature again (heat back up), and start over.

New Developments:

Can now use RNA targets
Nested PCR
Multiplex PCR
PCR sequencing
Quantitative PCR: Used to quantitate the viral load of infection in AIDS.
Automated PCR will be here soon.
In situ PCR

Divalent Cations, degrading enzymes, and polymerase inhibitors can all inhibit PCR and thus screw up the reaction.

Transcription Mediated Amplification: Has the advantage that it is isothermal. A way to make tons of copies of an RNA target.

Procedure:

Start with RNA
Make DNA, add primer.
Replicate it to dsDNA.
Use that to make tons of copies (by transcription) of the original RNA.

Very sensitive -- can use it to pick up one Mycobacterium Tuberculosis in a sputum sample.

Probe Amplification:

Ligase Chain Reaction is used for the detection of chlamydia.
This is similar to PCR, but there are four primers instead of two primers.

Signal Amplification:

Hybrid Capture System: Produce a DNA/RNA hybrid of the target and then identify it by a probe.

This test is dependent upon an antibody that will only detect hybrids.
Good quantitative test.
Can be used for CMV, HPV. Can be used to monitor CMV levels after a liver transplant.

Multiple Probe / Multiple Enzyme System: Utilizes branched DNA plus a probe.

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VIRUSES

VIRAL CULTURES:

TUBE CULTURE: Grown in tissue culture, in cells attached along the walls of a tube.

Viruses that can be detected:

Entero viruses
Adenoviruses
Respiratory Syncytial Virus (RSV)
MMR (Measles, Mumps, Rubella)
HSV1 and HSV2
CMV
Varicella-Zoster

SHELL-VIAL CULTURE: A small vial is used instead of a tube, and fluorescent antibodies are added. This method is more specific. This method is centrifugation-enhanced.

Viruses detected in shell-vials

Herpes Simplex
CMV
Varicella-Zoster
RSV
Chlamydia

DIRECT-VIRAL ANTIGEN DETECTION: For viruses that cannot be cultured, direct viral antigens are looked for.
SERODIAGNOSIS: ELISA, RIA, FA, Western Blot.

RESPIRATORY VIRUSES:

INFLUENZA VIRUS: Types A and B. Readily culturable.

Causes the lungs and bronchi to lose the ciliated carpet (ciliostasis), which results in secondary bacterial pneumonia. Patient will say that they were sick (flu), got better, and now they are really sick again.
TREATMENT: Don't treat symptoms with aspirin if it is a child under 18. Reye's Syndrome can result.

PARAINFLUENZA VIRUS: Types 1, 2, and 3. Readily culturable.
ADENOVIRUS: Infected cells have dark nuclei which are viral inclusion bodies.
RESPIRATORY SYNCYTIAL VIRUS (RSV):

DISEASE:

In a normal adult it causes no problems.
In infants under 1, RSV can be serious. It can cause severe pneumonia, as swelling closes up their tiny bronchi.
Major cause of nosocomial pneumonia in the pediatric wards. It has a high mortality rate for those who have congenital heart defects.

MORPHOLOGY: RSV inclusions appear within the nuclei of syncytial cells.

They appear very similar to measles Giant Cells.

HANTAVIRUS: Cause of fatal Hantavirus Pulmonary Syndrome. Very high fatality rate.

INFECTION from aerosolized mouse urine, often inhaled when sweeping.

VIRAL EXANTHEMS and VESICULAR LESIONS:

MEASLES (RUBEOLA):

MANIFESTATIONS:

Maculopapular Rash
Pneumonia.

MORPHOLOGY: Lung will show Warthin-Finkeldey Giant cells similar to RSV syncytial cells, with up to 50 nuclear viral inclusions.

May also see hyaline-like cytoplasmic viral inclusions.

MUMPS

Symptoms: Swelling of the Parotid gland and orchitis.

RUBELLA
VARICELLA-ZOSTER INFECTION: A type of Herpesvirus.

Chicken-Pox (Varicella): Primary infection with Varicella-Zoster.

SYMPTOMS:

General systemic viral symptoms of fever, chills, myalgia.
Eruption of fluid-filled vesicles.

COMPLICATIONS: Meningoencephalitis, pneumonitis, hepatitis.
MORPHOLOGY: Fluid-filled vesicles contain infected cells. Typical looking syncytial giant cells are visible microscopically.

Shingles (Herpes-Zoster): Reactivation-infection with latent Varicella-Zoster.

MORPHOLOGY: Vesicular lesions distributed unilaterally over a single dermatome. Virus infects the neurons.
Often infects the face unilaterally.

VACCINE is available, but some people think that actual infection is more protective.

HERPES SIMPLEX VIRUS (HSV): Types 1 and 2.

MANIFESTATIONS:

Lifelong infection alternating between latent and active infection.
Cold Sores: On lips, HSV-1.

Infection may also present fever, malaise, diarrhea, cervical lymphadenopathy.

Genital Herpes (HSV-2): She says that it can be caused by both types 1 and 2.

Both anal and genital lesions.

Herpes Keratitis: Acute keratoconjuctivitis, a common cause of blindness due to scarring.

HUMAN PARVOVIRUS B19: Cannot be cultured. Must use DNA or serology.

Erythema Infectiosum: Mild infection usually. Called the "fifth disease," after MMR and chicken pox. Looks like slapped red cheeks.
Populations at risk for high severity: Sickle Cell (can provoke crisis), pregnant women (can cause hydrops fetalis), immunocompromised.

INTESTINAL VIRUSES:

ROTAVIRUS: Cannot be cultured. Antigen test is used.

Causes Viral Enteritis, the most common cause of diarrhea worldwide.

HEPATITIS VIRUSES:

HEPATITIS-A VIRUS (HAV): An enterovirus.

MANIFESTATIONS: Generally not fatal; no chronic-carrier state.

Incubation period of about 25 days.

DIAGNOSIS: Serological detection of IgM detects a recent infection. IgG antibodies would only indicate that you have been infected before.

