Exam 4-Diseases

Strep Throat
Strep Throat
**BACTERIAL** UPPER RESPIRATORY
Causative agent: Streptococcus pyogenes; beta hemolytic (causes pus)Portal of Entry: inhalation/ingestion (i.e.: sharing drinks; droplet transmission)

Signs & Symptoms: Sore red throat often with white, pus follicles on tonsils or back of throat; tenderness of lymph nodes of throat

Pathogenesis: multiple virulence factors (**NOT S. pyogenes on its own!)

Epidemiology: direct contact and droplet infection

Treatment: antibiotics

Other: **untreated cases can subsequently produce rheumatic fever or glomerulonephritis (decreased kidney function) in some patients

Portal of Exit: nose and mouth

Diptheria
**BACTERIAL** UPPER RESPIRATORY
Causative agent: Corynebacterium diptheriae (look like check marks; pleomorphic)Portal of Entry: Inhalation-nasal cavity or throat

Signs & Symptoms: Sore throat, fever, fatigue and malaise; a white pseudomembrane often forms on the tonsils. Tonsils look gray and dead, with a layer of dead cells over the surface.

Pathogenesis: upper respiratory infection; exotoxin (A-B toxin) is released and absorbed by the body; toxin kills cell by blocking protein synthesis

Epidemiology: inhalation of droplets; direct contact with patient; indirect contact with for mites

Treatment: antitoxin; antibiotics to prevent transmission

Other: prevention is vaccination with diptheria toxoid in a childhood vaccination series with periodic adult boosters

Portal of Exit: respiratory secretions (i.e: coughing, hacking and sneezing)

**classic disease that Standard Precautions knock out**

Pink-eye (conjunctivitis); Earache (otitis media); Sinus infection (sinusitis)
Pink-eye (conjunctivitis); Earache (otitis media); Sinus infection (sinusitis)

*BACTERIAL* UPPER RESPIRATORY

Causative agents: Haemophilus influenzae & Streptococcus pneumoniae

Signs & Symptoms:
1.) Pink-eye: increased tears, red and swollen conjunctiva, sensitivity to light, large amounts of pus
2.) Earache: Severe earache, sometimes producing vomiting; sometimes fever
3.)Sinus infection: facial pain and pressure in sinus area, headache, severe malaise, thick green nasal discharge and sometimes pus and blood

Pathogenesis: direct contact and droplet infection of eyes and nose

Epidemiology: carriers can reach 80% in the absence of disease; virulence of bacteria and levels of respiratory viruses are all important factors. If you have another infection, it will make you more likely to develop these diseases. *With the development of sinus infections, allergies can trap some pathogens into the tissues*

Treatment: strain specific antibiotic drops for pink-eye (2-3 formulations); amoxicillin for the other two (decongestants and antihistamines are NOT recommended, because these diseases are not allergic reactions and the use of these can cause tissues to dry out and get infected better)

Other: Earache is common between 2-5 years, when most become immune to H influenzae; Pink-eye is common in teens; Sinusitis typically occurs in older children and adults

The Common Cold
*VIRAL* UPPER RESPIRATORY
Causative agent: Rhinovirus (100 or more types)Signs & Symptoms: Scratchy throat, nasal discharge, malaise, headache, cough

Pathogenesis: upper respiratory specific, prolific reproducers-cell damage produces the nasal discharge and histamine reactions; infection stopped by interferon (type of cytokine), cell-mediated, and humoral immunity

Epidemiology: Inhalation of droplets, direct contact (transfer of mucous)

Treatment: No generally accepted treatment. Can be prevented through handwashing and avoidance

Portal of Exit: nose and mouth

Pneumococcal pneumonia
*BACTERIAL* LOWER RESPIRATORY
Causative agent: Pneumococcus pneumoniae *capsulated* (only caused by the capsulated varieties; the more capsulated, the more virulent)Signs & Symptoms: cough, fever, *single shaking chill*; rust-colored sputum from degraded blood; shortness of breath; chest pain

Pathogenesis: inhalation of bacteria; colonization of alveoli; incites inflammatory response; plasma, blood, and inflammatory cells fill the alveoli (unable to breathe, may cause permanent lung damage); pain from nerve involvement

Epidemiology: high carrier rates; increased rates from transient or chronic immunocompromised states (including infection by other respiratory viruses) that impair mucocilliary escalator

Treatment: antibiotics; vaccine raised to 23 capsule antigens available (vaccine for pneumonia is for this strain)

Other: affected patients can become dusky in color; untreated patients that survive often regain normal color and their temperature drops after 7-10 days

**Pneumococcal pneumonia is the most common strain of pneumonia; Klebsiella is the most dangerous, causing tissue death, unlike the others (death, permanent damage and sepsis possible; antibiotic resistant) Mycoplasma pneumonia is mild compared to the others, and is known as “walking pneumonia.”**

Pertussis (whooping cough)
*BACTERIAL* LOWER RESPIRATORY
Causative agent: Bordatella pertussisSigns & Symptoms: runny nose followed by a number of days of 1-2 minute bouts of violent coughing (with long intervals of no coughing); vomiting, possible convulsions

Pathogenesis: upper respiratory specific-tracheobronchial; cilliary action slowed; A-B type exotoxin released causes cell death of epithelial cells; fever, excessive mucous, rise in circulating lymphocytes

Epidemiology: inhalation of droplets; older children have milder symptoms *very serious disease in infants/small children

Treatment: antibiotics if given before coughing starts; acellular vaccine for infants and children (DTaP) *On rise here in MI this year*

**adults are the carriers**

Tuberculosis (TB)
*BACTERIAL* LOWER RESPIRATORY
Causative agent: Mycobacterium tuberculosisSigns and Symptoms: Chronic fever, weight loss, cough, sputum production

Pathogenesis: lower respiratory specific; colonization of alveoli incites inflammation; ingestion by macrophages follows, and they are infected, and carry the bacterium to the lymph nodes, lungs and other body tissues; tubercle bacilli multiply; granulomas form (via delayed hypersensitivity)
= bacteria are gobbled up by the macrophages, but the macrophages do not kill them; bacteria are then carried throughout the body

Epidemiology: Inhalation of airborne organisms; latent infections can return *Recent outbreaks of completely resistant strains*

Treatment: two or more antiturbecular medications given simultaneously long term; DOTS; BCG vaccination (outside of US); TB tests used to give earl treatment; many false positives
When the TB test is given, if the bump on the arm becomes 10 mm or larger in size, the test is positive; the bump will appear irregular, glossy, pussy, etc.

Influenza (The Flu)
*VIRAL* LOWER RESPIRATORY
Causative agent: Influenza virus (primarily a bird disease; not immunologically adapted for humans)Signs & Symptoms: Fever, muscle aches, lack of energy, headache, sore throat, nasal congestion, cough (all strictly respiratory; in actual lung tissue)

Pathogenesis: lower respiratory epithelium; cells destroyed and virus released to infect other cells; possible bacterial secondary infection from damaged mucocilliary escalator (often followed by bacterial/viral bronchitis)

Epidemiology: antigenic drift and antigenic shift prevent immunity; spreads readily via droplet transmission

Treatment: specific antibiotics are sometimes effective for preventing Type A, but not B disease; neuramidase inhibitors are effective against both; meds are only effective if there is an early treatment; take meds in first 24-38 hours or they become ineffective **Vaccines are 80-90% effective**

Portal of Exit: coughing (droplet)

Hair follicle infections (folliculitis, furuncles, boils/carbuncles)
*BACTERIAL* SKIN DISEASE
Causative agent: Staph. aureus (usually several virulence factors)Signs & Symptoms: usually mild, but can become serious or bloodborne

Pathogenesis: minor infections of hair follicles can be relieved by pulling the hair and releasing the pus; more advanced infections produce a necrotic plug, a minor epidermal lesion and a more extensive dermal lesion; pus accumulates from inflammatory reaction; left unchecked can spread to multiple follicles (carbuncles), produce fever and large amounts of pus.

Epidemiology: direct contact, contact with fomites; S. aureus can acquire virulence factors from horizontal gene transfer; people with boils shed lots of bacteria and should not work with food, near patients with surgical wounds, or chronic illnesses.

Treatment: no preventative except cleanliness and keeping skin dry; sometimes minor surgery required (draining), minor course of antibiotics. *Resistant strains (VRSA, VISA, MRSA) can cause complications (VRSA= Very Resistant Staph. aureus)*

Staphylococcal Scalded Skin Syndrome (SSSS)
*BACTERIAL* SKIN DISEASE
Causative agent: Staph. aureus (with exfoliation gene, 5%)Signs & Symptoms: general redness, sometimes affecting the entire body; malaise, irritability, fever; later, the nose, mouth, or genitalia may be painful; later yet, clear, liquid-filled blisters appear; skin wrinkles, skin appears scalded or burned, feels like sandpaper, and starts peeling.

