Microbiology Test #4

Staphylococcal Disease: Localized cutaneous infections

invade skin through wounds, follicles, or glands

• Folliculitis

• Furuncle

• Carbuncle

Folliculitis

type of staphulococcal diease

superficicial inflammation of hair follicles and glands; usually self limiting

Furuncle

staphlococcal disease

boil; inflammation of hair follicle or sebaceous gland progesses into abscess or pustule, relatively small

Carbuncle

staphylococcal diease

larger and deeper lesion created by aggregation and interconnection of a cluster of furncles

• think furuncle and more furnaces

Staphylococcus

• common inhabitant of skin and mucous membranes

• irregualar clusters

• virulence factor: may have capsules

• has catalase

What are three important species of staphylococcus

S. aureus

S. epidermis

S. saprophyticus

Staphulococcal Diease: Toxigenic disease

Exfoliative toxin

Staphyloccoal scalded skin syndrome

Bullous impetigo

Stapyloccoal scalded skin syndrome

toxin (systemic) induces bright red flush, blisters, then desquamation of the epidermis,

usually in babies because weak immune system

Bullous Impetigo

-same toxin (staph. aureus)- can affect at any age

Toxigenic disease

super antigen

ex: food intoxication, toxic shock syndrome

Food intoxication

• toxigenic diease caused by super antigens

• ingestion of heat stable exterotoxcins; gastrointestinal distress; self- limiting

Toxic shock syndrome

• toxigenic diease caused by super antigen

• toxemia leading to shock and organ failure because it enters the bloodstream

Clinical concerns in Staphylococcal Infections

• MRSA- methicillin-ressitant S. aureus- carry multiple resistance. “superbugs”

• abscesses have to be surgically perforated

• systemic infections require intensive lengthy therapy

What are the two examples of staphylococcal Infections in clinical settings or MRSA?

• Nosocomial (HA-MRSA)

• Community (CA-MRSA)

Nosocomial (HA-MRSA)

hospital associated, much more resistant to antibiotics, but not more pathogenic

Community (CA-MRSA)

• everyday life, pathogenic, but more treatable

Streptococcus

• arranged in long chains or pairs

• non-spore-forming, nonmotile

• can form capsules and slime layers

• do not form catalase

What are the three ways to divide streptococcal into subgroups?

• lancefield groups

• hemolysis

• major extracellular toxins

Lancefield groups

• based on cell wall carbohydrates- 20 groups ( A, B, C..)

• based on C-carbohydrate found in cell wall

• one of the streptococcal subgroups

Hemolysis

Beta hemolysis: A, B,C, G and some D strains

Alpha hemolytic- hemolytic- S. pneumoniae and viridans (usally oral based)

• one of the streptococcal subgroups

Major extracellular toxins

Streptolysins- hemolysis: streptolysin O (SLO) and streptolysin S (SLS)- both cause cell and tissue injury

• one of the streptococal subgroups

Streoptococcus pyogenes

• skin infection

• Most common strain of group A

• group A beta-hemolytic streptococci

Impetigo

• streptococcal skin infection

• presents as red sores on the face, around a child’s nose

• the sores burst and develop honey-colored crusts

• epidermal layer

• group A beta-hemolytic streptococci

Erysipelas

• acute infection of the dermis and subsutaneous tissue

• group A beta-hemolytic streptococci

Necrotizing fasciitis (flesh-eating disease)

• Invasice Group A Streptococal infection

• enters and cuts and abrasions on skin and spreads rapidly through subcutaneous tissue

• enzymes digest connective tissue while toxins poison the epidermal and dermal tissues

What are the virulance factors that help necrotizing fasciitis away from the localized area?

Extracellular enzymes such as…

Streptokinase- digests fibrin clots

Hyaluronidase- breaks down connective tissue

Pyrogenic exotoxin A - superantigen

Streptococcal throat infections

Streptococcal pharyngitis (strep throat)

scarlet fever

Streptococcal pharyngitis

• streptococcal throat infection

• classic

• puulent exudate, pus containing nodules, inflammed tissue

Scarlet fever

• variety of strep throat but different because of the toxin

• strain of S. pyogenes carrying a prophage that codes for erythrogenic toxin

• strawberry tongue

What are long term complications of group A infections?