HEPATITIS-B VIRUS (HBV):

MANIFESTATIONS
DIAGNOSIS: Hepatitis-B Surface Antigen (HbsAg) in the serum indicates that you have an active, communicable infection.

IgM goes up early, and IgG goes up later.
The surface-antigen levels may go back down in chronic infection.

VACCINE: IgG against the surface antigen. IgG indicates vaccination, while IgM indicates infection.
MORPHOLOGY: You will see many dark nuclei in the liver -- lymphocytes. In chronic hepatitis, the liver is full of lymphocytes.

HEPATITIS-C VIRUS (HCV): It is an RNA virus.

EPIDEMIOLOGY: Get it from blood transfusions, and may be sexually transmitted. Route of transmission often is not known.
DIAGNOSIS: Look for antibody to HCV.
MANIFESTATIONS: Chronic hepatitis, slow course.

POLIOVIRUS: Affects CNS.

RABIES: Infection with Rabies Virus.

MANIFESTATIONS: Uniformly 100% fatal if not treated. Widespread spastic paralysis.

INFECTION is often from bats (especially lately), or dogs, racoons, etc.
Virus travels from muscle up peripheral nerve (retrograde up axon) to the CNS.

MORPHOLOGY: Rather large viral particles.

Negri Bodies are cytoplasmic inclusions found in the infected brain.

TREATMENT: 10-year vaccine

Post-Exposure PROPHYLAXIS consists of both PASSIVE (antibodies) and ACTIVE (toxoid) immunity, giving simultaneously in each arm. Due to the distinct location, the two vaccines will not interact with or cancel out each other.

JC POLYOMAVIRUS: The cause of Progressive Multifocal Leukoencephalopathy (PML), which is demyelination of white matter, occurring in AIDS patients. Fatal.

VIRAL HEMORRHAGIC FEVERS: Ebola virus and others.

Transmitted by chronically infected rodents. Tend to be seasonal. Fatal.
YELLOW FEVER
DENGUE FEVER: Found in Texas.

EPSTEIN-BARR VIRUS (EBV) INFECTION:

INFECTIOUS MONONUCLEOSIS

CYTOMEGALOVIRUS (CMV) INFECTION:

EPIDEMIOLOGY: Transmitted by close contact.
MANIFESTATIONS: CMV infects lymphocytes and monocytes.

Congenital CMV, Mononucleosis
Infection is usually subclinical in immunocompetent hosts.

MORPHOLOGY: gigantic cells (hence the virus' name) with nuclear and cytoplasmic inclusions.

HUMAN PAPILLOMAVIRUS (HPV) INFECTION:

MANIFESTATIONS

Verrucum Vulgaris: Skin Warts
Condylomata Acumulata: Perianal / Genital warts

Types 16, 18, 31, 33, 35 are associated with squamous cell carcinoma of the cervix.
Types 6 and 11 are not associated with carcinoma.

HUMAN POXVIRUS:

MANIFESTATION: Molluscum Contagiosum

Causes a wart-like lesion, with characteristic inclusion-bodies called Molluscum Bodies recoverable in the center of the lesion.
The wart has an umbilicated center, and the molluscum bodies are shed through the opening.
Transmitted by direct-contact (may be sexual).

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BACTERIAL INFECTIONS

SUSCEPTIBILITY TESTING:

E-TEST: Is a quantitative susceptibility testing-strip, used in cases where a quantitation is needed, such as osteomyelitis, endocarditis, and other hard-to-reach places.

STAPHYLOCOCCUS AUREUS:

MANIFESTATIONS:

Cutaneous:

Furuncle: Boil, infected hair follicle.
Carbuncle: Boil resulting from cluster of furuncles.

Bacteremia: Targets kidneys, lungs, hearts, bone. Possible coagulopathy.

The first thing you will see is an isolated abscess in an organ -- a clue that systemic S. Aureus infection is occurring.
You may also see petechial hemorrhages in fingernails, toes, and digits.
Endocarditis can result.

Septic embolus can break off of the vegetations and go to a distal peripheral artery (such as finger) to cause an infarct.

Osteomyelitis can also result. Used to occur in children. Septic arthritis occurs in adults, associated with heroin IV-needle use.

Scalded Skin Syndrome: Bullous lesions leading to desquamation in infants.

It is a result of the toxin Exfoliatin. No bugs are found in the lesion.
It will heal without scarring, if treated carefully and not spread.

Toxic Shock Syndrome: Result of TSS-Toxin.

High-grade fever, headache, myalgia, hypotension, rash, diarrhea.

Food Poisoning: Abdominal cramps, diarrhea, vomiting, 2-12 hours after eating. Staph Aureus is the most common cause of food poisoning in the U.S.

Associated with mayonnaise kept at room temperature, such as at a picnic.
Results from Enterotoxins A-E

VIRULENCE:

COAGULASE: Staph Aureus is Coagulase (+) and thus virulent. Coagulase Negative Staph (CNS) are far less virulent.
Catalase, Fibrinolysins, Hyaluronidase.

Methicillin-Resistant Staph Aureus (MRSA): Must be treated with Vancomycin.
Coagulase-Negative Staph (CNS): Less virulent. S. Saprophyticus causes UTI's in young females.

STREPTOCOCCI:

STREPTOCOCCUS PYOGENES (GROUP-A)

MANIFESTATIONS

SUPPURATIVE:

Pharyngitis: 5-15 yrs old.
Scarlet Fever: Pronounced oropharyngeal infection and rash.

Strawberry tongue, with desquamation ------> raspberry tongue.
Desquamation of outer skin layer on trunk.
Caused by the virulence factor, Erythrogenic Toxin.

Toxic-Shock Like Syndrome: Similar to Staph, it occurs as a result of Superantigen Erythrogenic Toxin A (SEA).

These are the so-called Flesh-eating bacteria.

Pyoderma:

IMPETIGO: Cutaneous lesions in kids, usually on face. Very similar to the Staph bullous lesions, except that these are vesicular lesions because these are actually full of bugs.
ERYSIPELAS: Cutaneous lesions in adults. Painful. Again contains organisms.