Pathogenesis: infection is usually small, but the toxin spreads throughout the body, and causes the epidermis to separate from the dermis; the loss of body fluids can be very dangerous, and the possibility of secondary infection from other bacteria (like Pseudomonas sp.) is high.

Epidemiology: can appear in any age group, but most common in newborn infants (their immune system is weak); the elderly and immunocompromised are susceptible. *Transmission is from person to person*

Treatment: antibiotic therapy, usually methicillin (handles possible secondary infections as well); dead skin is removed as with traditional burns. Prompt therapy usually leads to full recovery.

Impetigo
*BACTERIAL* SKIN DISEASE
Causative agent: Streptococcus pyogenes (sometimes S. aureus); “strep throat in the wrong spot”Signs & Symptoms: blisters that break, releasing plasma and pus (pyoderma); *formation of golden-colored crusts* (hallmark); lymph node enlargement (2-5 day incubation period) *comes on quick*

Pathogenesis: Organisms enter the skin through minor breaks; certain strains of S. Pyogenes that cause impetigo can also cause glomerulonephritis

Epidemiology: Spread by direct contact with carriers or patients with impetigo, insects, and fomites

Treatment & Prevention: An oral penicillin if cause is known to be S. pyogenes; otherwise, an anti-staphylococcal antibiotic orally or topically. Cleanliness, care os skin injuries.

Rocky Mountain Spotted Fever
*BACTERIAL* SKIN DISEASE
Causative agent: Rickettsia rickettsii (the wood tick is the main vector in the western United States)Signs & Symptoms: headache, pain in muscles and joints, and fever, followed by a hemorrhagic rash that begins on the extremities; characteristically, the rash begins on the arms and legs, spreads centrally, and becomes hemorrhagic (4-8 day incubation period)

Pathogenesis: Organisms multiply at site of the tick bite; invade the bloodstream and then infect endothelial cells; vascular lesions and immune response to endotoxin account for pathologic changes.

Epidemiology: A zoonosis transmitted by bite of infected tick, usually Dermacentor sp.

Treatment & Prevention: Treated with doxycycline or chloramphenicol (therapeutic index is low, but they work well). Prevented by avoiding tick-infested areas, using tick repellent, removal of ticks within 4 hours (tick must be drinking your blood for four hours to become infected)

Lyme disease
*BACTERIAL* SKIN DISEASE
Causative agent: Borrelia burgdoferi (the black legged (deer) tick is the most important vector of Lyme disease in the eastern and north-central United States)Signs & Symptoms: Early localized infection includes an enlarging rash at the site of the bite, lymph node enlargement near bite, and flulike symptoms; Early disseminated infection brings about heart and nervous system involvement; Late persistent infection involves chronic arthritis and nervous system impairment (approx. 1 week incubation period)

Pathogenesis: Spirochetes injected into the skin by and infected tick multiply and spread rapidly; the spirochetes enter the bloodstream and are carried throughout the body; the immune reaction to bacterial antigen causes tissue damage.

Epidemiology: Spread by the bite of ticks, usually found in association with animals such as white-footed mice and white-tailed deer living in wooded areas.

Treatment & Prevention: Early treatment with doxycycline and others; prolonged antibiotic therapy in chronic cases. Protective clothing and tick repellents.

**target rash is distinctive of Lyme disease; the rash usually has a target-like or bull’s eye appearance**

Chickenpox
Chickenpox
*VIRAL* SKIN DISEASE
Causative agent: Varicella-zoster virus (VZV); a herpes virus (goes latent, then comes back)Signs ; Symptoms: itchy bumps and blisters (papules), fever; latent infections can reactivate, resulting in shingles years later

Pathogenesis: multiplies in the upper respiratory tract followed by spread via bloodstream to the skin; giant cell formation

Epidemiology: Highly infectious; Portal of Entry is the upper respiratory: spread via skin lesions or respiratory secretions. The only source of infection is people with active chickenpox or shingles.

Treatment: Acyclovir or other antiviral for prevention and treatment. Attenuated vaccine. Passive immunization for immunocompromised with zoster IgG (VZIG)

Rubeola (Measles)
Rubeola (Measles)
*VIRAL* SKIN DISEASE
Causative agent: Rubeola virus (in same family as Herpes virus)Signs ; Symptoms: rash, fever, weepy eyes, cough and nasal discharge; Koplik spots are characteristic of measles, and resemble grains of salt on a red base (term used when spots are fully developed)

Pathogenesis: upper respiratory replication; spreads to lymphatic tissues and then rest of the body, notably the skin, lungs, and brain; damage to the respiratory tract epithelium leads to secondary infection of ears and lungs.

Epidemiology: Acquired by respiratory route; *highly contagious; humans only* (easier to eliminate)

Treatment: No treatment. Attenuated vaccine after age 1, with second dose before entering grade school (vaccine mediates death)

Rubella (German measles)
*VIRAL* SKIN DISEASE
Causative agent: Rubella virusSigns ; Symptoms: Mild fever and cold symptoms, rash beginning on forehead and face, enlarged lymph nodes behind the ears. Symptoms are often mild, but the effects on a fetus can be devastating.

Pathogenesis: Replication in the respiratory tract; the virus spreads across the body and across the placenta; surviving fetuses often develop abnormally and they excrete the virus for months after birth.

Epidemiology: Lives in nose and throat a week before and after the rash appears. Portal of Entry: respiratory. *Humans are the only reservoir* (great shot to eliminate this with vaccine)

Treatment: none. Attenuated vaccine administered at 12-16 months and again before grade school

**measles and German measles are NOT related; 2 different viruses**

Superficial cutaneous mycoses (athlete’s foot, jock itch, ringworm)
*FUNGAL* SKIN DISEASE
Causative agent: Epidermophyton (jock itch), Microsporium (ringworm) or Trichophyton (athlete’s foot)Signs ; Symptoms: Most have no symptoms; some complain of itching, bad odor, or rash. Ringworm can produce a scaly area surrounded by a reddened ring. This group includes dandruff, beard itch, nail fungus, etc.

Pathogenesis: Normal skin is generally resistant to all but the most virulent varieties. Some produce kertanaise, which is a virulence factor (allows fungi to break down dead skin tissue and get to the fresh dermis which allows them to thrive and grow). Infections that progress to the dermis provoke an immune reaction like asthma, eczema, or allergies.

Epidemiology: Patient age, strain virulence, and moisture availability are the major factors (obesity, tight clothing, plastic or rubber footwear, etc.)

Treatment: Numerous over the counter medications can be used to treat superficial skin conditions. Nail infections, however, may require oral antifungals and/or removal of the nail

Necrotizing fasciitis (Group A Streptococcal); “Flesh Eating Disease”
*BACTERIAL* WOUND INFECTION
Causative agent: Streptococcus pyogenes (SPE-producing) *skin eating bacteria*Signs ; Symptoms: sudden, severe pain at the wound site (which can be trivial); rapid swelling, fever and confusion; overlying skin becomes stretched and translucent; death occurs rapidly in the absence of treatment *rapidly progresses and URGENT*

Pathogenesis: S. pyogenes requires F-protein, exotoxins A (a superantigen that causes toxic shock) and B (tissue-destroying protease), M-protein, and often multiple other virulence factors-including a variety of SPEs (streptococcal pyrogenic exotoxins)
*know in general that it requires SPE and multiple toxins*

Epidemiology: in the US, cases are sporadic- of all deaths from an invasive S. pyogenes, less than 2% are necrotizing fasciitis. Invasive infections seldom occur in healthy individuals with minor injuries.

Treatment: Toxins spread so fast that almost immediate surgery is required to reduce the pressure from the swollen tissue and to remove dead tissue; penicillin can be helpful if caught very early, but surgery (even amputation) is the best treatment.

**DEATH IN HOURS**

Tetanus (“lockjaw”)
*BACTERIAL* ANAEROBIC BACTERIAL WOUND INFECTION
Causative agent: Clostridium tetaniSigns ; Symptoms: restlessness, irritability, difficulty swallowing; muscle pain and spasm in the jaw, abdomen, back, or the entire body.

Pathogenesis: results from tetanospasmin, a neurotoxin produced by C. tetani. The toxin is carried to the brain and spinal cord by motor nerve axons or circulating blood; the toxin inhibits nerves that inhibit muscle contraction (nerves that cause relaxation). Unopposed, the contractile nerves then produce spasm.