• Rheumatic fever

• acute glomerulonephritis

Rheumatic fever

• long term complications of Group A infection

• follows pharyngitis

• antibodies raised against bacterial antigens target body proteins

• inflammation- carditis (valve damage possible), arthritis

• type two hypersensitivity

Acute glomerulonephritis

• kidney

• long term complications of Group A infection

• immune complexes in blood filtered by nephron and damage the filtration system (glomerulus)

• can lead to increased blood pressure, Heart or kidney failure in extreme cases

• hypersensitivity 3

Group B: Streptococcus agalactiae

• beta-hemolytic streptococci

• regulary resides in human vagina, pharynx, and large intestine

• can be transferred to infant during delivery and cause servere infection

• most prevalent cause of neonatal pneumonia, sepsis

• meningitis

• antibiotics administered during labor

Streptococci: The Viridans Group

• large complex group; apla hemolytic

• streptococcus mutans, salivarus, mitis etc.

• residents of the gums and teeth, oral cavity; less in pharynx and on skin

Streptococcus mutans

• produce slime layers that adhere to teeth, basis for plaque

• involved in dental caries

• apart of the Viridans Group

Subacute endocarditis

• blood-borne bacteria settle and grow on Heart lining or valves

• colonication of Heart by forming biofilms

Streptococcus pneumoniae: Pneumococcus

• all pathogenic strains form large capsules

• normal flora

• cause most of bacterial pneumonias

• leading cause of bacterial meningitis

• cayse middle ear infections

Gram-Negative Cocci

• mucous membranes

• neisseria, branhamella, moraxella

two primary human pathogens in the

• neisseria gonorrhoeae

• neisseria meningitidis

bean-shaped, diplococci

• no flagella or spores

• capsules on some pathogens

• fimbriae

Neisseria gonorrhoeae

• causes gonorrhea

• gram- negative cocci

What are factors contributing to gonococcal pathogenicity?

• fimbriae, other surface molecules for attachment; slows phagocytosis

• IgA protease- cleaves secretory IgA

What is the Epidemiology and pathology of gonorrhea?

• strictly a human infection

• in top five stds

• inflammation of epithelium and connective tissue

• often asymptomatic

Genital Gonorrhea

• Men- Urethritis: pus discharge, scarring, and infertility

• Woman- Urethritis: scar tissue, infertility

Pelvic Floor diease

• N. gonorrhae and or Chlamydia Mixed infection: Mycoplasma,
  Ureaplasma, Haemophilis, enterics,
  etc. All can lead to minor urethritis
  as well

Salpingits

• inflammation of fallopian tube

• 
  

Vaginitis

inflammation

Gardnarella vaginalis –
normal flora; Clue cells

Gonococcal Infections in Children

• infants born to gonococcus carriers are in danger of being infected as they pass through the birth canal

• eye inflammation, corneal ulceration- blindness

• sexually transmitted infections

• prevented by prophylaxis immediately after birth

Neisseria Meningitidis: meningococcus

• 
  Human reservoir
  • nasopharynx; 10% of adult
  population carry it without
  symptoms
  • Starts as a throat infection
  • Can enter bloodstream, cross the
  blood-brain barrier, permeate the
  meninges, and grow in the
  cerebrospinal fluid
  • Very rapid onset; neurological
  symptoms
  • Virulence factors:
  • Capsule, fimbriae, IgA protease,
  Endotoxins
  • 12 strains; serotypes A, B, C, and Y
  cause most cases; vaccine for some
  serotypes
  • Prevalent cause of meningitis

Bacillus Anthrax

Majority of cases in cattle/livestock
• 3 types of anthrax:
• Cutaneous – bacterial
• Pulmonary –inhalation of toxin
• Gastrointestinal – bacterial

Gas Gangrene/Myonecrosis

Clostridium perfringens most frequent
clostridia involved in soft tissue and wound
infections

• infection after surgery

• wound area needs ischemia (less oxygen)

• bubble of tissue sometimes

Tetanus (lock jaw)

Clostridium tetani

• puncture wound or cut umbilical cord

• muscles contract more frequently “spastic”