Pneumonia:
Bacteremia: Can lead to arthritis, osteomyelitis, endocarditis, meningitis.

NON-SUPPURATIVE: Sequelae

Rheumatic Fever: 2-3 weeks after soar throat, low-grade fever and polyarthritis.

Heart Murmur found, due to inflammatory process in heart.
Theories to cause:

Antibody to MAP protein cross-reacting with heart muscle.
Small Strep protein may bind to cardiac muscle.
Strep actually infect the heart valve, exposing our own antigens which are not normally exposed.

Acute Glomerulonephritis: Can follow skin or throat infections.

Associated with T-Antigen. Presence of DNAse Type B antigen is diagnostic.
Renal shutdown, oliguria, and hypertension.
Thought to be immune-complex disease.

TREATMENT: Penicillin. No problem with resistance.

STREPTOCOCCUS AGALACTIAE (GROUP B): Important cause of perinatal and neonatal meningitis, because it colonizes the birth canal.
STREPTOCOCCUS PNEUMONIAE

MANIFESTATIONS: Lobar pneumonia; wedge-shaped.

Empyema, pus in a pre-existing body space, can result.

VIRULENCE: Highly encapsulated.

BACTERIAL INFECTIONS OF CHILDHOOD

DIPHTHERIA: CORYNEBACTERIUM DIPHTHERIAE

MANIFESTATIONS: primarily affects respiratory tract and skin.

Skin: Not systemic disease. Local cutaneous pseudomembranous necrosis of hands and feet. Host response contributed to damage.
Bull neck: Characteristic appearance found (similar to Mono), with enlargement of cervical lymph nodes.
Pseudomembranous Necrosis: Found in oropharynx in initial respiratory infection.
Systemic Toxemia: Diphtheria toxin affects three organs, in order:

Heart:
Nerves: Polyneuritis, anesthesia of palate
Kidney: Only late course.

Special culture requirements -- notify lab.

PERTUSSIS: BORDETELLA PERTUSSIS

EPIDEMIOLOGY: Big problem in countries other than U.S. 1 million deaths annually.
MANIFESTATIONS:
WHOOPING COUGH: Bugs adhere to cilia up and down the airway. Systemic infection from a toxemia -- not a bacteremia. The organisms are non-invasive.

Incubation Stage: (7-10 days). Mild respiratory manifestations.
Catarrhal Stage: (1-2 weeks). More serious respiratory infections.

This is the best time to collect the bugs, when the bugs are in the greatest number.

Paroxysmal Stage: (2-4 weeks). Paroxysmal, rapid coughs, anoxia, followed by the "Whoop" sound to recover breath.

Intense lymphocytosis is found, unusual for bacterial infection -- more common with viral infection.
Vomiting

Convalescent Stage: (3-4 weeks or longer). Pneumonia, convulsions from anoxia, other complications.

Subconjunctival Hemorrhaging found in the eyes (red around iris) in babies who have had Whooping Cough.

HAEMOPHILUS INFLUENZAE (Hib)

MANIFESTATIONS:

Infantile Meningitis: #1 cause in kids older than 3 months.
Epiglottitis in kids 2 - 5, possibly with sepsis.
Cellulitis in kids.
Bacteremia
Otitis Media
Bronchitis and pneumonia

NEISSERIA MENINGITIDIS

EPIDEMIOLOGY: Normal flora of mouth of 15-20% of people.
MANIFESTATIONS: Meningitis and sepsis.

Waterhouse-Friderichsen Syndrome, adrenal necrosis,

SEXUALLY TRANSMITTED:

GONORRHEA: NEISSERIA GONOCOCCUS
CHANCROID: HAEMOPHILUS DUCREYI
GRANULOMA INGUINALE

ENTEROPATHOGENIC INFECTIONS:

LAB:

Normally cultured organisms: Salmonella, Shigella, Campylobacter. All other organisms require a special request.
A toxin assay will be done on Clostridium Difficile.

Diarrhea: Defined as more than 0.3L / day of fluid in the stool.
Enteritis: General host response to enteric infection can lead to Malabsorption Syndrome

Increased rate of mucus secretion by goblet cells.
Goblet cell metaplasia
Regressive changes in the intestinal chief cells.
Inflammatory reaction, which can ruin the brush border.

ENTERIC ESCHERICHIA COLI

GI MANIFESTATIONS:

Enterohemorrhagic E. Coli (EHEC): Causes hemolytic crisis and is associated with the O157:H7 serotype. This is the E. COLI food poisoning you get from hamburger.
Enteroinvasive E. COLI: Virtually indistinguishable, both microbiologically and clinically, from Shigella.

UTI MANIFESTATIONS:

As a quick urine assay, you can look for leukocyte esterase and nitrites in the urine as evidence of bacteruria and thus UTI.

TYPHOID FEVER: SALMONELLA TYPHI

Symptoms:

First Week: Constipation with step-wise fever and malaise.
Second week: Bacteremia. Sustained fever.

Rose Spot Rashes are discrete rashes on the trunk.

Diarrhea: Intestinal necrosis, severe bleeding, thrombophlebitis, cholecystitis, pneumonia, focal abscesses.
Carrier State following resolution -- may last up to a year. Bugs localize to the bile ducts.

PATHOGENESIS:

Organisms multiple in the lamina propria, lymphatics, and monocytes of the small intestine.
They then invade and disseminate to reticuloendothelial system, leading to sustained bacteremia.
At the liver, organisms reinvade the GI-Tract via the gallbladder.

COMPLICATIONS:

Intestinal perforations
Thrombophlebitis.
Cholecystitis and gallstones
Patchy necrosis caused by complement fixation and PMN inflammation.
DIC and focal abscesses.

ENTERIC FEVER: SALMONELLA ENTEROCOLYTICA

Enterocolitis self limiting to 2-7 days.

Nausea, vomiting, non-bloody diarrhea, fever, abdominal cramps, headache.
Can be asymptomatic.
Can penetrate mucosa but doesn't cause much damage.