Epidemiology: bacteria common in soil (NEVER going to get rid of it); spores contaminate wounds, germinate in anaerobic conditions, particularly in dirty or puncture wounds.

Treatments: antibiotics, tetanus antitoxin. Immunization at ages 2 months, 4 months, 6 months, and 18 months; booster dose when starting school and at 10 year intervals. Tetanus IgG (TIG) available.

**recovery is more limited in adults**

Clostridial myonecrosis (“gas gangrene”)
*BACTERIAL* ANAEROBIC BACTERIAL WOUND INFECTION
Causative agent: usually Clostridium perfringesSigns ; Symptoms: severe pain; gas and fluid seep from wound, blackening of overlying skin; shock and death commonly follow. **horrible smell**

Pathogenesis: organisms grow in dead and poorly oxygenated tissues and release *alpha-toxin*; toxin kills leukocytes and normal tissue cells by degrading lecithin in their cell membranes; involvement of muscle causes shock by an unknown mechanism. Sometimes puncture wounds, often war wounds (reason for many amputations in previous wars) *liquefication of muscle causes shock*

Epidemiology: Wounds of war; dirt contamination of wounds, tissue death, impaired circulation to tissue as in people with diabetes or arteriosclerosis; self induced abortions.

Treatment: Surgical removal of dirt and dead tissues of primary importance; hyperbaric oxygen of possible value; antibiotics to kill negative C. perfringes of marginal value. NO VACCINE

Actinomycosis (“lumpy jaw” – named incorrectly)
*BACTERIAL* ANAEROBIC BACTERIAL WOUND INFECTION
Causative agent: usually Actinomyces isrealii (normal bacteria that grows in the wrong spot)Signs ; Symptoms: Chronic disease; recurrent, sometimes painful swellings open and drain pus, heal with scarring; usually involves face and neck; chest, pelvis, and abdomen are other common sites.

Pathogenesis: usually begins in a mouth wound (i.e: bite inside of mouth), extends to the face, neck, or upper chest; sometimes begins in the lung, intestine, or female pelvis. A. isrealii is usually accompanied by the normal microflora. In tissue, grows as *dense, yellowish colonies*.

Epidemiology: Part of normal microflora. *No person to person spread* Dental procedures, abdominal surgeries, or IUDs (intrauterine devices) can initiate infections.

Treatment: Due to slow growth, treatment is prolonged. Multiple antibiotics are effective. No specific prevention.

Human bites
*BACTERIAL* BACTERIAL INFECTION OF BITE WOUND
Causative agent: mixed aerobic and anaerobic species, usually normal mouth microbiota (so many bacteria in the mouth; may not be normally pathogenic, but when put into a sterile spot all at one time, can work together and go out of control).Signs ; Symptoms: rapid onset (approx. 1 hour), pain, massive swelling, drainage of foul-smelling pus.

Pathogenesis: Various mouth bacteria act synergistically to destroy tissue. Wounds often produce irreversible tendon and tissue destruction.

Epidemiology: Alcohol-related violence; forcible restraint (mentally ill, drugs, etc.); poor mouth care and extensive dental disease.

Treatment: Treatment is usually surgical. Prompt cleaning of wound and application of antiseptic is advised. Possibly days of IV antibiotics.

Animal bites
*BACTERIAL* BACTERIAL INFECTION OF BITE WOUND
Causative agent: usually Pasturella multocida (gets rolling in our flesh)Signs ; Symptoms: Spreading redness, tenderness, swelling, discharge of pus.

Pathogenesis: Introduced by bite, the bacteria attaches to tissue, resisting phagocytes because of its capsule; *probably cell-destroying toxins*. Extensive swelling, abscess formation. Opsonins develop, allowing phagocytic killing, which limits spread (do NOT need to know for exam)

Epidemiology: Carried by many animals in their mouths and upper respiratory systems.

Treatment: Penicillin, other antibacterials, effective if given promptly. *NO VACCINES*

Rat bite fever
*BACTERIAL* BACTERIAL INFECTION OF BITE WOUND
Causative agent: Streptobacillus monoliformisSigns ; Symptoms: Chills, fever, muscle aches, headache and vomiting. *Later, rash and pain in one or more large joints (HALLMARK)*; looks similar to the beginning of pneumonia, but large joint aches set it apart.

Pathogenesis: Bite wound heals normally, but bacteria travels in the bloodstream. Fevers come and go irregularly. Most victims recover without treatment; in others, infection of organs can be lethal. Rodent teeth are long and sharp, so acts much like a puncture wound.

Epidemiology: Wild and laboratory lab rats. Bites of other rodents and those that prey upon them can transmit the disease to humans. Food or drink contaminated with rodent feces can also transmit the infection.

Treatment: effectively treated with penicillin, other antibacterials. Control of wild rats and mice; proper handling in labs.

Rose Gardener’s Disease
*FUNGAL* WOUND INFECTION
Causative agent: Sporothrix schenckii (fungi)Signs & Symptoms: painless, ulcerating nodules, appearing in sequence in a linear pattern (HALLMARK)

Pathogenesis: Spores multiply at the site of introduction by thorn, splinter, or other plant material, causing a small nodule that ulcerates. *Spores carried by lymph flow repeat the process along the lymphatic vessel*. May spread beneath the skin, regardless of lymph vessels. Fungal disease which moves up the lymph system and progresses along the arm/extremity.

Epidemiology: Distributed worldwide in tropical and temperate climates, Occupational risk for plant workers.

Treatment: most cases can be treated with potassium chloride (VERY odd; usually used to euthanize animals or stop the heart). Generalized infections require specific antifungals.

*RARE*

Heliobacter pylori Gastritis
*BACTERIAL* UPPER DIGESTIVE
Causative agent: Heliobacter pylori (microaerophilic, sheathed); requires oxygen, but cannot stand full environmental areas of it; secretes a sheath to protect itSigns & Symptoms: sometimes asymptomatic; peptic ulcers can cause abdominal pain, tenderness, and bleeding; possibly stomach cancer, heart valve colonization/damage

Pathogenesis: produce urease (ammonia from urea lowers local pH), motile, and burrow in stomach lining mucous; produce CagA (type 3 secretion system) that can make cells pre-cancerous; immune damage can cause decreased local mucous production and ulceration. Once they get into blood, go right to aortic valve, colonize it, and destroy it.

Epidemiology: probably fecal-oral transmission (i.e: fecal-oral transmission); can get into blood when having teeth cleaned and they are knicked.

Treatment: no preventative; treatment with 2 antibiotics plus stomach acid inhibitor; immunocompromised take antibiotics prior to teeth cleanings in which they are highly susceptible

Mumps
*VIRAL* UPPER DIGESTIVE
Causative agent: Mumps virus (a paramyxovirus)Signs & Symptoms: fever, loss of appetite, headache; followed by the *painful swelling of the parotid (salivary) glands* (occasionally elsewhere). Stiff neck and headache can be a sign of additional viral meningitis. Swelling and muscle spasm may make it difficult to talk and chew

Pathogenesis: droplets of saliva in upper respiratory; then transported throughout the body via the bloodstream (meninges, ovaries, testicles, parotid glands)

Epidemiology: *mumps is human reservoir ONLY*; only one antigenic type, so immunity is lifelong. Incubation time is 15 to 21 days, where the virus may be transmitted for up to 7 days before symptoms occur.

Treatment: *no treatment.* A very effective attenuated vaccine is available. *Mumps is a good candidate for eradication.*

Mumps has the capability of becoming meningitis; more problematic for adults

Salmonella Gastroenteritis
*BACTERIAL* LOWER DIGESTIVE
Causative agent: Salmonella enterica (cousin of E. coli)Signs & Symptoms: Diarrhea, vomiting, headache, abdominal pain, fever (all universal)

Pathogenesis: induced uptake (type III secretory system) by epithelial cells between the small and large intestine; bacteria multiply in the phagosome and are discharged at the base of the cells; inflammatory response increases fluid secretion.

Epidemiology: ingestion of food contaminated by animal feces, especially poultry; poor meat preparation.

Treatment: treatment with antimicrobial medication is NOT advised. Prevention relies on adequate cooking and food handling practices.

Other: 1.4 million cases occur each year in the US, resulting in *400 deaths.* (usually the immunocompromised) Large outbreaks occasionally occur due to the use of commercially distributed foods. The Salmonella family are showing increased drug resistance. RARELY FATAL

Clostridium difficile- Associated Disease (C-diff)
*BACTERIAL* LOWER DIGESTIVE
Causative agent: Clostridium difficileSigns & Symptoms: variable; mild diarrhea to pseudomembranous colitis-a potentially fatal inflammation of the colon.