Tetanospasmin (exotoxin) – binds motor neurons; moves to
the spinal cord. Toxin inhibits release of GABA
• Stops relaxation pathways of muscles - spastic
• Death by paralysis of respiratory muscles if untreated
• Prevention by vaccination with tetanus toxoid (DTaP) and
booster or treatment with tetanus immune globulin

Botulism

Clostridium botulinum

• muscles impacted because no acetylcholine to contract, flaccid paralysis

• treatment: supportive care and antitoxcin, proper canning, food preservatives (nitrates)

C- diff Colitis

Clostridioides difficile– part of normal intestinal flora
• Extended use of antibiotics – causes overgrowth
• Enterotoxins cause diarrhea and can damage intestines
• Pseudomembranous colitis – patches slough off
• Ulceration and perforation of the intestinal wall
• Treatment: stop antibiotics, probiotics, fecal transfer

Listeria monocytogenes

inhabits soil and water
• Resistant to cold, heat, salt, pH extremes, and bile
• Virulence: induces phagocytosis & replicates inside; avoids humoral immune system; moves cell to cell

Listeriosis

most cases associated with dairy products (soft
cheeses) and meat (processed)
• Often mild or subclinical in normal adults
• Immunocompromised patients and fetuses (can cross placenta) –
miscarriage, fetal death, neonatal meningitis

Gram-Positive Irregular Non-Spore-Forming Bacilli

Irregular: pleomorphic, stain unevenly
• Medically important genera:
• Corynebacterium
• Propionibacterium
• Mycobacterium
• Actinomyces
• Nocardia

Diphtheria

Corynebacterium diphtheriae
• Rods have pleomorphic variants with internal
granules
• Resides in healthy carriers
• Acquired via respiratory droplets from carriers or
infected individuals
• Diphtherotoxin produced by lysogenized C.
diphtheriae
• Cutaneous diphtheria: Infected skin wound leads to
slow healing ulcer
• Upper respiratory tract (most common location)
• Diphtheria membrane of fibrin, dead tissue, and
bacteria
• Pseudomembrane formation can cause
asphyxiation
• Systemic toxin targets heart & nervous system
• Prevented by DTaP and Td vaccine (Diphtheria
toxoid)

Mycobacterium tuberculosis

Tubercle bacillus – long, thin rod that
grows in masses or strands called cords
• No exotoxins nor enzymes that contribute
to infectiousness
• Virulence factors –complex cell wall and
cord factor
• Transmitted human to human by airborne
respiratory droplets
• Estimate 1/3rd of world population and 15
million in U.S. carry tubercle bacillus
• 5% to 10% of infected people develop
clinical disease
• Untreated, the disease progresses slowly
• Majority of TB cases contained in lungs

Primary tuberculosis

Phagocytosed by macrophages and
multiply inside
• Immune system will form tubercles
• Centers can become necrotic (caseous),
then calcify

Secondary tuberculosis (reactivation or
reinfection)

Tubercles with latent bacilli can expand
and drain into respiratory tract
• Severe symptoms develop: violent
coughing, bloody sputum, fever, anorexia,
weight loss, fatigue – “Consumption”

Disseminated (extrapulmonary)
tuberculosis

During reactivation, bacilli disseminate
any tissue

Tuberculosis Diagnosis

Tuberculin skin test
screening
• positive = current or previous
infection
• Followed by X-ray, acid-fast
staining of sputum, culturing
bacteria

Treatement of Tuberculosis

Prolonged treatment with multiple
antibiotics
• Vaccines: BCG, live, avirulent M.
bovis.
• Not widely used in U.S.
• Europeans frequently positive
in Tb test due to vaccine

Leprosy (Hansen’s Disease)

Mycobacterium leprae – strict parasite
• Grows best at cooler temperature (30°C)
• Transmission unclear
• Macrophages phagocytize the bacilli, but a or slow response may not kill
bacillus
• If untreated, bacilli grow slowly in the skin macrophages and Schwann
cells of peripheral nerves

Two forms of leprosy (hansen’s diease): Tuberculoid (paucibacillary) and Lepromatous (multibacillary)

Can have both forms, and one type can progress to another
• Tuberculoid form: superficial, dermal nerve damage, loss of sensation in skin areas, skin lesions with bacilli
• Lepromatous form: Disseminated bacilli cause skin thickening and nodules; nerve damage, trauma, secondary infections lead to disfigurement

