Chapter 21: Microbial Diseases of the Skin

Staphylococcus species: Gram-positive cocci (clusters): opportunistic pathogens

• S. epidermidis (coagulase negative); nosocomial pathogen; possess slime layer

  • Can penetrate skin via catheter insertion

• S. Aureus (coagulase positive); possesses a number of virulence factors:

  • Toxins: anti-phagocytic

  • Resists opsonization

  • Neutralizes AMPS of host

  • Lysozyme resistant

  • Antibiotic resistant (MRSA,VRSA)

Staphylococcal Skin Infections

• Folliculitis - Infection of the hair follicles

• Sty - folliculitis of an eyelash

• Furuncle (boil) - abscess; pus surrounded by inflamed tissue

• Carbuncle - Inflammation of tissue under the skin

• Impetigo - crusting (nonbullous) sores, spread by autoinoculation

Scalded skin syndrome (bullous): form of impetigo due to toxins; causes separation of skin layers

Streptococcus species: Gram-positive cocci (in chains)

• Classified based on their hemolytic properties (via hemolysis)

• Culture Streptococci on blood agar

  • a-hemolysis: partial hemolysis (S. pneumoniae)

    • Green, partial hemolysis

    • → Viridans: S. mutans

      • → Dental caries plaque, biofilms, Endocarditis

    • → S. pneumoniae

      • → Pneumonia, Meningitis

  • b-hemolysis: complete hemolysis (GAS → S. pyogenes)

    • Clear complete hemolysis

    • → S. pyogenes

      • → Strep throat, Scarlet fever, necrotizing fascitis

  • y-hemolysis: no hemolysis (Enterococcus)

    • no hemolysis

    • Enterococcus species

      • → rarely harmful

Streptococcus pyogenes:

• best known for causing sore throats

Rheumatic fever → secondary immunological response (sequelae)

• M protein: body produces antibodies to M proteins; these cross-react with heart muscle proteins

Erysipelas - infects dermal layer of skin; toxins cause tissue destruction → can lead to sepsis

Necrotizing fasciitis (“flesh-eating” disease): deep tissue layers affected; toxins causes death of tissues, can affect muscles

Virulence factors:

• M protein: prevents complement activation; facilitates adherence

• Hyaluronic acid capsule: non-antigenic

• Produces streptokinase, hyaluronidase, streptolysin, exotoxin A (superantigen)

Chapter 22: Microbial Diseases of the Nervous System

Bacterial Meningitis - infection of the membrane surrounding the brain & spinal cord (meninges); cross the blood-brain barrier

• Initial symptoms of fever, headache, and stiff neck, followed by nausea and vomiting → may progress to convulsions and coma

• Diagnosis by Gram stain and agglutination test of CSF

Viral meningitis: more common; serious but rarely fatal

Viral Skin Disease: Chicken pox → Shingles

• Herpesvirus-varicella zoster; acquired via respiratory route and localizes in skin cells → forms vesicular rash, then pustules

  • Mild disease, very low mortality

  • Virus can remain latent within the body → enters peripheral nerves, moves to ganglia of CNA; viral DNA persists

• Reactivation of virus: new virions move down peripheral nerves to sensory nerves of skin → shingles

• Appears as a vesicular rash; severe burning/stinging; occasionally nerve damage occurs

• Prevention: live attenuated vaccine

• Acyclovir may lessen symptoms

Neisseria virulence factor → opa protein

Neisseria meningitidis (meningococcal meningitis)

• Caused by N. meningitidis; Gram-negative, aerobic diplococci with a capsule

• Possess number of virulence factors:

  • OPA protein → entry into cell

  • Endotoxin; capsule; pilli

  • Phase variation

• 40% of people are healthy nasopharyngeal carriers

• Begins as throat infection, rash leading to bacteremia → crosses blood-brain barrier into cerebrospinal fluid

• Death can occur a few hours after onset of fever; require antibiotic therapy

• Various capsule serotypes: A, B, C, X, Y, W-135; vaccination (A,C,Y, W-135 capsule) recommended for college students

Clostridium species; Gram-positive endospore formers

• C. botulinum (“Botox”)

Anaerobe, grows in canned food releasing toxin; spores survive unless autoclaved

Toxins interferes with neural transmission by blocking release of acetylcholine

• Causes flaccid paralysis

Clostridium toxins:

• C. tetani: tetanus toxin (tetanospasmin)

Anaerobe, grows in puncture wound; blood flow interrupted; tissue becomes anaerobic

Toxins block release of GAB, inhibitory transmitter.