Pathogenesis: toxins disrupt host cellular transport, with lethal effect in intestinal epithelium; turn on all efflux pumps and the cells leak themselves to death.

Epidemiology: Primarily occurs in hospitalized patients on antibiotic therapy.

Treatment: when feasible, STOP ANTIBIOTIC THERAPY; otherwise, the antibiotics of last resort. *Fecal transplants have been found to be a very effective treatment to repopulate the colon (microflora repopulation)

Rotoviral Gastroenteritis
*VIRAL* LOWER DIGESTIVE-INTESTINAL TRACT
Causative agent: Rotovirus (a reovirus)Signs & Symptoms: vomiting, abdominal cramping, *diarrhea lasting 5 to 8 days.*

Pathogenesis: Infection produces epithelial cell death in the cells of the upper intestine and decreased production of digestive enzymes. Damaged lining fails to absorb fluids, leading to watery diarrhea. Also produces a toxin that increase fluid secretion.

Epidemiology: Fecal-oral; *represents 25% of traveler’s diarrhea.*

Treatment: no treatment; but IV replacement of fluids if often lifesaving.
Prevention: attenuated vaccine

Other: before the vaccine, there were 500,000 ER cases and over 55,000 admissions in the US per year. Worldwide, more than 500,000 children still die from rotovirus infection each year.

*LONGER AND LESS SEVERE WHEN COMPARED TO NOROVIRUS*

Noroviral Gastroenteritis
*VIRAL* LOWER DIGESTIVE-INTESTINAL TRACT
Causative agent: Norovirus (a calicivirus)Signs ; Symptoms: vomiting, abdominal cramps, *diarrhea lasting 12 to 16 hours*

Pathogenesis: Infection produces epithelial cell death in upper small intestine and decreased production of digestive enzymes. The damaged lining usually repairs itself within two weeks. *Immunity is short term, lasting only a few months.* Immune system will get involved, but a B-cell response will never occur

Epidemiology: Fecal-oral, vomit. Low infections dose (~10 viral particles), viruses are very stable and resist sanitization methods (handwashing does nothing but washes them off the surface of the skin). Common outbreaks in dorms and on cruise ships. *Represents 90% of all epidemic bouts or non-bacterial gastroenteritis around the world*

Treatment: none; NO VACCINE. Handwashing and disinfectants help to limit the spread.

*SHORT, SHARP, SEVERE, THEN SHORT RECOVERY WHEN COMPARED TO ROTOVIRUS*

Hepatitis (A, B ; C)

*VIRAL* LOWER DIGESTIVE-LIVER

*Hepatitis A*
Causative agent: Naked, single-stranded RNA picornavirus, HAV

Transmission: Fecal-oral; come in from Mexico on lettuce, strawberries, etc.

Incubation period:3-5 weeks (range, 2-7 weeks)

Prevention: *inactivated vaccine*; immune globulin

Other: Usually mild symptoms, but often prolonged; full recovery; no long term carriers; *combined Hep. A and Hep. B vaccine available*

*Hepatitis B*
Causative agent: Enveloped, double-stranded DNA hepadnavirus, HBV

Transmission: *Blood*, semen

Incubation period: 10-15 weeks (range 6-22 weeks)

Prevention: Subunit vaccine (get a vaccine, wait 3 months, get another, wait, get a titer); immune globulin

Other: Acute symptoms often more severe than Hep. A; chronic disease can lead to cirrhosis and cancer; chronic carriers; can cross the placenta; *combined Hep.A and Hep.B vaccine available*

*Hepatitis C*
Causative agent: Enveloped. single-stranded RNA flavivirus, HCV

Transmission: Blood, possibly semen

Incubation period: 6-7 weeks (range 2-24 weeks)

Prevention: *NO VACCINE*; Nothing you can do, eventually terminal

Other: Usually few or no symptoms; progressive liver damage can lead to cirrhosis and cancer; chronic carriers

*HEPATITIS IS GROUPED BY AFFECT*

Giardiasis
*PROTOZOAN* LOWER DIGESTIVE
Causative agent: Giardia lamblia (a pear-shaped protozoan with 2 nuclei; fluorescent); aggressive swimmersSigns ; Symptoms: *Mild*: indigestion, flatulence, nausea; *Severe*: vomiting, diarrhea, abdominal cramps, weight loss

Pathogenesis: ingested cysts survive stomach acid and become active in the small intestine; some attach to epithelium and others move freely; mucosal function is impaired and creates a host immune response. Like a bacterial endospore, but wrap themselves like a fungal endospore, resisting stomach acid and other fluids.

Treatment: several antibiotics. *Prevention*:boiling, filtering, or disinfecting drinking water.

Other: *This is the most commonly identified waterborne illness in the US, and is responsible for many cases of traveler’s diarrhea.* A single human stool can contain 300 million Giardia cysts. Can be infected from just ONE cyst.

*”DON’T DRINK THE WATER” BUG*

Bacterial Vaginosis
*BACTERIAL* GENITAL SYSTEM DISEASE
Causative agent: UnknownSigns & Symptoms: *Gray-white vaginal discharge and unpleasant fishy odor*

Pathogenesis: Uncertain. Marked change in normal microbiota composition. Increased sloughing of vaginal epithelium in the absence of inflammation. Odor due to metabolic products of anaerobic bacteria. May cause complications of pregnancy, including premature births.

Epidemiology: Associated with many sexual partners or a new partner, but can occur in the absence of sexual intercourse. *No evidence that it is a sexually transmitted infection*

Treatment and Prevention: Treatment with metronidazole is effective; no proven preventative measures

*2 TYPES OF VAGINOSIS; THIS IS THE FIRST TYPE*

Vulvovaginal candidiasis (VVC)
*FUNGAL* GENITAL SYSTEM DISEASE
Causative agent: Candida albicans (yeast)Signs & Symptoms: Itching, burning, *thick, white vaginal discharge*, redness and swelling

Pathogenesis: Inflammatory response to overgrowth of the yeast, which is normal microflora (imbalance issue); genetic components as well.

Epidemiology: *NOT CONTAGIOUS*. Usually not sexually transmitted. Associated with antibacterial therapy, use of oral contraceptives, pregnancy, uncontrollable diabetes, but mostly unknown factors.

Treatment: Intravaginal anti-fungal medications are usually effective. No proven preventative measures.

Staphylococcal toxic shock
*BACTERIAL* GENITAL SYSTEM DISEASE
Causative agent: Staphylococcus aureus (TSST-1-toxin producing strains)Signs & Symptoms: fever, vomiting, muscle aches, low BP, and a rash that peels.

Pathogenesis: 3-5 days after S. aureus infection with the TSST-1 toxin; TSST-1 is a superantigen causing cytokine release and drop in BP. *The disease can be fatal within a few hours; HAPPENS VERY FAST AND IS VERY DANGEROUS.*

Epidemiology: associated with certain high absorbency tampons, leaving tampons in place for long periods of time, and the abrasion of the vagina from tampon use. Occasionally, SA infection from other locations. Use of intravaginal contraceptive sponges also increases risk. Currently, 6 or fewer cases per 100,000 in the US (a significant decrease).

Treatment: Hospitalization; antimicrobial treatment against S. aureus; IV fluids. Awareness of symptoms. Prompt treatment of S. aureus infections; frequent change of tampon by menstruating women.

**Toxic shock syndrome is a collapse of BP due to a circulating toxin such as one of the superantigens produced by S. aureus or S. pyogenes**

Gonorrhea
*BACTERIAL* STI
Causative agent: Neisseria gonorrhoeae (tough to culture/study)Signs & Symptoms: *Men*: painful urination, discharge; complications include urinary flow, sterility, and arthritis. *Women*: pain on urination, discharge, fever, pelvic pain, sterility, ectopic pregnancy, arthritis. *Men(20%) and women(60%) can be asymptomatic (carriers for months to years).*

Pathogenesis: organisms attach to certain non-ciliated epithelial cells by pili; phase and antigenic variation help it to attach to different cells and evade the immune system. Inflammation, scarring, can be spread by bloodstream. Scarring of fallopian tubes.

Epidemiology: transmitted by sexual contact-throat, genital, and anal. Asymptomatic carriers. *NO IMMUNITY*. Oral contraceptive can increase chance of infection due to biological effects (can produce wetter/dryer surfaces that can perturb normal microflora)

Treatment: ceftriaxone (the cephalosporins). *Prevention*: abstinence, monogamous relationships, condoms, early treatment of sexual contacts.

