Normal Microbiota of the Skin
Has large numbers of Gram-positive bacteria that are
resistant to drying and high salt concentrations
Ex: Staphylococci
Micrococci
Diphtheroids
Washing reduces numbers, but microbes in hair
follicles and sweat glands quickly repopulate
Skin Lesions (Fig. 21.2)
A. Vesicles
Small fluid-filled lesions
B. Bullae
Larger fluid filled lesions
C. Macules
Flat, reddish lesions
D. Papules
Raised lesion
If contain pus à pustules
Bacterial Diseases of the Skin
A.
Staphylococcal Skin Infections
1.
Folliculitis – infection of the hair follicles
Etiology: Staphylococcus
aureus
Transmission:
Direct contact
Pathogenesis:
infection of a hair follicle
Characteristics:
Pimple à mild inflammation
Furuncle à abscess (pus + inflammation)
Carbuncle à hard, round deep inflammation of tissue under skin
Treatment: topical or oral antibiotics
2. Scalded Skin Syndrome (Fig. 21.4)
Etiology: S.
aureus lysogenized by certain page types
Transmission:
Direct contact (esp. newborns and children)
Pathogenesis:
toxin causes epidermis to separate from dermis
Characteristics:
Blisters, reddening, extensive peeling.
Resembles a burn.
Treatment: Antibiotics
B.
Streptococcal Skin Infections
Classification of Streptococci
Hemolytic groups – based on reactions with blood agar
Gamma-hemolytic à non-hemolytic à normal flora
Alpha-hemolytic à hemoglobin reduced à green zone around colony à usually normal flora
Beta-hemolytic à lyse red blood cells à clear zones around colonies à many pathogenic
Lancefield groups – based on different surface
antigens A through T
1. Erysipelas
(Fig. 21.6)
Etiology: Streptococcus
pyogenes (= Group A beta-hemolytic streptococci)
Transmission:
Direct contact (probably through fissures in skin)
Pathogenesis:
Infects dermal layer of skin
à local tissue destruction à sepsis
Characteristics:
Reddish patches with raised margins
Treatment:
Penicillin
2. Impetigo
(Fig 21.7)
Etiology: Streptococcus
pyogenes
Transmission:
Direct contact (contagious, esp. in children)
Pathogenesis: Skin infection
Characteristics:
pustules that become crusted and rupture
Treatment: Penicillin
3. Invasive
group A streptococcal infection “flesh-eating bacteria” (Fig. 21.8)
Etiology: Streptococcus
pyogenes
Transmission:
Direct contact
Pathogenesis: Infection and rapid destruction of skin
and muscle tissue
Characteristics:
pustules that become crusted and rupture
Treatment: Penicillin
C.
Pseudomonas Skin infections
Etiology: Pseudomonas
aeruginosa
Transmission:
Opportunistic pathogen
Direct contact from swimming pools à dermatitis or swimmer’s ear
Nosocomial à resistant to disinfectants and antibiotics
esp.