Syphilis

Treponema pallidum
• Strict parasites; difficult to
culture
• Sexual and transplacental
transmission
• Invades the mucosa or through
skin breaks and enters the
bloodstream
• Induces an inflammatory
response
• Three clinical stages
• Interspersed with latency

Syphilis stages

Primary stage: chancre at
site of infection (non-painful);
overlooked, infectious
• Secondary: Skin and
mucosal rashes; affect many
body tissues; infectious
• Tertiary: Gummas on many
organs, skin. Benign but
painful
• Primary & secondary stages
treated with penicillin

Congenital Syphilis

Can cross placenta during
any trimester
• Inhibits fetal growth and disrupts critical periods of development
• Surviving infants have skin lesions and/or profuse nasal discharge
• Hutchinson’s Triad:
• Deafness
• Impaired vision
• Notched, peg-shaped teeth

Nonsyphilitic Treponematoses

Subspecies of T. pallidum; not transmitted sexually nor congenitally

Nonsyphilitic Treponematoses: Bejel

deforming childhood infection of the mouth, nasal cavity, body, and hands

Nonsyphilitic Treponematoses: yaws

invasion of skin cut, causing a primary ulcer that seeds a second crop of lesions

Nonsyphilitic Treponematoses: pinta

superficial skin lesion that depigments and scars the skin

Lyme Disease

Borrelia burgdorferi
• Reservoir: Mice & Deer
• Vector: Tick nymphs (Ixodes)
• First symptom
• bull's eye rash
(80%)
• Untreated can progress to cardiac and neurological symptoms, followed by severe arthritis Lyme Disease
Disease first identified in 1975 in Lyme, CT; Northeast and Midwest

Prompt removal of tick including all mouth pieces.
Prevention it to avoid the vector

Relapsing Fever

caused by Borrelia spp.
• Transmitted by soft ticks that feed on wild
rodents, squirrels, etc
• Arthropod vector
• Humans are usually accidental host
• Fever caused by immune response
• Fluctuates – returns every few days
• Due to immune evasion by antigenic variation
Relapsing Fever

Cholera

Vibrio cholerae
• Favored in warm, alkaline, and
saline conditions
– Noninvasive
– Produces the cholera toxin
 Toxin causes the host cells
to secrete electrolytes and
water.
 Causes “rice water stools”
• 50% mortality if untreated
• Cholera increases when
sanitation is compromised.

Campylobacter Enteritis

Campylobacter jejuni
• Residents of the intestinal and
genitourinary tract of birds and
mammals
• Transmitted by contamination
• Invade mucosal cells of ileum
• Enterotoxin CJT stimulates a
secretory diarrhea like cholera
• Symptoms: headache, fever,
abdominal pain, bloody or watery
diarrhea
• Usually resolves in a week without
treatment
• Possible sequela: Guillain-Barré
syndrome

Gastritis & Peptic Ulcer disease

Helicobacter pylori – produces urease
• Disrupts stomach mucosa, causing inflammation and
damage to epithelium; leads to gastritis/ulceration.
• Carcinogenic

O
Rickettsias

intracellular pathogens that rely on an arthropod vectors

Chlamydias

intracellular pathogens that alternate between elementary and reticulate bodies

Epidemic typhus

Rickettsia prowazekii
• Reservoir: humans
• Vector: Pediculus humanus
corporis (lice)
• Passed through defecation
• Seen in warfare

Endemic murine typhus

Rickettsia typhi
• Reservoir: Rodents
• Vector: Xenopsylla cheopsis (flea)
• Passed through defecation

Spotted Fevers (Rocky Mountain spotted fever)

Rickettsia rickettsii
• Zoonotic disease
• Measles-like rash including palms
and soles
• Invasion of endothelial cells
• Nervous system involvement
• Vectors  Dermacentor spp. (wood
tick in west/dog tick in east)
• Reservoir  Ticks; mammals
• Most cases found in SE USA
• Diagnosis via serological methods

Rickettsial-Related Diseases: Ehrlichious

Caused by Ehrlichia chaffeensis
• rickettsia-like, obligately intracellular
• Form aggregates (morulae) in monocytes/macs
• Human monocytic ehrlichiosis (HME)
• Vector is the Lone Star tick