Chlamydia
*BACTERIAL* MAJOR STI
Causative agent: Chlamydia trachomatsis (obligate intracellular bacterium, certain serotypes)Signs & Symptoms: *Men*: thin, grey-white penile discharge, painful testes. *Women*: vaginal discharge, vaginal bleeding, lower or upper abdominal pain.

Pathogenesis: attaches to epithelial cells as an elementary body, produces reticulate body after endocytosis, replicates elementary bodies in the phagosome until the cell bursts. Release of cytokines results in inflammatory response; cell-mediated immune response can produce extensive damage; scar tissue can form, in women producing ectopic pregnancy and infertility.
=it gets in there, phagocytes come, inflammatory issues, cytokines released, and scarred tissue results in overall infertility.

Epidemiology: *The leading reportable bacterial infection in the US.* Large numbers of asymptomatic carriers of both genders. Asexual transmission via non-chlorinated swimming pools.

Treatment: Antibacterials. *Prevention*: abstinence, monogamous relationships, condoms. Test sexually active people yearly to reduce carriers.

Syphillis
*BACTERIAL* STI
Causative agent: Treponema pallidumSigns & Symptoms: Painless red chancre at site of infection (primary), fever, rash, stroke; nervous system deterioration; can imitate other disease (aka “The Great Imitator”). Incubation 10-90 days. Once it has proceeded to secondary (mouth lesions) and tertiary (gumma) stage, it is swimming around the body and destroying everything.

Pathogenesis: primary lesion (site of infection) heals after 2-6 weeks; T. palladium is spread via blood throughout the body, causing fever, rash, mucous membrane lesions; damage to the brain, arteries, and peripheral nerve appears years later.

Epidemiology: Sexual contact with infected partner; kissing; transplacental passage. *From 1900-1950, syphilis was a major source of mental illness and blindness, and a significant cause of heart disease and stroke.

Treatment: Penicillin. *Prevention:* abstinence, monogamy, condoms, safer sex practices, treatment of sexual contacts, reporting of cases.

Syphilis goes through several phases and can be hard to diagnose; can be passed on from parents to fetus, resulting in Hutchinson teeth later on in the person who was born with syphilis (deformed incisors)

Genital Herpes
*VIRAL* STI
Causative agent: Usually herpes simplex virus type 2 (type 1 is cold sores, but the two are close cousins); herpes simplex 1 can also be responsible. Herpes viruses are enveloped and contain double stranded DNA. 1 week incubation periodSigns & Symptoms: Itching, burning pain at the site of infection, painful urination, tiny blisters with underlying redness (look like cold sores in the wrong spot). The blisters break, leaving a painful superficial ulcer, which heals without scarring. Recurrences are common.

Pathogenesis: Lysis of infected epithelial cells results in fluid-filled blisters containing infectious virions. Vesicles burst, causing a painful ulcer. The acute infection is controlled by immune defenses; genome persists within nerve cells in a non-infectious form beyond the reach of immune diseases. Replication of infectious virions can occur and cause recurrent symptoms in the area supplied by the nerve. Newborn babies can contract fatal generalized herpes infection if their mother has a primary infection at the time of delivery.

Epidemiology: *NO ANIMAL RESERVOIRS; HUMANS ONLY* Transmission by sexual intercourse, oral-genital contact. Transmission risk greatest first few days of active disease. Transmission can occur in the absence of symptoms. Herpes simplex increases the risk of contracting HIV.

Treatment and Prevention: No cure. Medications help prevent recurrences, shorten duration of symptoms. *Prevention*: abstinence, monogamy, and correct use of condoms help to prevent transmission.

Genital warts/HPV
*VIRAL* STI
Causative agent: Human papillomavirusSigns & Symptoms: *often asymptomatic. Warts (papillomas) of the external and internal genitalia are the most common symptom.* Symptoms are strain specific (there are 27 different types of HPV)

Pathogenesis: Virus enters via abrasion, infects deep epithelium; establishes latency; cycles of replication occur when the host cells begins maturation; cancer-related strains can insert into the host cell chromosomes and produce pre-cancerous lesions. Can hop around like transposons and mutate multiple cells/genes.

Epidemiology: Asymptomatic individuals can transmit the disease; multiple sex partners are the greatest risk factor; warts can be transmitted to the mouth with oral sex and to babies at birth. *40 million American (1 in 10)*

Treatment: Wart removal by multiple techniques (i.e: liquid nitrogen), but does NOT cure the infection. *Prevention*: avoid risky partners. Pap smears yearly for sexually active women. Vaccines are effective against some strains.

HIV
*VIRAL* STI
Causative agent: Human Immunodeficiency Virus type-1 (HIV-1)Signs & Symptoms: *No symptoms, or flu-like symptoms early in the illness.* An asymptomatic period typically lasting years. Symptoms of lung, intestine, skin, eyes, brain, and other infections, and certain cancers follow.

Pathogenesis: Infects specific lymphocytes and macrophages, thereby destroying the ability of the immune system to fight infections and cancers (low amount of T cells)

Epidemiology: HIV is present in blood, semen, and vaginal secretions in symptomatic and asymptomatic infections; spread by sexual intercourse, sharing of needles by injected drug-abusers, and from mother to infant at birth. Other STIs can foster infection.

Treatment: reverse transcriptase inhibitors and protease inhibitors in combination (HAART). *Prevention*: abstinence, no drug abuse, monogamy, consistent use of condoms; avoidance of sexual contact with high-risk or infected individuals. Anti-HIV meds for pregnant women and newborns. Circumcision and pre-expose prophylaxis.

Trichimoniasis (“trich)
*PROTOZOAL* STI
Causative agent: Trichomonas vaginalis (have spikes on front that beat their way into cells and eat; how they get in. Looks like fluorescent paint.)Signs ; Symptoms: *Women*: itching, burning, swelling, vaginal redness; frothy, sometimes malodorous, *yellow-green discharge* and burning on urination. *Men*: discharge from penis, burning on urination, painful testes, tender prostate. *Many women and men are asymptomatic*

Pathogenesis: Unexplained. Inflammatory changes and pinpoint hemorrhages suggest mechanical trauma from the motile organisms.

Epidemiology: Worldwide distribution; asymptomatic carriers foster spreading; killed easily by drying due to lack of cyst form, transmission by intimate contact; high rate of infection with multiple sex partners. Newborns can acquire the infection at birth.

Treatment: metronidazole. *Prevention*: abstinence, monogamy, and consistent use of condoms.

Listeriosis
*BACTERIAL* NERVOUS SYSTEM
Causative agent: Listeria monocytogenesSigns ; Symptoms: fever and muscle aches, with or without gastrointestinal symptoms; *headache and stuff neck mark the onset of meningitis* One of the causes of meningitis (there are multiple; see Table 26.2)

Pathogenesis: ingested bacteria (from food such as soft cheeses, non-pasteurized milk, hot dogs, or smoked fish) penetrate the intestinal epithelium and enter the bloodstream; the bacteria then spread to the meninges.

Epidemiology: Epidemics from contaminated food sources. Pregnant women get bacteremia, fetal infection, miscarriage, infants contract at birth and develop meningitis within a month.

Treatment: Antibiotics. Care in the handling and cooking of raw meats; thorough washing of vegetables; reheating of cold cuts, hot dogs, and refrigerated leftovers. Use of ListShield in commercially sold meat products, in which viruses which only hurt Listeria monocytogenes are placed into products that it most inhabits.

Hansen’s Disease (aka leprosy)
*BACTERIAL* NERVOUS SYSTEM
Causative agent: Mycobacterium lepraeSigns & Symptoms: skin lesions that lack sensation; deformed face; loss of fingers and toes.

Pathogenesis: invasion of the small nerves of the skin; multiplication in macrophages; course of disease depends on the immune response of the host; activated macrophages limit growth of bacteria; attack of immune cells against the infected nerve produces nerve damage, leading to deformity; in lepromatous leprosy, lymphocytes fail to react to the bacteria allowing the bacteria to replicate unchecked. Mycobacterium leprae prefer a temp. of 30 degrees Celsius, not 37 degrees Celsius like most other bacteria, making them not adaptive to humans; because they like it cooler, they grow better in cooler areas of the body such as the nose, fingers, and toes. Cleared areas on the skin is a result of the activation of the immune system; if lymphocytes cannot respond, the bacteria will begin degrading flesh and bones, resulting in a loss of fingers and toes.

Epidemiology: direct contact with M. leprae from mucous membrane secretions

Treatment: Specific antibiotics for months or years; another added for lepromatous disease. *NO VACCINE*

Botulism
*BACTERIAL* NERVOUS SYSTEM
Causative agent: Clostridium botulinum, an anaerobic, Gram-positive, spore-forming, rod-shaoed bacterium. *STRICTLY ANAEROBIC*Signs & Symptoms: Blurred or double vision, weakness, nausea, vomiting, diarrhea; generalized paralysis and respiratory insufficiency. 12-36 hour incubation period.