SHIGELLOSIS: Dysentery
CHOLERA: Watery diarrhea with no dysentery and no damage to mucosa.
CAMPYLOBACTER: Bloody diarrhea, not as severe as Shigella but can disseminate.

GRAM-NEGATIVE PNEUMONIAS:

LEGIONNAIRE'S DISEASE: LEGIONELLA PNEUMOPHILA

STAIN: Dieterle Silver stain. It doesn't show up well on Gram-stain.

PSEUDOMONAS AERUGINOSA: Nosocomial, immunocompromised pneumonia.
KLEBSIELLA PNEUMONIA:

CLOSTRIDIAL DISEASES:

FOOD POISONING
CLOSTRIDIUM PERFRINGENS:

FOOD POISONING
NECROTIZING ENTERITIS
GAS GANGRENE

TETANUS: CLOSTRIDIUM TETANI
BOTULISM: CLOSTRIDIUM BOTULINUS
CLOSTRIDIUM DIFFICILE COLITIS: Most common cause of nosocomially acquired (exogenous or endogenous) diarrhea.

ZOONOTIC INFECTIONS:

BRUCELLOSIS: BRUCELLA, gram-negative coccobacilli.

SPECIES

B. Melitensis goat
B. Abortus cattle
B. Suis pig
B. Canis dog

AT-RISK: Zoonotic disease; ranchers, meat-processors.
MANIFESTATIONS: Undulating Fever

Infecting organisms go into bloodstream and then are taken up by fixed RES macrophages, where they reside happily.
Organisms are occasionally released from fixed macrophages and go back into the bloodstream. Fever waxes and wanes according to the presence of organisms in the blood stream.
Chronic disease causes microabscesses, granulomas, and caseation in the spleen and liver.

This results from Type-IV cell mediated response to the bugs.

PLAGUE: YERSINIA PESTIS

MANIFESTATIONS

BUBONIC FORM: Flea bite.

Bite become indurated and necrotic.
Buboes (swollen lymph node) results from initial flea bite.
Bugs undergo large temperature increase from 25C to 37C, which initiates new virulence properties (YOP's and F1 antigen).
High fever, bacteremia, pneumonia, sepsis.

PNEUMONIC FORM: Inhalation of aerosolized droplets spread by human to human contact (coughing).

Fever, malaise, pulmonary edema, death within 24 hrs.

Special culture requirements -- notify lab.

TULAREMIA: FRANCISELLA TULARENSIS. Small gram-negative coccobacillus.

MANIFESTATIONS: Four distinct forms of the disease

Ulceroglandular Tularemia: Most common type. Ulcer and glandular (lymph node) swelling. Often epitrochlear or axillary nodes, because initial exposure was on the hands.
Oculoglandular Tularemia: If it contacts your eyes. Also fairly common.
Typhoidal Tularemia: Infection of the gut.
Pneumonic Tularemia: Pneumonia.

ANTHRAX: BACILLUS ANTHRACIS -- Large gram-positive, spore-forming rod.

SOURCES: Goat, sheep, cattle, horses, pigs, dogs
PATHOPHYSIOLOGY:

The organism multiples extremely rapidly.
Anthrax Toxin causes the rapid hemorrhagic necrosis in the mediastinal lymph nodes in the lungs.

MANIFESTATIONS: Four different forms

Malignant Pustules: Most common by far. Skin infection with formation of an eschar.

First it forms a bullae, then ruptures, then necroses to form an eschar.

Pulmonary Anthrax: Inhalation of the spores. Very high mortality rate.

Wool Sorter's Disease
Hemorrhagic mediastinitis.

Septicemic Anthrax:
Gastrointestinal Anthrax:

LISTERIOSIS: LISTERIA MONOCYTOGENES

INFECTION: Get from food, soil, water, and plants.

Cole slaw and raw hot dogs.
Pregnant woman is at risk

PATHOPHYSIOLOGY: Starts as a bacteremia and then is tropic for the CNS, meningitis.

In-utero infection results in spontaneous abortion or stillbirth.
Sequelae: You may see an antibody-mediated aseptic meningitis as a sequela, after the initial infection is gone. Rash will appear, too.

CAT-SCRATCH FEVER: ROCHALIMAEA HENSELAE

MANIFESTATIONS

Unilateral lymphadenopathy and fever are most common manifestations.
Can have RES and CNS involvement.
Will disseminate in AIDS patients.

MORPHOLOGY: Can form necrotic abscesses, with liquefactive necrosis. The abscesses tend to have a stellate (star-like) appearance.

FILAMENTOUS INFECTIONS:

ACTINOMYCOSIS: ACTINOMYCES
NOCARDIOSIS: NOCARDIA

SPIROCHETAL INFECTIONS:

SYPHILIS: TREPONEMA PALLIDUM

PRIMARY SYPHILIS: Chancre, painless lesion with serous exudate and loads of bugs in the lesion.

Between primary and secondary phases, there is an asymptomatic spirochetemia, during which the bugs replicate.

SECONDARY SYPHILIS: Rash all over, including palms and soles.

Rashes are also loaded with bugs and highly infectious.

Latency:

Early Latency: Lots of antibodies and symptoms present.
Late Latency: Asymptomatic

TERTIARY SYPHILIS: Not infectious, due to immune response.

Skin: patchy loss of hair.
Neurosyphilis: Tabes Dorsalis, dementia, seizures, paresis.
Cardiovascular: Dissecting Aortic Aneurysm
Congenital: Stillbirth, abortion, or structural (but not intellectual) defects if the baby is born.

LYME DISEASE: BORRELIA BURGDORFERI:

CHLAMYDIAL INFECTIONS:

CHLAMYDIA TRACHOMATIS:
LYMPHOGRANULOMA VENEREUM: CHLAMYDIA TRACHOMATIS

Sexually transmitted but not manifested in the genital tract.
Suppurative infection of inguinal lymph nodes.