catheter and burn patients
Pathogenesis:
Produces toxins that damage tissues
Characteristics:
Mild cases à dermatitis
Burn patients à green wounds with blue-green pus
Treatment: Newer antibiotics
Viral Diseases of the Skin
A. Warts
Etiology:
Human Papillomavirus (HPV)
Transmission:
Direct contact
Pathogenesis:
Infection causes benign tumors (warts)
Characteristics:
Warts
Treatment: Freezing or burning off
B. Smallpox
(Variola) (Fig. 21.9)
Etiology:
Variola virus
Transmission:
Respiratory route
Pathogenesis: infect internal organs, then skin
producing lesions
Characteristics:
fever, pain, scarring rash, death
Treatment:
Immunization:
Vaccinia (cowpox) vaccine
C. Chickenpox
(Varicella) and Shingles (Herpes Zoster) (Fig. 21.10a)
Etiology:
Varicella-Zoster virus (herpesvirus)
Transmission:
Respiratory route
Pathogenesis: Virus carried by bloodstream from
respir. tract to skin
à minor pustles
But Chickenpox + aspirin à Ryes syndrome à neurological damage, death
Characteristics: Children à Fever and Rash
May reoccur later à painful lesions à shingles (Fig. 21.10b)
Treatment:
Active infection:
Acyclovir (shortens by 1 or 2 days)
Immunization:
Chickenpox vaccine
D. Herpes
Simplex (oral herpes, cold sores) (Fig. 21.11) (Fig. 21.12)
Etiology:
Type 1 Herpes simplex virus (HSV-1)
Transmission:
Oral or respiratory route
90% of population infected, but usually subclinical
Pathogenesis: Virus latent in trigeminal nerve à Virus replicates in oral mucosa à inflammatory response
Characteristics:
painful, short-lived vesicles on lips, “cold sores”
Treatment: Acyclovir reduces duration of symptoms
E. Measles
(Rubeola) (Fig. 21.14)
Etiology:
measles virus
Transmission:
Respiratory route (very contagious)
Pathogenesis: virus invades bloodstream infects cells
lining small blood vessels à immune response causes rash
Characteristics:
rash (raised spots), Koplik’s spots (tiny red patches with central white
specks on oral mucosa opposite the molars)
Complications:
middle ear infections,
pneumonia,
encephalitis à brain damage
Subacute sclerosing panencephalitis
Occurs
mostly in males, 1-10 years after recovery from measles
Treatment:
Immunization:
MMR vaccine
F. Rubella
(German measles) (Fig. 21.15)
Etiology:
Rubella virus
Transmission:
Respiratory route
Pathogenesis:
Infect respiratory membranes
Characteristics: light fever, macular rash (spots not
raised)
Complications:
pregnant woman à
miscarriage or congenital rubella syndrome à heart defects, impaired vision/hearing, mental
retardation
Treatment:
Immunization:
MMR vaccine
Chapter
22 Microbial Diseases of the Nervous
System
Bacterial Diseases of the Nervous System
A. Bacterial
Meningitis
(Meningitis = inflammation of meninges)
(Encephalitis = inflammation of the brain)
Etiology:
More than 70% of cases caused by:
Streptococcus pneumoniae
Transmission:
Respiratory route
Pathogenesis:
Capsule prevents Phagocytosis by immune cells, transfers across blood
brain barrier, infects meninges, shock and inflammation
Characteristics:
headache, fever, stiff neck
à nausea, vomiting
à convulsions, coma, death
Treatment:
Active infection:
Penicillin, cephalosporin
Immunization:
Hib vaccine (Haemophilus influenzae b vaccine) for children (Fig.
22.3)
B. Tetanus
(Fig. 22.6)
Etiology: Clostridium
tetani
Transmission:
Direct à
from soil through wound
Pathogenesis:
C. tetani grows in wound, produces tetanospasmin, blocks muscle
relaxation pathway
Characteristics:
muscle spasms à
rigid paralysis à
respiratory failure
Treatment: Tetanus vaccine (toxoid)
C. Botulism
Etiology:
toxin produced by Clostridium botulinum
Transmission:
GI Route
Suspect foods à Low acid canned foods (meat, green beans, etc.)
75% of botulism in US due to home canned foods
Pathogenesis:
In adults:
Bacteria grow in food à produces neurotoxin
Person ingests neurotoxin in food à Blocks release of acetylcholine across motor
synapses
In infants:
Infant eats food with C. botulinum endospores (esp.
honey)
Infant intestinal microbiota not established so
endospores germinate and grow à neurotoxin produced
Characteristics:
weakness, blurred vision initially
à flaccid paralysis à respiratory or cardiac failure à death
Treatment: antitoxin (antibodies to toxin)
Viral Diseases of the Nervous System
A.
Poliomyelitis
Etiology:
Poliovirus
Transmission:
Ingestion of water contaminated with infectious feces
Pathogenesis:
Infects throat and small intestine à Spreads to lymph nodes à Enters blood
In 1% of people infected à infect central nervous system à nerve cells die
Characteristics:
Most cases à asymptomatic or sore throat and nausea
In 1% of people infected à paralysis or death from respiratory failure (Fig.