Pathogenesis: C. botulinum endospores germinate in food and release neurotoxin. Toxin is ingested, absorbed, and is carried by the bloodstream to motor nerves; toxin acts by blocking the transmission of nerve signals to the muscles, producing paralysis; C. botulinum can also colonize intestines and cause generalized weakness or paralysis. Can infect host via improperly canned food; very hard to kill and is the result of a swelled can. Likes sugar, acid, and is HEAT RESISTANT.

Epidemiology: Ingestion of toxin produced by vegetative C. botulinum cells growing in a food, *often an improperly processed home-canned, low-acid food.* Endospores widespread in soil, aquatic sediments, and dust. Organisms can colonize the intestines of adults and infants with deficiencies in normal microbiota, and wounds containing dirt and dead tissue, including those caused by injected drug-abuse.

Treatment & Prevention: *Treatment:* Enemas and stomach washing to remove toxin, cleaning infected wounds of dirt and dead tissue, IV administration of antitoxin, and artificial respiration (bacteria destroy the nerves which control the lungs). Education in proper home-canning methods; heating food to boiling for 15 minutes just prior to serving.

**Injected into face to purposely damage nerves (Botox)
= kills nerves of forehead to make muscles relax to prevent wrinkles; however, the bacteria circulates in the bloodstream and is a very potent neurotoxin. VERY DANGEROUS!

Viral meningitis
*VIRAL* NERVOUS SYSTEM
Causative agent: usually Enterovirus (cocksackie or echovirus; can be mumps virus, if unvaccinated)Signs & Symptoms: abrupt onset, fever, severe headache, stiff neck, often vomiting; sometimes sore throat, large parotid glands, rash, or chest pain. Milder than bacterial version, recovery in 7-10 days. *Fever is the distinction; picked up right away as opposed to the bacterial meningitis.* Lumbar puncture will make the CSF cloudy with bacteria, but clear with viruses (viruses do not eat sugar, so glucose level will be normal; glucose is the primary food for bacteria, so glucose levels will be low with bacterial meningitis). Mumps in fall and winter; Enteroviruses in spring/summer (resistant to chlorine)

Pathogenesis: Viremia from primary infection spreads to meninges. Fewer leukocytes enter CSF than with bacterial infections, and many are mononuclear, usually no decrease in CSF glucose.

Epidemiology: fecal-oral transmission of Enteroviruses, mumps via respiratory secretions and saliva. Enteroviruses mainly in summer and early fall; mumps in fall and winter.

Treatment: No specific treatment. Handwashing, avoiding crowded swimming pools during enterovirus epidemics; mumps vaccine (mumps leads to meningitis)

epidemic viral encephalitis
*VIRAL* NERVOUS SYSTEM
Causative agent: LaCrosse/St.Louis/West Nile encephalitis virus, Eastern and Western equine encephalitis virus (all zoonotic *arboviruses*)
*ALL CARRIED BY MOSQUITOES*Signs & Symptoms: Abrupt onset, fever, headache, vomiting, disorientation, paralysis, seizures, deafness, coma *lack of stiff neck is the distinguishing factor from meningitis*

Pathogenesis: replication at the site of the mosquito bite, replication in the lymph nodes, then viral invasion of brain tissue. Nerve cells in the brain destroyed. Process halted by neutralizing antibody.

Epidemiology: Viruses transmitted to humans from birds or rodents via mosquitoes.

Treatment: No accepted treatment for arborviruses. Chicken sentinels to warn of arbovirus epidemics. Insecticides and other anti-mosquito preventative measures.

Poliomyelitis (Table 26.9)
*VIRAL* NERVOUS SYSTEM
Causative agent: Polioviruses 1,2,3; members of the picornavirus familySigns & Symptoms: Headache, fever, stiff neck, nausea, pain, muscle spasm, *followed by paralysis.* (muscle spasm and paralysis are hallmarks)

Pathogenesis: Virus infects the throat and intestine, circulates via the bloodstream, and enters some motor nerve cells of the brain or spinal cord; infected nerve cells lyse upon release of mature virus. Lytic virus that produces toxins.

Epidemiology: Spreads by the fecal-oral route,; asymptomatic and non-paralytic cases common.

Treatment & Prevention: *Treatment:* artificial ventilation for respiratory paralysis (“iron lung”); physical therapy and rehabilitation. Prevented by injecting Salk’s inactivated vaccine or by Sabin’s orally administered attenuated vaccine in areas of epidemic or endemic disease. Polio vaccine is given to kids before starting school.

POLIO IS A HUMANS ONLY DISEASE

Rabes
*VIRAL* NERVOUS SYSTEM
Causative agent: Rabes virusSigns & Symptoms: fever, headache, nausea, vomiting, sore throat, cough at onset; later, *spasms of the muscles of the mouth and throat, coma, and death* (HALLMARKS) Similar to meningitis, but no stiff neck.

Pathogenesis: Virus multiplies at the site of the bite, then travels to the CNS; multiplies and spreads outward via multiple nerves to infect the heart and other organs.

Epidemiology: *Bite of a rapid animal, usually a bat.* Inhalation is another possible mode (inhaling dried bat feces). Once it gets hold, it is fatal.

Treatment: *effective post-exposure measures:* immediately wash wound and apply antiseptic; inject rabies vaccine and human rabies antiserum as soon as possible. No effective treatment once symptoms begin. Avoid suspect animals; immunize pets (lower population of potential contact).

SKUNKS ARE A MAIN RESERVOIR FOR RABIES

Cryptococcal meningoencephalitis (fungal)
*FUNGAL* NERVOUS SYSTEM
Causative agent: Cryptococcus neoformans and C. gattiiSigns & Symptoms: headache, vomiting, confusion, and weight loss; slight to no fever; symptoms may progress to seizures, paralysis, coma, and death. Not real quick; usually appears in the immunocompromised; often an onset of AIDS.

Pathogenesis: infection starts in lung; encapsulated organisms multiply, enter bloodstream, and are carried to various parts of the body; phagocytosis is inhibited; *meninges and adjacent brain tissue becomes infected.*

Epidemiology: Inhalation of material contaminated with the fungus; other sources; most people resistant to the disease (if you have a healthy immune system, this never takes hold).

Treatment: Antifungals. No preventative measures.

Other: It is the defining infection of AIDS

African sleeping sickness
*PROTOZOAL* NERVOUS SYSTEM
Causative agent: Trypanosoma bruceiSigns & Symptoms: tender nodule at the site of the *tsetse fly bite*; fever, enlargement of lymph nodes; later, involvement of the CNS, *uncontrollable sleepiness* (HALLMARK), headache, poor concentration, unsteadiness, coma, death.

Pathogenesis: Multiplication at the bite site, then enter the blood and lymphatic circulation; as new cycles of parasites are released, their surface protein changes, requiring new types of antibodies to be made. Very clever in that they modify their surface proteins, and the body has trouble adapting to them.

Treatment: suramin; when CNS is involved, other drugs are added. Protective clothing, insecticides, clearing of brush where flies breed.

ONLY OCCURS IN ZONES WHERE THE TSETSE FLY IS PRESENT; ZOONOTIC

Transmissible spongiform encephalopathy (CID- Creutzfeld-Jacob Disease)
*DISEASE CAUSED BY PRIONS* NERVOUS SYSTEM
Causative agent: PrionsSigns & Symptoms: *usually in over 45 year old men;* behavioral changes, anxiety, insomnia, fatigue, progressing over weeks or months to muscle jerks, lack of coordination, dementia.

Pathogenesis: Prions increase in quantity by converting normal protein to more prion; transmission to the brain; aggregations into masses outside nerve cells; cell malfunction and death (similar to Alzeihmer’s/Parkinson’s)

Epidemiology: Human-to-human transmission by corneal transplant and by contaminated surgical implements; probably transmission of cattle prions to humans by eating contaminated beef; sporadic CJD in those over 45 years; media age of variant CJD only 28 years. *Only 0.5 to 1 case per million humans.* VERY RARE

Treatment: No treatment, invariably fatal. Prions are inactivated by autoclaving in concentrated sodium hydroxide.

Subacute bacterial endocarditis (SBE)
*BACTERIAL* BLOOD VASCULAR SYSTEM
Causative agent: Skin or mouth normal microflora (enter during a dental procedure)Signs & Symptoms: fever, loss of energy over a period of weeks or months; sometimes a stroke.