TRACHOMA:
PSITTACOSIS (ORNITHOSIS): CHLAMYDIA PSITTACI

RICKETTSIAL INFECTIONS: Gram-negative rods.

ROCKY MOUNTAIN SPOTTED FEVER: RICKETTSIA RICKETTSIAE

Early Infection: Full bodied rash, including palms and soles.
Later Infection: Severe gram-negative infection: DIC, hypotension, high fever.

EPIDEMIC TYPHUS

MYCOPLASMAL INFECTIONS:

MYCOPLASMA PNEUMONIAE

MYCOBACTERIAL INFECTIONS:

TUBERCULOSIS: MYCOBACTERIUM TUBERCULOSIS

MANIFESTATIONS:

Miliary Tuberculosis: Tuberculosis that has spread through the blood, either through the lung, or disseminated to other places in body.

Infection-Immunity: Once you get Tb, you always have it, and you are then immune to reinfection.
Ghon Complex: Combination of granulomas found in lung, plus hilar lymphadenopathy, both identifiable on X-Ray.
RESISTANCE: Multiple Drug-Resistant (MDR) Tuberculosis is a big problem. High mortality rate, and you can go to jail for not taking your drugs.

MYCOBACTERIUM-AVIUM (MAC) COMPLEX: MYCOBACTERIUM AVIUM-INTRACELLULARE
LEPROSY: MYCOBACTERIUM LEPRAE

MANIFESTATIONS:

TUBERCULOID LEPROSY: Forms good granulomas, and really requires a dermatologist to diagnose.

Few organisms are in the lesions.
Lots of lymphocytes are found in the lesions.

LEPROMATOUS LEPROSY: Anergic state against the bugs.

Lots of organisms in the lesions.
Lots of epithelioid cells -- incompletely formed granulomas.

CULTURE: It has never been cultured in artifical medium (Koch's postulates not fulfilled).

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FUNGI

OPPORTUNISTIC MYCOSIS:

CANDIDIASIS: CANDIDA ALBICANS

MORPHOLOGY:

YEAST: Candida in yeast form is part of our endogenous mucocutaneous flora, and exists in healthy people in small numbers in oral and vaginal mucosa.
Pseudohypha: When Candida is in the form of pseudohypha, it can escape neutrophilic attack. Other forms of Candida are susceptible to neutrophilic attack.
HYPHAE: Candida only exists in hyphal state when it is disseminated.

DEFENSE: Neutrophils are the most important defense. They can phagocytose yeast form, and can release oxidative enzymes onto mycelial form to degrade it.

Neutropenia can thus lead to Candidiasis.

LOCALIZED INFECTION: Mucocutaneous Candida infection, originating from endogenous flora.

THRUSH: Oral Candidiasis on the tongue. White cheesy stuff. Esophageal Candida can also be found.
Other skin infections: diaper rash, intertrigo (infection of apposed skin surfaces)
RISK FACTORS: Immunocompromise, Diabetes, antibiotic therapy.

Vaginal yeast (Candida) infections (from normal GI flora) is a common side effect of Antibiotic therapy.

DISSEMINATED INFECTION: AIDS

Likes to go to kidneys.

ASPERGILLOSIS: ASPERGILLUS FUMIGATUS

MORPHOLOGY: Characteristic finger-like conidia.

SEPTATE Hyphae
ACUTE angles of branching, in Y-Shape.

SOURCE:

AIR CONDITIONERS in hospitals can blow their conidia all over the place when they are turned on initially. The Aspergillus can collect in condensations around the air conditioner, and conidia are dispersed when it's turned on.

PATHOPHYSIOLOGY:

Likes to invade (grow into) blood vessels in the lungs, leading to wedge-shaped infarcts.

ALLERGY to Aspergillus is very common. Allergy is usually to the galactomannans (against which we have antibodies) or glycoproteins.
DISSEMINATED ASPERGILLOSIS: Septate Hyphae can disseminate in immunocompromised host.

RISK: Immunocompromised. It is a problem on the bone-marrow transplant ward.
SYMPTOMS: Lung is most common site of immunocompetent and immunocompromised infection.

Acute Pneumonia is common in immunocompromised patients.
Bad prognosis with dissemination to other organs common.

Spread: Hyphae (not conidia) spread to all organ systems. Dissemination is deadly and is often only detected post-mortem.

CRYPTOCOCCOSIS: CRYPTOCOCCUS NEOFORMANS

MORPHOLOGY: In tissue, it is a yeast with an enormous polysaccharide capsule.

The Capsule is susceptible to attack only by activated macrophages, hence AIDS renders us helpless.
Stains poorly with H&E and Gram stain. In lungs, appears as bubbles or holes in tissue stain.

SOURCE: PIGEON POOP -- Desiccated cryptococcal yeast are found in pigeon poop. Initially it is inhaled.
DISEASE:

Inflammation is scanty, due to the capsule evading the immune response.
DISSEMINATED: CRYPTOCOCCAL MENINGITIS is the most common disseminated form of the disease. Very common in AIDS.
LUNGS: Cryptococcal pneumonia also occurs.

SYSTEMIC DIMORPHIC INFECTIONS:

HISTOPLASMOSIS: HISTOPLASMA CAPSULATUM

INFECTION: Histoplasma is found in CHICKEN SHIT.
PATHOPHYSIOLOGY: Acute Histoplasmosis is most similar to tuberculosis in its histology and pathophysiology.

Pulmonary Infection will leave little caseating granulomas that can be silent in immunocompetent patients, and that eventually calcify.
Histoplasma live intracellular, inside alveolar macrophages. This is their route of dissemination, hence primary sites of dissemination are reticuloendothelial.

DISSEMINATION: Histoplasmosis disseminates primarily to Reticuloendothelial System (liver and spleen).
AIDS: It is common in AIDS, suggesting that CD4⁺ is essential to host defense.

BLASTOMYCOSIS: BLASTOMYCES DERMATIDES

GEOGRAPHIC LOCATION: The southeast, Tennessee valley.
MORPHOLOGY: Big yeasts with broad-based budding.
PATHOPHYSIOLOGY: Blasto also has huge conidia, but in yeast form it is primarily extracellular rather than intracellular.