• Causes nerve impulses to go unchecked; spastic paralysis via excessive nerve signaling

• Both botulism & tetanus toxins have 30-40% identity, similar modes of action. Each are A-B type toxins

Listeriosis → foodborne illness

• Ingestion of contaminated food → milk, dairy foods, processed meats (deli meats, hot dogs), smoked seafood, raw vegetables

• Characterized by flu-like symptoms & GI symptoms

  • For most: asymptomatic or a mild illness

  • Serious form: septicemia → meningitis, meningoencephalitis; >24% mortality

• Illness primarily among pregnant women, infants, elderly, immunocompromised persons

Etiologic agent → Listeria monocytogenes

• Small, gram-positive rods

• Widely distributed in soil/water

• In mammals, birds, fish, insects

Listeria monocytogenes → pathogenesis/virulence factors

• Adherence: D-galactose on surface binds host cell receptors

• Produce Invasins: allows for penetration of host cells → induces phagocytosis

  • Infect epithelial cells of GI; multiplies intra- and extracellularly

  • Host defense → primarily T cells (Tc) Interferon

• Polymerization of host cell actin → form “actin rockets”; propels cells into, within, and between host cells

• Produce

  • Hemolysins

  • Phospholipase C

  • Protease

• Growth at low temperature

• Non invasive/invasive listeriosis

• Pregnant women: cross placenta; can lead to stillborn, aborted, or acutely ill infant

• Prevention: effective sanitation of food contact surfaces; refrigerate foods <4ºC

Rabies

• Caused by the rabies virus (ss RNA); transmitted by animal bite; typically leads to fatal encephalitis

• Virus multiplies in skeletal muscles and then brain cells, causing encephalitis

• Initial symptoms may include muscle spasms of the mouth and pharync and hydrophobia

Furious rabies - animals are restless, then highly excitable

Paralytic rabies - animals seem unaware of surroundings

• Once in peripheral nerves, the virus is inaccessible to the immune system until CNS neurons destroyed

• Once symptoms appear, the disease is usually fatal

• Diagnosis: detect viral antigen via fluorescent antibody test

Negri bodies - viral inclusions present in affected nerve cells

Pre-exposure prophylaxis - injection of human diploid cells vaccine (HDCV)

Post exposure treatment - vaccine plus rabies immune globulin (RIG)

Chapter 23: Microbial Diseases of the Cardiovascular System

Many pathogenic bacteria produce septicemia and disseminate throughout the body (sepsis/septic shock)

Plague - caused by bacterium Yersinia pestis

• Bite of flea introduces organism; moves to lymph nodes

  • bubonic plague - form “bubbles” - enlarged nodes

• Then moves to blood stream = septicemic plague

• In the lungs = pneumonic plague → highly infectious, passed by airborne droplets

• A number of virulence factors inhibits phagocytes

• Plague is endemic in western U.S.; normally transmitted from animal to animal (rats, prairie dogs) by bite of infected fleas

Chapter 24: Microbial Disease of the Respiratory System

Respiratory tract infections are common and most are of viral origin

Bacteria can be the primary cause of respiratory infections or follow a viral infection (i.e., a secondary infection)

Upper Respiratory Tract Infections

• Streptococcal pharyngitis (strep throat; B-hemolytic strep → S. pyogenes)

  • Resistant to phagocytosis; streptokinases lyse clots; streptolysins are cytotoxic

• Scarlet fever

  • Erythrogenic toxins produced by lysogenized S. Pyogenes

  • Causes pinkish-red skin & fever

• Diphtheria

  • Corynebacterium diphtheriae: aerobic, Gram-positive rod; exhibits pleomorphic morphology

Diphtheria

• 1835: leading infectious killer of children in U.S.