Pathogenesis: Normal microbiota enter through dental procedures or another trauma; in an abnormal heart, turbulent blood flow causes formation of a thin clot that traps circulating organisms; a biolfilm forms, protecting the bacteria from phagocytes; pieces of the clot break off and block important vessels, leading to tissue death. High levels of antibodies to bacteria found in blood; immune complexes can cause other problems, like glomerulonephritis. Not as bad, do not affect heart valves (slow growth)

Epidemiology: Risk factors are congenital heart defects, or in hearts previously damaged by rheumatic fever; may develop after dental procedures, or other situations that can produce bacteremia (large accidents).

Treatment: Bactericidal antibiotics given in pairs. *Prevention:* giving an antibiotic immediately before anticipated bacteremia (i.e: before dental work)

Tularemia
*BACTERIAL* LYMPH NODES AND SPLEEN
Causative agent: Francisella tularensisSigns & Symptoms: *Ulcer at site of entry*, enlarged lymph nodes in area, fever, chills, achiness.

Pathogenesis: Organisms are ingested by phagocytes, grow within these cells, and then spread throughout the body. Usually on hands when skinning animals; infects lungs when inhaled. VERY FATAL.

Epidemiology: Present in wildlife throughout the US. *Risk mainly to hunters and other that handle wildlife.* Acquired when the organism enters a mucous membrane or enters broken skin, as may occur when skinning rabbits, for example; bite or infected insect or tick bite.

Treatment: Antibiotics. *Prevention:* avoid insects; wear rubber gloves when skinning rabbits; cook wild meat thoroughly; taking safety precautions in lab.

Other: Tularemia is a Class A bioterrorism agent, though non-communicable.

Plague
*BACTERIAL* LYMPH NODES AND SPLEEN
Causative agent: Yersinia pestisSigns & Symptoms: Sudden onset of high fever, large lymph nodes called buboes, skin hemorrhages; sometimes blood sputum

Pathogenesis: Enters by bite of infected fleas. Bacteria is engulfed by macrophages. The intracellular environment causes them to transform into encapsulated organisms capable of producing multiple virulence factors that allow the attachment to host cells, and provide defense form the immune system. Get inside, transform a little bit, and spread around.

Epidemiology: endemic in rodents and other wild animals, and their fleas, particularly in the western US. *The plague is transmitted by fleas;* the pneumonic plague can be transmitted person-to-person in respiratory droplets. *Pneumonic plague is the most dangerous because Y. pests is fully virulent at the time of transmission.* A small percentage of the time, this can start infecting/multiplying in the lungs and can begin spreading through coughing.

Treatment: Prompt diagnosis; antibacterial treatment necessary to prevent high mortality. *Prevention:* no vaccine, though 2 in evaluation. Rodent control!

Infectious mononucleosis (“mono”; “the kissing disease”)
*VIRAL* LYMPHATIC AND BLOOD VASCULAR SYSTEMS
Causative agent: Epstein-Barr virus (EBV)Signs & Symptoms: *fatigue*, fever, sore throat, and enlarged lymph nodes.

Pathogenesis: Productive infection of epithelial cells of throat and salivary ducts (reason for lymph node swelling); latent infection of B-lymphocytes; hemorrhage from enlarged spleen is rare but can be a serious complication.

Epidemiology: Spread by saliva (“kissing disease”); lifelong recurrent shedding of virus into saliva of asymptomatic latently infected individuals. Usually the shedding is never enough to pass it on, but sometimes you can; if it is not active, it does nothing.

Treatment: Antivirals like acyclovir inhibit productive infection by the virus and are helpful in serious cases; it has no activity against the latent infection. Cortisone-like medication can help in relieving airway obstruction from swollen tissue. *Prevention:* stop kissing, sharing anything that can share saliva (drinks). NO VACCINE.

VERY COMMON IN TEENS.

Yellow fever
*VIRAL* LYMPHATIC AND BLOOD VASCULAR SYSTEMS
Causative agent: Yellow fever virusSigns & Symptoms: *Often only a headache and fever.* Severe cases characterized by high fever, jaundice, black vomit, and hemorrhages into skin. Usually appears in 3-6 days from infection.

Pathogenesis: Virus multiplies at the site of the mosquito bite, spreads to the liver, and throughout the body to the bloodstream. Virus destroys liver cells, causing jaundice and decreased production of blood-clotting proteins. Hemorrhages and decreased strength of the heart result in circulatory failure and kidney failure.

Epidemiology: Reservoir in forest primates and their mosquitoes in Africa, Central and South America; human epidemics occur when the virus infects human household mosquitoes. Normally a tropical disease; not common in the US. Due to climate changes, cases have occurred in the Florida Keys.

Treatment: NONE. There is highly effective attenuated vaccine.

TRANSMITTED BY MOSQUITO!!

Dengue fever
*VIRAL* LYMPHATIC AND BLOOD VASCULAR SYSTEMS
Causative agent: Dengue virus (transmitted by mosquito)Signs & Symptoms: *Often asymptomatic* (this is in the initial infection; the real problems come in the secondary infection). Fever, headache, rash and severe joint pain. In dengue hemorrhagic fever (DHF) (bleeding from mucous membranes), bleeding and shock can occur, as well as disseminated intravascular coagulation (DIC).

Pathogenesis: Infect and distributed via macrophage. Infected macrophages produce pro-inflammatory cytokines, producing leaky blood vessels and hemorrhaging. *DHF is the result of a re-infection;* the second time, the macrophages die, producing massive blood clotting and DIC (CAN BE FATAL).

Epidemiology: Transmitted by the *Aedes* mosquito. Primarily exists in tropical and subtropical regions with high rainfall. Zone are increasing. DHF usually occurs in children under 15 years old.

Treatment: None, but symptomatic: analgesics, ORT (oral rehydration therapy), platelet transfusion of bleeding occurs. *Prevention:* mosquito control; vaccine development is underway.

PARTICULARLY DIC IS A PROBLEM IN CHILDREN.

Hemorrhagic fever
*VIRAL* LYMPHATIC AND BLOOD VASCULAR SYSTEMS
Causative agent: Ebola virus and Marburg virusSigns & Symptoms: rapid onset of fever (HOURS), headache, abdominal pain, joint and muscular pain, sore throat, rash, and bleeding. Later, leaky capillaries, bleeding from all mucous membranes, no clotting, bloody vomit and diarrhea; multi-organ failure or shock; DEATH. Inactivates the entire clotting system. For Ebola, this can happen in less than 3 days, from infection to death. Zoonotic; unsure of exact reservoir multiple animals?)

Pathogenesis: Contact with infected animals or people. HIGHLY INFECTIOUS. The worst; extremely rapid. Class A bioterror agent.

Epidemiology:*50%-80% death rate.* Social and economic conditions favor epidemic in these African countries. The reservoir is unknown, though may be fruit bats for Ebola.

Treatment: There is no standard treatment. Patients are kept hydrated, and blood and oxygen levels maintained. Plasma containing coagulation factors are given to control bleeding. Quick diagnosis and rapid responses by healthcare workers is essential; stringent use of protective gear and infection control measures.

Malaria
*PROTOZOAL* BLOOD AND LYMPHATIC INFECTIONS
Causative agents: Plasmodium (gets in and infects RBCs)Signs & Symptoms: recurrent cycles of violent chills and fever, alternating with feeling healthy.

Pathogenesis: Cell burst and release of protozoa causes fever; spleen enlarges in response to removing large amounts of foreign material and many abnormal blood cells from circulation; infected red blood cells stick to each other and to the walls of the capillaries; vessels block, depriving the tissue of oxygen.

Epidemiology: Transmitted from person to person by the bite of the *Anopheles mosquito.* Some individuals are genetically resistant to infection (those with sickle-cell anemia)

Treatment: usually ACTs; other medicines if sensitivities are known. *Prevention:* choloroquines; doxycyclines-whichever works for the infective strain. Other meds. for liver stage. Mosquito netting soaked in insecticides, vaccines in development.

ENDEMIC IN AFRICA; PREVENTS POPULATION FROM GETTING AHEAD.

HIV disease
*VIRAL*
Causative agent: Human Immunodeficiency Virus (HIV)Signs & Symptoms: Over 50% develop fever, sore throat, head and muscle aches, rash and enlarged lymph nodes early in infection. After an asymptomatic period, symptoms result from immunodeficiency and include unusual malignant tumors, pneumonia, meningoencephalitis, diarrhea, etc. (ARC symptoms; mark the onset of AIDS).