It forms uncalcified granulomas in the lungs in immunocompetent people. These granulomas are similar to the cutaneous ones formed by Sporothrix.
Response can be both suppurative and granulomatous, even in the same infection, in the lung.

DISSEMINATION: It often disseminates to skin, bone.
AIDS: It is NOT seen in AIDS, suggesting that CD4⁺ is not essential to host defense. They don't know what is, though.

COCCIDIOMYCOSIS: COCCIDIODES IMMITIS

INFECTION: Initial infection is also pulmonary, and calcified granulomas are formed.
PATHOPHYSIOLOGY:

VALLEY FEVER: It forms valley fever and is found in the desert southwest. This is usually self-limiting.

Usually infects the lung, but it can also infect the skin.

MORPHOLOGY: Forms a tissue cyst similar to Toxoplasma Gondii.

Spherules usually do not provoke an inflammatory response until the cyst ruptures.

DISSEMINATION: Relatively common. Can be found in skin, bone, meninges, and later, mucocutaneous.

PARACOCCIDIOMYCOSIS: PARACOCCIDIOIDES BRASILIENSIS

ZYGOMYCOSIS:

RHIZOPUS:

PATHOPHYSIOLOGY:

ESCHAR: Infarcted skin commonly around orbit and maxillary.

They like to invade blood vessels, causing acute infarcts.

Deadly disease
RISK: Prolonged Acidosis. The fungi like to grow in acidotic environment.

Chronic respiratory acidosis
Diabetic Ketoacidosis

MORPHOLOGY:

BROAD BASED hyphae
RIGHT-ANGLE branching
NON-SEPTATE for the most part.

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PARASITES

PROTOZOA:

MALARIA (Plasmodium): A SPOROZOAN. The mosquito is the definitive host (in which sexual reproduction takes place), and the human is the intermediate host, in which larvae are disseminated.

Species:

PLASMODIUM FALCIPARUM: The most virulent of all of them. It will attack all RBC's indiscriminately.

Identification: Small rings on inside of cell; sometimes multiple parasites inside each erythrocyte. Infected and uninfected erythrocytes may or may not be the same size.

The Schizont forms a ring or double-ring inside the erythrocyte.

Erythrocytic Cycle: 48 Hrs. -- infected erythrocytes rupture 48 hours after initial invasion into RBC.
Malignant Tertian Malaria: It is the most virulent because it has the shortest pre-erythrocytic cycle, and it produces the greatest number of merozoites.

PATHOGENESIS: Schizont in the RBC produces adhesins that bind to ICAM-1, CD46, causing endothelial cell adhesion. RBC's stick to walls and stick to each other.
RBC LYSIS can also occur. This can result in anemia, and if rapid, hemoglobinuria which is known as BLACK WATER FEVER

PLASMODIUM VIVAX: Can be RELAPSING (Hypnozoites in liver)

Benign Tertian Malaria: Intermediate in severity. It can give profound anemia after a week to a month.

PLASMODIUM MALARIAE

Quartan Malaria: Slowest acting disease. After immunity is formed, immune complexes can accumulate in the kidney.

PLASMODIUM OVALE: Can be RELAPSING (Hypnozoites in liver)

Benign Tertian Malaria

LIFE-CYCLE

SEXUAL CYCLE: Sporogony in the mosquito, taking 1 to 3 weeks.

Sporozoites are released into mosquito, rendering it infectious to humans.

ASEXUAL CYCLE: Schizogony, formation of the Schizont.

Infected mosquito bites another human.
PRE-ERYTHROCYTIC PHASE: It occurs in the liver.

Sporozoites from mosquito's salivary glands make way to human liver.

Mosquito saliva has anti-coagulant properties.

HYPNOZOITES: P. Vivax and P. Ovale: Some sporozoites stay in hepatocytes and reside in a dormant state.
Sporozoites undergo asexual reproduction to make 2000 - 40,000 MEROZOITES.

ERYTHROCYTIC PHASE: Formation of more Merozoites from Merozoites.

Merozoites (larvae) enter erythrocytes by receptor-mediated endocytosis, where they mature to ring-shaped TROPHOZOITES
Erythrocytic Schizogony: The Trophozoite then undergoes nuclear division to make multinucleated SCHIZONT.
Schizont then creates from 8 to 24 MEROZOITE daughter cells.

Some daughter cells will be transformed to gametocytes, where they can be picked up by mosquitos.

CLINICAL STAGES OF MALARIA:

ACUTE: All organ systems can be involved. Hepatosplenomegaly, renal failure, CNS vascular problems.

P. Falciparum has the worst acute phase. P. Malaria has virtually no acute phase.

CHRONIC: Some immunity has been acquired, but there are still organisms in the erythrocytic stage.
RELAPSING: Re-activation of Hypnozoites of P. VIVAX and P. OVALE.
RECRUDESCENT: Recurrent malaria due to immunodeficiency, such as from corticosteroids, stress, or chemotherapy. This differs from relapsing because the organisms did not come from the Hypnozoite stage, but rather from an erythrocytic stage.

Malaria is NOT a problem in AIDS.

TOXOPLASMOSIS: TOXOPLASMA GONDII: Usually asymptomatic

SOURCES: Cat shit, pig meat (they like to eat cat shit)
DISEASE:

CONGENITAL TOXOPLASMOSIS (TORCH), leading to Necrotizing Encephalitis

Women are only infectious if they are in acute disease during childbearing age.

IMMUNOCOMPROMISED Toxoplasmosis in Brain: multifocal necrotizing encephalitis.

Ring-enhanced lesion is frequently seen on CT with AIDS patients. Other diseases must be a part of the Ddx:

HIV Encephalopathy
Progressive Multifocal Leukoencephalopathy (PML)
Cysticercosis

Center of lesion is often necrotic and devoid of bugs. Bugs are around the perimeter of the lesion, which is where biopsy should be taken.