Rickettsial-Related Diseases: Anaplasmoisis

Caused by Anaplasma phagocytophilum
• Targets neutrophils and other granulocytes
• Human granulocytic anaplasmosis (HGA)
• Vector is the Ixodes tick

Q fever

• Coxiella burnetii
– Obligately parasitic, intracellular
bacteria
– Makes spore like structure
• Transmitted to farm animals from
tick bites
– Transmitted to humans by
contamination from the
inhalation of aerosols from
animal products and
unpasteurized milk
– Usually inhaled causing
pneumonitis, fever, aches, etc

Ocular trachoma Chlamydia

severe infection, deforms eyelid and
cornea, may cause blindness
• Greatest cause of blindness worldwide
• Infection causes permanent scarring of the cornea

Inclusion conjunctivitis Chlamydia

passed to baby through
genitourinary tract secretion during birth
• prevented by prophylaxis

Chlamydiosis

Chlamydia trachomatis

Most prevalent STD. Long term reproductive
damage. Asymptomatic in females (70%) and male (90%)

Nongonococcal urethritis (NGU) in males

Chlamydia trachomatis

Inflammation of
the urethra. Mimics gonorrhea, yet do not involve gonococci

Pelvic inflammatory disease (PID) in women

Chlamydia trachomatis
Cervicitis with
a white drainage, endometritis, and salpingitis

Lymphogranuloma venereum (LGV)

Chlamydia trachomatis

disfiguring disease of
the external genitalia and pelvic lymphatics

Cavities

Dental plaque
– Biofilms involved in the formation of dental caries
– Streptococcus mutans is the most important cariogenic
organism
– use dietary carbohydrates to secrete glucans
• Caries - acid dissolves tooth enamel leading to caries and
tooth damage; can penetrate into the dentin
• Other species can then attach to the biofilm

Gingivitis

Inflammation and infection of the gums
– Started by calcified plaque (calculus)
– Caused by streptococci, actinomycetes, and anaerobic
gram-negative bacteria

Periodontitis

Bone and tissue supporting the teeth are destroyed (plaque bacteria and immune reaction)

Pseudomonas aeruginosa

Opportunistic pathogen
• Common inhabitant of soil and water
• Intestinal resident in 10% normal people
• Otitis externa; nosocomial infections post-burn
• Multidrug resistant strains
• Many virulence factors

Melioidosis

Melioidosis
• Burkholderia pseudomallei –acquired by penetrating
injury or inhalation
• Wound infections, bronchitis and pneumonia, septicemia
• Occurs in moist soils - Opportunistic
• Commonly affects immunocompromised
• Chronic infection – endotoxic shock, organ abscesses,
death

Undulant Fever (Brucellosis)

Brucella spp, gram-
negative cocco-bacillus;
opportunistic pathogen
• Transmitted via milk from
infected animals or
contact with infected
animals
• Bacteria reproduce in
macrophages
• Fluctuating fever (malaise,
night sweats, muscle
aches)
• Not usually fatal

Tularemia

Francisella tularensis –
zoonotic pathogen
• Seen in wild rabbits;
transmitted by vectors or
direct contact
• Bacteria reproduce in
macrophages
• 10% death rate in systemic
and pulmonic forms
• Low infectious dose

Pertussis (Whooping Cough)

Bordetella pertussis: encapsulated coccobacillus
• Virulence: Tracheal cytotoxin of cell wall damaged ciliated
cells; Pertussis toxin; adhesion to cells
• Reservoir –healthy carriers; transmission - inhalation of
aerosols. Acute respiratory syndrome – severe in babies
• Prevented by DTaP vaccine (acellular Pertussis; toxoid)
• Stage 1: Catarrhal stage, like common cold
• Stage 2: Paroxysmal stage: Violent coughing

Legionellosis (Legionnaires’ disease)

Legionella pneumophila
• Opportunistic in older men – rarely seen in young &
healthy
• Widely distributed in water, in close association with
amoebas (or macrophages in the body)
• Transmitted by inhaling aerosols, not transmitted from
human to human
• Pneumonia-like disease
• Pontiac fever (mild disease)
Legionellosis (Legionnaires’ disease)

Enteropathogenic E. coli (EPEC)

Cause the host cells to form
pedestals where the bacteria
attach