Pathogenesis: HIV infects various body cells, notably those of the immune system (CD4 + T-cells & antigen-presenting cells). T-cells are killed, with declining numbers until the immune system cannot resist normal issues. Nails the T-helper cells, causing the antibodies and Tc cells to go; no humoral/adaptive immune system.

Epidemiology: *Transmission routes:* sexual contact, transfer of blood or blood products, mother to child around childbirth. Can be transmitted via breast milk, and possibly oral-genital contact.

Treatment: HAART Therapy, which delays progression of the disease to AIDS. *HAARRT is NOT a cue and is too expensive for most of the world’s patients.* No vaccine yet available. Medications can prevent many of the infections that complicated HIV disease. Anti-HIV meds and C-sections can decrease mother-newborn transmission. *Prevention:* sex education, needle exchange, condoms.

SOME STDS ENHANCE HIV TRANSMISSION; predominantly found in heterosexuals, but percentage wise, is it said to be transferred most through homosexual men and the least through lesbians. Circumcision also reduces the potential for HIV significantly.

B lymphocyte tumors (lymphomas)
*COMPLICATIONS OF ACQUIRED IMMUNODEFICIENCIES* MALIGNANT TUMORS
Causative agent: Epstein-Barr virus (EBV)Signs ; Symptoms: Weight loss, fever, and night sweats.

Pathogenesis: HIV infection causes activation of latent EBV. B-ce;;s proliferate rapidly, mutate, producing enlarged lymph nodes, rapid spreading, and cancer. *Non-Hodgkins and cerebral lymphomas.* (both rare)

Epidemiology: In AIDS, the incidence of non-Hodgkin’s lymphoma, primary cerebral lymphoma and Hodgkin’s disease are all increased. There are three different varieties of AIDS-related lymphoma. *Lymphoma accompanies 3% of all HIV diagnoses.*

Treatment: Varies by type of lymphoma (3 types). *Prevention:* keeping viral load as low as possible over the long term.

Cervical and anal carcinoma
*COMPLICATION OF ACQUIRED IMMUNODEFICIENCY*
MALIGNANT TUMORS
Causative agent: Certain strains of HPV (warts)Signs ; Symptoms: *Anal:* bloating and change in bowel habits, a lump near the anus, rectal bleeding, itching or discharge. *Cervical:* usually asymptomatic, sometimes vaginal bleeding, contact bleeding, or a vaginal mass (RARE). Major reason why women need to go for pap smears (usually never have symptoms whatsoever).

Pathogenesis: Infection of tissue with certain types of HPV. Decreased immune clearance of abnormal or infected cells encourages progression to cancer.

Epidemiology: *Cervical cancer is the second most common and fifth deadliest cancer in women in the US.* Only 10% os anal cancer is metastatic or recurrent with proper treatment. Incidence spikes dramatically in combination with HIV disease.

Treatment: Various anti-cancer therapies. *Prevention:* vaccination, condoms.

Kaposi’s sarcoma
*VIRAL* COMPLICATIONS OF ACQUIRED IMMUNODEFICIENCIES; MALIGNANT TUMORS
Causative agent: Human herpes virus-8 (HHV-8 aka KSHV)Signs & Symptoms: Infection is usually asymptomatic. In immunocompromised, papular nodules appear that are red, brown, purple, or black in color, typically found in skin, but can develop in the mouth and respiratory and GI tracts.

Pathogenesis: Pathogenesis is complex, with viral infection being held in check in healthy individuals. *In immunocompromised:* infected blood or lymphatic vessel cells multiply rapidly and mutate, becoming cancerous. *KS cells have a characteristic spindle shape (HALLMARK)* Inflame the lining of the blood vessels and cause large lesions.

Epidemiology: Spread by saliva, widespread, emerges rarely in the elderly; 50% of the HIV infected develop KS after HHV-8 infection. *KS is 500 times more common in HIV patients then in transplant immunocompromised patients.*

Treatment: restoration of the immune system. Surgical removal of lesions is not recommended. Limit deep kissing, using commercial lubricant rather than saliva. Normally, the immune system keeps this in check, but it is common in the immunocompromised and the elderly of Middle-Eastern decent.

Pneumocystitis pneumonia (PCP)
*FUNGAL* COMPLICATIONS OF ACQUIRED IMMUNODEFICIENCY; INFECTIOUS DISEASES
Causative agent: Pneumocystitis jiroveci (fungus)Signs & Symptoms: Gradual onset, shortness of breath, rapid breathing, non-productive cough, slight or absent fever, dusky skin color. Typically manifests in low pulse ox. patients.

Pathogenesis: Can be a reactivated latent infection (by immunocompromised state or inhalation of new spores), or new infection. Spores are inhaled, attach to alveoli, and multiply. Alveoli fill with fluid, macrophages and fungus; the walls thicken, impairing oxygen transfer.

Epidemiology: Widespread in domestic and wild animals as latent lung infection. Reservoir there unknown. Most humans become infected in early childhood. Disease usually arises when immunocompromised; epidemics among nursing home elderly and hospitalized premature infants.

Treatment: *Formerly the leading cause of death in those with AIDS*; usually prevented by anti-fungal medication, started as soon as T-cell counts drop to 200 cells/microliter or less, and continues for life (or until HAART raises T-cell counts above 200).

Toxoplasmosis
*PROTOZOAL* COMPLICATION OF ACQUIRED IMMUNODEFICIENCIES; INFECTIOUS DISEASES
Causative agent: Toxoplasma gondii (protozoa)Signs & Symptoms: *Healthy:* sore throat, fever, enlarged lymph nodes, rash; *with fetal infections:* miscarriage, stillbirth, birth defects, epilepsy, intellectual disability, retinitis; *in immunocompromised:* confusion, poor coordination, weakness, paralysis, seizures and coma.

Pathogenesis: Organisms penetrate host cells causing necrosis, With the development of immunity, cell destruction stops, tissue cysts develop. Most healthy people have few to no symptoms unless the infective dose is very large, Organisms released from cysts when immunity is impaired.

Epidemiology: Occurs worldwide, less in cold and dry areas. Infection from ingesting oocysts from dried cat feces or eating poorly cooked meat.

Treatment: Antibiotics. *Prevention:* avoid listed sources of oocysts. *With HIV:* antibiotics pairs given when T-cell count drops below 100 cells per microliter and antibodies to T. gondii are present (blood test done to check for antibodies).

EASILY SPREAD; MOST CATS ARE NOW SCREENED FOR THIS

Cytomegalovirus disease
*VIRUS* COMPLICATION OF ACQUIRED IMMUNODEFICIENCIES; INFECTIOUS DISEASES
Causative agent: Cytomegalovirus (CMV) (herpes family)Signs & Symptoms: Symptoms are rare, but resemble infectious mononucleosis. Infection of the mother during pregnancy can result in fetal infection. *Immunocompromised:* blindness, lethargy, dementia, coma, and brain damage. (HALLMARK= blindness and dementia)

Pathogenesis: Many tissues susceptible to infection and damage, especially eyes, brain, and liver. Latent CMV can reactivate. CMV can reduce CD4 + T-cell counts, thus enhances the deleterious effects of HIV; reduces active T-cells that are left in a person infected with HIV.

Epidemiology: Common worldwide, lifelong infection. More than 50% of 18-25 years olds are infected. Congenitally infected infants can shed virus for months or years. Body fluids, including breast milk, blood, urine, semen and vaginal secretions can transmit the disease. Hard to avoid.

Treatment: Antivirals. NO VACCINE. *Prevention:* condoms, handwashing, testing blood and tissue transplants. CMV specific antivirals in HIV patients with T-cell count below 50 cells per microliter.

Mycobacterial (MAC) diseases
*BACTERIAL* COMPLICATION OF ACQUIRED IMMUNODEFICIENCIES; INFECTIOUS DISEASES
Causative agents: Mycobacterium species (leprae, TB, etc.)Signs & Symptoms: *Healthy:* asymptomatic. *Children:* chronic localized enlargement of lymph nodes. *Elderly:* chronic cough as tuberculosis. *Immunodeficient:* cough, fever, sweating, marked weight loss, abdominal pain, diarrhea. Very common symptoms; stains required.

Pathogenesis: Enter via lungs and GI tract and taken up by macrophages. *In immunocompromised:* most are destroyed and infection is controlled by cell-mediated immunity. In the severely immunocompromised, bacteria resist phagocytosis and get transported throughout the body before growing to enormous numbers in tissues because there is no inflammatory reaction. Hop on macrophages, get moved around through tissues and may or may not cause a problem.

Epidemiology: MAC organisms are widespread in food, water, and soil.

Treatment: Antibiotics. No proven prevention aside from prophylactic antibiotics.

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