MORPHOLOGY:

Trophozoites are banana-shaped
Cysts are formed in brain, which eventually rupture. Immunocompetent folks then kill all the bugs.

Bradyzoites remain within the cyst: slowly-reproducing toxoplasma.
Tachyzoites is the name of the bugs that rupture from the cyst. Rapidly proliferating if not checked by immunity.

PNEUMOCYSTIC CARINII PNEUMONIA: AIDS Pneumonia

MORPHOLOGY:

Cup shaped cysts that like Type 1 alveolar cells.
Proteinaceous stuff is put into lungs -- there will be no solid calcifications (cellular exudate) as in bacterial pneumonias.
Ground-glass appearance is what the chest x-ray looks like.

TREATMENT: Trimethoprim

AMEBIASIS: ENTAMEBA HISTOLYTICA

AMEBOMA: Accumulations of amoeba that form in areas of fecal stasis -- the cecum and recto-sigmoid colon. Trophozoites invade through the intestinal epithelium where they can form flask-shaped ulcers in the submucosa.

The intestinal ulcers result in dysentery, or bloody diarrhea. If they ulcerate all the way through, complications are Amebic Peritonitis or Bacterial Peritonitis.

LIVER ABSCESS: Supposed to resemble anchovy paste. Major complication.

Amoeba like to eat red cells. They get into the blood and go through portal circulation to liver, where they form Liver Abscesses.

DIAGNOSIS: Take a fresh stool sample and look for motile trophozoites in the stool. This finding is intermittent, and you should check at least three times before ruling out amebiasis.

GIARDIASIS: GIARDIA LAMBLIA

MORPHOLOGY: Flagellate (tuft of flagella), and it has a sucker.
PATHOPHYSIOLOGY:

The creatures adhere to the enterocyte glycocalyx epithelium. This leads to malabsorption and facilitates bacterial metabolism, resulting in non-bloody diarrhea and immense foul-smelling flatulence.

LEISHMANIASIS: Resembles Leprosy in its appearance and pathophysiology.

SOURCE: Sand flies.
PATHOPHYSIOLOGY

Skin Ulcer is most common, innocuous form.
ANERGIC: Can have an anergic case of Leishmaniasis, which is terribly disfiguring and can lead to disseminated disease.

MORPHOLOGY: The bugs live intracellular
KALA-AZAR: VISCERAL LEISHMANIASIS

The bugs infect macrophages, and the macrophages disseminate. Immunity can control it, but 5% are anergic.
Invasion of Reticuloendothelial System. Cachexia and massive splenomegaly.

CHAGAS DISEASE (AMERICAN TRYPANOSOMIASIS): TRYPANOSOMA CRUZI

ACUTE DISEASE:

CHAGOMA, ROMANA SIGN: Periorbital edema is a sign of infection with Chagas.

CHRONIC DISEASE:

Myocarditis, dilated heart. Infiltrates and a dilated heart. Dysrhythmias.
Megaesophagus: Dilated esophagus from constricted, inflamed LES (Achalasia). Results from destruction of parasympathetic ganglion cells in the wall of the lower esophagus.
Megacolon: Similar to megaesophagus, in the mesenteric plexus of the colon. Progressive aganglionosis causes severe constipation.

AFRICAN SLEEPING SICKNESS (TRYPANOSOMIASIS):

Destructive vasculitis of the small vessels of the CNS.

TRICHOMONAS VAGINALIS:

DISEASE: Simple trophozoite infecting vaginal or penile mucosa. Non-invasive.

Often coexists with other vaginal infections.
Infection may cause non-gonococcal urethritis in males, or it may be asymptomatic (in males or females).

MORPHOLOGY: Flagellate

FILARIAL NEMATODES:

LYMPHATIC FILARIASIS: Bancroftian Filariasis

TRANSMISSION: Mosquitos infect us and are the vectors.
DIAGNOSIS: Filaria (larvae) circulate through the blood only in early evening and early morning. Blood must be taken at those times.
Adult worms obstruct lymph channels, leading to Elephantiasis and lymphedema.

ONCHOCERCIASIS: ONCHOCERCA VOLVULUS

TRANSMISSION: Simulium black flies. Endemic to areas where there is running water (hence river)
MANIFESTATIONS: River Blindness
PATHOPHYSIOLOGY: Microfilariae migrate to skin, eyes, and lymph nodes to cause disease. In the eye, the microfilariae infiltrate to all parts of the eye including the optic nerve.

INTESTINAL NEMATODES: AHEATS

(A) ASCARIS LUMBRICOIDES: ROUNDWORMS. They are the largest intestinal nematodes.

INFECTION: Eating food contaminated with the eggs.
PATHOGENESIS / CLINICAL: Intestinal ascariasis is usually asymptomatic or may cause pain or obstruction.

Pulmonary Ascariasis may occur if larva get in lungs. This will result in an eosinophilia.

DIAGNOSIS: Look for eggs in the feces.
LOCATION: Worldwide, in USA found in the south.

(H) HOOKWORMS -- NECATOR AMERICANUS

INFECTION: Skin penetration from filariform larvae in moist soil. They then migrate to lungs, are coughed up, and then are swallowed.
MANIFESTATIONS: Biggest clinical problem is BLOOD-LOSS -- Microcytic Hypochromic Anemia, an iron-deficiency (not hemolytic) anemia. The hookworms suck blood in small intestine.

Cachexia, round face, and edema can also occur.

DIAGNOSIS: Look for eggs in the feces. May see worms attached to intestinal wall in a tissue biopsy.

Larva is kind of long and bent, like Strongyloides.

LOCATION: In western hemisphere: USA found in the south, Brazil, Phillippines.

(E) ENTEROBIUS VERMICULARIS -- PINWORM

INFECTION: Ingestion of eggs.
MANIFESTATIONS: Perianal itching (pruritus) is most common symptom.

Can result in secondary Staph or Strep perianal infection from scratching.

DIAGNOSIS:

SCOTCH TAPE on the ass at night can recover eggs.
The eggs are not found in stools. They are only found in perianal region.
Most commonly affects children.