• Disease begins with a sore throat & fever; spread by droplet transmission

• Tough, grayish membrane forms in the throat; can restrict airflow

  • grayish membrane → pseudomembrane

• Toxin producer: toxin circulates in the bloodstream; interferes with protein synthesis

• Immunization (DTaP vaccine) has limited reported diphtheria cases to <5/year

• Cutaneous diphtheria

Lower Respiratory Tract Infections

Pertussis (whooping cough)

• Bordetella pertussis: aerobic, Gram-negative coccobacillus

  • Inhibits the mucociliary escalator by binding to lung ciliated cells in the trachea, then progressively destroying them

  • Virulence factors: capsule, toxins

  • Tracheal cytotoxin: damages ciliated cells

  • Pertussis Toxin: enters blood, results in systemic symptoms of disease

  • Catarrhal stage: resembles common cold

  • Paroxysmal stage: violent coughing; gasping for air; 1-6 weeks

  • Convalescence stage: months

  • DTP to DTaP (cell-free) vaccine

  • 2012 epidemic

Pneumonia - a disease, not a specific infection, caused by many types of microbes

• Streptococcus pneumonia (a-hemolytic)

  • Typically a secondary infection

  • Spread by airborne droplets

  • Has capsule that prevents phagocytosis

  • In lungs, proliferates in alveolar spaces & potentially the bronchi; fluid build-up occurs

  • Pneumococcal polysaccharide vaccine (PPV)

  • Can spread to bloodstream & brain (meningitis)

• Legionella pneumophila

  • Legionnaires disease - form of atypical pneumonia

  • Gram-negative, non-encapsulated, aerobic bacillus with a single, polar flagellum

  • Found in freshwater; a facultative intracellular parasite → invades and replicate inside amoebae in the environment

  • In human, L. pneumophila invades and replicates inside macrophages via invasins

  • Human infection: inhalation of aerosols provided by cooling towers, air conditioners, hot tubs

Legionnaires disease

• Signs and symptoms: 2-10 days after exposure → cough, shortness of breath, high fever, muscle pains, headaches; may have nausea & vomiting

• Legionnaires accounts for 2-9% of pneumonia cases that occur each year

• 10% of those who are infected die

• Diagnosis: good maintenance of water systems

• Treatment: with antibiotics

• History: outbreak at 1967 American Legion convention in Philadelphia

• 182 of 2000 attendees contracted the disease and 29 died

• Traced to the cooling tower of the hotel’s air conditioning system; Bellevue-Stratford Hotel

Chapter 25: Microbial Diseases of the Digestive System

Streptococcus mutans (a-hemolytic): primary agent in initiating dental caries

S. mutans metabolize wide variety of sugars; tolerates acidity, synthesizes dextran → biofilm & plaque formation

Gastrointestinal Tract Infections

• Inflammation of GI tract due to viral or bacterial growth, and/or toxin production; results in loss of water & electrolytes

• Most gastroenteritis is caused by viruses

  • Retroviruses (dsRNA virus); highly infectious; can cause lethal dehydration

• bacterial (Gram-negatives):

  • types that invade cells of epithelial mucosa (Invasive)

    • Shigella dysenteriae: enterotoxin producer

    • E. coli (EIEC) (enteroinvasive): Shiga toxin via phage

    • Salmonella enterica (salmonellosis): non-toxin producer

  • Types that remain outside epithelial cells (Non-invasive)

    • E. Coli (EHEC(O157:H7); enterohemorrhagic: O157=LPS serotype; H7 = flagella serotype; produce Shiga toxin

Shiga toxin - blocks host protein synthesis, damages endothelial causing capillary damage, loss of blood, clots

Staphylococcus aureus - secrete enterotoxins into prepared foods

• Protozoal infections causing gastroenteritis

  • Giardia lamblia - enters host as a cyst from contaminated drinking water; also found in rodents & pets

    • Cyst dissolved by acid pH; trophozoite attaches to intestinal wall

    • A major cause of diarrhea throughout the world

Treating GI tract infections: rehydration therapy (electrolytes/water)

Chapter 26: Sexually Transmitted DIseases

STD pathogens are susceptible to drying & generally require direct physical contact w/ mucous membranes for transmission

• Syphilis - caused by the spirochete Treponema pallidum

  • Several stages; during 2-6 week incubation stage following transmission, bacterium multiplies & spreads in body

  • Primary syphilis: chancre(s) at site of infection; painless, full of spirochetes → if untreated, enters primary latent stage

  • Secondary syphilis: after several years effects on heart and CNS

  • Congenital syphilis: pregnant mother → fetus; congenital defects