22.9)
Treatment: (Fig. 22.10)
Salk vaccine – inactivated virus
Sabin vaccine – attenuated virus (oral vaccine)
More effective, but 1 in 750,000 cases virus
reacquires virulence à
causes polio
B. Rabies
Etiology:
Rabies virus
Transmission:
Animal bites, esp. Raccoons, skunks, dogs (Fig 22.12)
Pathogenesis:
Virus replicates in muscle, then invades nervous system (Fig. 22.11)
Characteristics:
30 – 50 day incubation
Increased salivation, irrational behavior,
convulsions, hydrophobia
Once symptoms develop à 100% mortality
Treatment: Rabies vaccine immediately after bite (6
injections over 28 days) and Rabies immune globulin
C. Arboviral
(mosquito-borne viruses) Encephalitis
1. St. Louis
encephalitis
Etiology: St.
Louis encephalitis arbovirus
Transmission:
by mosquitoes in summer months
Pathogenesis:
blood to brain à
encephalitis
Characteristics:
Most cases asymptomatic
In 1% of cases, chills, headache, fever à mental confusion, coma, permanent neurological
problems or death
Treatment: none
Prevention: control mosquito populations
2. West Nile
Etiology:
West Nile virus
Transmission:
by mosquitoes in summer months
Pathogenesis:
blood to brain à
encephalitis
Characteristics:
Most cases asymptomatic
In small number of cases, esp. in elderly à chills, headache, fever à paralysis or fatal encephalitis
Treatment:
none
Prevention:
control mosquito populations
Protozoan Diseases of the Nervous System
A. African
Trypanosomiasis (African sleeping sickness)
Etiology: Trypanosoma
brucei gambiense or T. brucei rhodesiense (Fig 12-13)
Transmission:
Bite of the tsetse fly
Pathogenesis:
Infect blood à
Invade nervous system
Characteristics:
mental deterioration à coma à death
Treatment:
Eflornithine (also reduces facial hair on women)
Chapter
23 Microbial Diseases of the
Cardiovascular and Lymphatic Systems
Bacterial Diseases of the Cardiovascular and
Lymphatic Systems
A. Rheumatic
Fever (Fig. 23.5)
Etiology: Streptococcus
pyogenes
Transmission:
Respiratory route (often following episode of “Strep throat”)
Pathogenesis:
Infection à
autoimmune reaction à
joint damage and heart valve damage
Characteristics:
Fever, subcutaneous nodules, arthritis, heart failure, death
Treatment:
Penicillin
B. Tularemia
“rabbit fever”
Etiology: Francisella
tularensis
Transmission:
Zoonose à carried and transmitted by many animals, esp.
rabbits.
Most prevalent in hunters (skinning game) (Fig. 23.6)
Enters body
1. Through
minor skin wounds or tick bites
2.
Respiratory route – inhaling dust contaminated by infected animals
Pathogenesis:
Infect lymph and blood and organs
Characteristics:
ulcer at inoculation site à swollen lymph nodes à organ damage or pneumonia (if inhaled)
Treatment:
Streptomycin
C. Anthrax
Etiology: Bacillus
anthracis
Three forms in humans
1. Cutaneous
anthrax (90% of cases)
Transmission:
Endospore from animal hide or wool enters through minor lesion
Pathogenesis:
Localized infection of skin
Characteristics:
Vesicles that rupture and ulcer covered by black scab, slight fever,
malaise (Fig. 23.7)
2.
Gastrointestinal anthrax (rare)
Transmission:
Ingestion of undercooked food containing endospores
Pathogenesis:
Lesions in GI tract
Characteristics:
Nausea, abdominal pain, bloody diarrhea, 50% mortality
3.