(A) ANISAKIS
(T) TRICHURIS TRICHURIA -- WHIPWORM

INFECTION: Eat food contaminated with the eggs.
MORPHOLOGY:

The worm has a thick body and thin tail.
The egg is a bi-operculate egg, which can be remembered by the mnemonic "tricky tricky."

MANIFESTATIONS: Most infections are asymptomatic. It may cause diarrhea.

TENESMUS is anal dry heaves. It can occur with Whipworm and can lead to rectal prolapse.

TREATMENT: Usually is not treated. Drugs are toxic.

(S) STRONGYLOIDES STERCORALIS -- THREADWORM

INFECTION: Penetration of skin by filariform larvae. They go to lungs, are coughed up and then are swallowed.

Adult worms lives in the crypts of the colon.
They spend their entire life-cycle (and can replicate) in the human host.
Amplification Cycle: Eggs can also form more filariform larvae which can go back to the lungs to repeat the cycle.

You will see a pulmonary eosinophilia in the lung.

MANIFESTATIONS: Strongyloidiasis. Can be asymptomatic, depending on worm-burden.

Watery diarrhea
Pneumonitis can occur in lung

DIAGNOSIS: Identify larva in stool sample.

TISSUE NEMATODES:

TRICHINOSIS: TRICHINELLA SPIRALIS

INFECTION: Rats ------> pigs eat the rats ------> humans eat the undercooked pork.

Human is the dead-end host.

MANIFESTATIONS: Worms mate in intestine, and larvae migrate to skeletal muscle.

Cysts form in skeletal muscle. The larvae die and undergo dystrophic calcification in the area. Then inflammatory response ensues, leading to muscle aching.
Other symptoms: Myalgia, chronic fatigue, periorbital edema.
Severe eosinophilia is also seen.

CREEPING ERUPTION

INFECTION: Caused by a long list of organisms. Humans are dead-end hosts and not part of their life-cycle. Worms migrate through skin.

In U.S., usually caused by domestic cat or dog hookworm.

MANIFESTATIONS: Migrate through skin; skin eruptions.

Toxocara = larval migration through skin to eyes, which can lead to blindness. This is a possible complication.

TREMATODES (FLUKES):

SCHISTOSOMIASIS:

DIAGNOSIS: Eggs in feces. May find eggs in tissue.
MANIFESTATIONS: All pathological findings are due to the presence of the eggs -- not the worms!

	HEPATOSPLENIC SCHISTOSOMIASIS	URINARY SCHISTOSOMIASIS
Species	*Schistosoma Mansoni* *Schistosoma Japonica*	*Schistosoma Haematobium*
Pathogenesis	Inflammatory granulomatous response to allergens from eggs in the colon	Inflammatory granulomatous response to allergens from eggs in the bladder and lower ureters.
ACUTE SCHISTOSOMIASIS	Eosinophilia Granulomatous Polyps in Colon Fever, anorexia, weight loss, anemia Portal Hypertension	Eosinophilia Hematuria Terminal Dysuria (pain, difficulty at end of micturition)
Secondary Sites of Infection	Eggs go back through portal circulation to liver, causing granulomatous inflammation in liver	Eggs go back through systemic circulation (iliacs) to Lungs, causing granulomatous inflammation in lungs.
Sequelae CHRONIC SCHISTOSOMIASIS	Portal Hypertension leads to Splenomegaly, esophageal varices, and ascites. Biliary cirrhosis and end-stage liver disease.	Obstructed urine flow results in Hydroureter and Hydronephrosis Risk for Squamous Cell Carcinoma of the bladder.

CLONORCHIASIS: CLONORCHIS SINENSIS

MANIFESTATIONS: Chinese liver fluke infection.

CESTODES (TAPEWORMS): Has a scolex (head), proglottids (segments), and suckers.

TAENIA SAGINATA (BEEF TAPEWORM): Cause of Taeniasis.

INFECTION: Ingestion of cysticerci in undercooked beef. Humans are definitive host and cattle intermediate host.
MORPHOLOGY: The largest of parasites. Up to 1 meter long.
MANIFESTATIONS: Unlike pork tapeworm, findings are largely asymptomatic. Proglottids may be found in stool, resulting in reinfection or spreading of infection.
TREATMENT: Must get rid of the scolex. Getting rid of the proglottids won't help.

Use a scope to get at the scolex. Look in the feces for the scolex to know you're cured.

TAENIA SOLIUM (PORK TAPEWORM): Cause of Cysticercosis.

INFECTION: Undercooked pork. Normally, people ingest the larvae, or cysticerci.
MANIFESTATIONS: Neurocysticercosis

Cysticerci go to brain where they occupy space (cystic, non-inflammatory). Once they die, inflammation ensues.
Neurocysticercosis is the leading cause of Epilepsy in Mexico, where they eat undercooked pork.
The larva don't have to occupy the brain. They can go to any organ. Heart cysts are also common.

DIPHYLLOBOTHRIUM LATUM (FISH TAPEWORM): Cause of Diphyllobothriasis.

MANIFESTATIONS: The worm likes to eat Vit B-12, thus Pernicious (Megaloblastic) Anemia can result from infection.

ECHINOCOCCUS GRANULOSUS (DOG, HYDATID TAPEWORM): Cause of Unilocular Hydatid Cyst Disease.

LIFE-CYCLE: Dogs are definitive hosts, and so are sheep. Humans are a dead-end intermediate host.
PATHOPHYSIOLOGY: It forms one fluid-filled cyst that is just jam-packed with scoleces from the parasite. Embedded daughter cysts can form within the main cyst, etc.

Cyst must be surgically removed. Parasite is antigenic, and if not careful, removal of cyst and exposure to antigen can result in anaphylaxis.
Cysts can form in: liver, spleen, lungs, elsewhere

MANIFESTATIONS: Often asymptomatic, but liver cysts, brain cysts can result. Cyst rupture can cause fatal anaphylactic shock.

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