Inhalational anthrax
Transmission:
Endospores inhaled into lungs
Pathogenesis:
Bacteria enter bloodstream from lungs, septic shock, death
Characteristics:
mild fever, coughing, chest pain à almost 100% mortality if untreated
Treatment:
Ciprofloxacin or doxycycline
D. Gas
Gangrene (Fig. 23.8)
Etiology: Clostridium
perfringens
Transmission:
Infected through wound
Pathogenesis:
produce enzymes that dissolve muscle and connective tissue
Characteristics:
Tissue swelling due to gas production and tissue necrosis, death
Treatment:
Penicillin
Surgical removal of necrotic tissue
Hyperbaric oxygen treatment (lethal to obligate
anaerobe) (Fig. 23.9)
E. Plague
“Black death”
Etiology: Yersinia pestis
Two forms in humans
1. Bubonic
plague
Transmission:
vector (fleas on rodents) (Fig. 23.11)
Pathogenesis:
Systemic infection and damage à 50 – 70% mortality if untreated
Characteristics:
Buboes (enlarged lymph nodes) (Fig. 23.10)
Tissue hemorrhage à black lesions on skin
2. Pneumonic
plague
Transmission:
Respiratory route from other infected human, very contagious
Pathogenesis:
Lung infection (no buboes)
Characteristics:
pneumonia, tissue hemorrhage (no buboes)
à almost 100% mortality if untreated
Treatment:
Streptomycin or tetracycline administered early
F. Lyme
Disease (Fig. 23.13)
Etiology: Borrelia
burgdorferi
Transmission:
Vector (deer tick)
Pathogenesis:
Infection spreads to nervous system and heart
Characteristics:
“Bulls-eye rash”, fever, fatigue à heart damage, arthritis, facial paralysis (Fig.
23.14)
Treatment:
Penicillin early in course of disease
G. Rocky
Mountain Spotted Fever
Etiology: Rickettsia rickettsii
Transmission:
vector (tick) (Fig 23.16)
Pathogenesis:
Multiply in endothelial cells lining blood vessels à capillary hemorrhage
Characteristics:
fever, muscle pain, rash similar to measles, often on palms or soles,
often fatal if untreated (Fig 23.18)
Treatment: Tetracycline
Viral Diseases of the Cardiovascular and Lymphatic
Systems
A. Infectious
Mononucleosis
Etiology:
Epstein-Barr Virus
Transmission: Transfer of saliva (kissing, sharing
cups and utensils)
Pathogenesis: viral replication in mouth and throat,
then B-cells à
immune response à
abnormal number of mononuclear lymphocytes
Characteristics:
fever, chills, headache, sore throat , fatigue
Complications:
Burkitt’s lymphoma à in young black Africans (Fig. 21.19)
Nasopharyngeal carcinoma à in southeast Asia
Treatment: none
Protozoan Diseases the Cardiovascular and Lymphatic
Systems
A. American
Trypanosomiasis (Chagas’ Disease)
Etiology: Trypanosoma
cruzi (Fig. 23.22)
Transmission:
Reduviid bugs (kissing bugs) bite lips and eyelids and defecate à you scratch contaminated feces into wound (Fig.
12.33d)
Usually seen in Texas, Mexico, Central and South
America
Pathogenesis:
Infect blood à
invade nervous system and heart
Characteristics:
heart damage, especially in children
Treatment:
none
B. Toxoplasmosis
Etiology: Toxoplasma
gondii
Transmission:
Eating undercooked infected meat or ingestion of infected cat feces
Life cycle: (Fig. 23.23)
Protozoan in cat feces
Mice ingest and are infected
Infected mice lose their avoidance behavior toward cats
(see handout “Bugs in Brain”)
Cats eat mice and are infected
Pathogenesis:
Infect and form cysts in neural tissue
Characteristics:
In most people à
asymptomatic
In immune compromised à neurological impairment
In pregnant women à serious fetal defects or miscarriage
Treatment:
none
C. Malaria
(Fig. 23.24a)
Etiology: 4
species of Plasmodium
Transmission:
Bite of Anopheles mosquito (Fig. 12.31b)
Pathogenesis:
Infect liver and red blood cells à lyse red blood cells (Fig. 23.25)
Characteristics:
severe fever and chills, vomiting, headache
Treatment:
Chloroquine
Helminthic Diseases of the Cardiovascular and
Lymphatic Systems
A.
Schistosomiasis
Etiology: Schistosoma
Transmission:
Fecal/oral
Most cases in developing countries
Life Cycle:
(Fig. 23.27)
Eggs from adult flukes in human à feces à water
Eggs hatch, larvae burrows into snail
Larvae develops, leaves snail
Larvae burrows into human, travels to intestinal
blood vessels
Pathogenesis:
Eggs lodge in tissue à damaging inflammation à local tissue damage (granulomas) (Fig. 23.28)
Characteristics:
Liver, lung, intestinal, bladder, nervous system damage
Treatment:
Oxamniquine