MICROBIAL DISEASES OF THE SKIN AND EYES ➢ Onycholysis

○ Separation of nail plate from nail bed

Bacterial Skin Infections Normal Microbiota of the Skin
➢ Skin ➢ Gram-positive, salt-tolerant bacteria
○ Salt inhibits microbes ○ Staphylococci
○ Lysozyme hydrolyzes peptidoglycan ○ Micrococci
○ Fatty acids inhibit some pathogens ○ Diphtheroids
○ Defensins are antimicrobial peptides ➢ Malassezia furfur
➢ Mucus Membranes Microbial Diseases of the Skin
○ Line body cavities ➢ Exanthem: Skin rash arising from another focus of
○ The epithelial cells are attached to an the infection
extracellular ➢ Enanthem: Mucous membrane rash arising from
○ matrix another focus of the infection
○ Cells secrete mucus Staphylococcal Skin Infections
○ Some cells have cilia
➢ Macule
○ Circumscribed lesion up to 5mm (in
diameter) characterized by flatness and
usually distinguished from surrounding skin
by its coloration
➢ Patch
○ Circumscribed lesion of more than 5mm in
diameter characterized by flatness and
usually distinguished from surrounding skin
by its coloration Differential Characteristics
➢ Papule ➢ Coagulase: Fibrinogen-Fibrin
○ Elevated dome-shaped or flat-topped lesion ➢ Mannitol Salts Agar (MSA)
5mm or less across Staphylococcal Skin Infections
➢ Nodule
○ Elevated lesion with spherical contour
greater than 5mm across
➢ Plaque
○ Elevated flat-topped lesion, usually greater
than 5mm across (may be caused by
coalescing papules)
➢ Vesicle
○ Fluid-filled raised lesion 5mm or less across
➢ Bulla
○ Fluid-filled raised lesion greater than 5mm
across
➢ Blister
○ Common term used for vesicle or bulla
➢ Pustule Clinical Manifestation/Disease
○ Discrete, pus-filled, raised lesion ➢ Skin
➢ Wheal ○ Folliculitis
○ Itchy, transient, elevated lesion with variable ○ Boils (furuncles)
blanching and erythema formed as the ○ Carbuncles
result of dermal edema
➢ Scale
○ Dry, horny, plate-like excrescence; usually
the result of imperfect cornification
➢ Lichenification
○ Thickened and rough skin characterized by
prominent skin markings; usually the result
of repeated rubbing in susceptible persons
➢ Excoriation
○ Traumatic lesion characterized by breakage
of the epidermis, causing a raw linear area
(i.e deep scratch); often self induced
 Metastatic Infections
Clinical Manifestations/Disease ➢ Bacteremia
➢ Impetigo (bullous & pustular) ➢ Osteomyelitis
➢ Scalded skin syndrome ○ Disease of growing bone
○ Neonates and children under 2 years ○ Pulmonary and cardiovascular infection

Staphylococcal Skin Infections

➢ Scalded skin syndrome Streptococcal Skin Infections
○ Bright red lesions that easily peels off in ➢ Streptococcus pyogenes
sheets ➢ Group A beta-hemolytic
○ Exfoliative toxin ➢ M proteins
○ Antibiotic tx ★ Alpha hemolysis is indicated by a greenish or
○ Part of toxic shock syndrome (TSS) brownish zone around the colonies
Staphylococcal Scalded Skin Syndrome (SSSS) ★ In beta hemolysis, the bacteria synthesize a
➢ Dermonecrotic toxin (exfoliative toxin) hemolysin that produces a complete zone of lysis
➢ Bullous exfoliative dermatitis around the colonies
Clinical Manifestations/Disease ★ Some bacteria grow on blood agar, but cause no
➢ Other infections change in the red blood cells
○ Primary staphylococcal pneumonia Streptococcus Pyogenes
○ Food poisoning vs. Foodborne disease ➢ Local infections
○ Toxic shock syndrome ○ Impetigo
Toxic Shock Syndrome ○ Erysipelas
➢ Toxic shock syndrome toxin (TSST-1) ○ Cellulitis
○ Superantigen ○ Necrotizing Fasciitis (flesh-eating bacteria)
○ Produced by 5-25% isolates ➢ Systemic effect
○ Tampon or infected wound ○ Streptococcal toxic shock-like syndrome
■ Fever (STSS)
■ Rash ■ SPE (similar to TSS by S. Aureus)
■ Exfoliation of skin ○ Scarlet fever (pyrogenic toxin by
■ Shock (death 3%) lysogenized)
Staphylococcal Skin Infections ➢ Post-infection
○ Rheumatic fever (associated with
pharyngitis)
○ Glomerulonephritis
Invasive Group A Streptococcal Infections
➢ M protein
➢ Streptokinases
➢ Hyaluronidase
➢ Exotoxin A, superantigen
➢ Cellulitis
➢ Necrotizing fasciitis
Virulence Factors
➢ Adhesins
○ M protein (fibrillar Ag)
 ○ Fibronectin Binding Proteins (Protein F) ○ Pyocyanin produces a blue-green pus
➢ Hyaluronic Acid Capsule ➢ Pseudomonas dermatitis
➢ Invasins ➢ Otitis externa
○ Streptolysins (S&O) ➢ Post-burn infections
○ Hyaluronidase
○ Streptokinases
○ Activates blood clot dissolving
protein-plasminogen (human specific)
■ Dnase
➢ Exotoxins
○ Pyrogenic (erythrogenic) toxin- SPE
■ Scarlet fever
■ Toxic shock syndrome
Streptococcal Infections

Acne
➢ Comedonal acne occurs when sebum channels are
blocked with shed cells
➢ Inflammatory acne
○ Propionibacterium acnes
■ Gram-positive, anaerobic rod
■ Treatment
➢ Inflammatory acne
○ Nodular cystic acne
○ Treatment: isotretinoin
★ Preventing sebum formation (isotretinoin)
★ Antibiotics
★ Benzoyl peroxide to loosen clogged follicles
★ Visible (blue) light (kills P. Acnes)
Propionibacterium Infections

Streptococcal Skin Infections

➢ Erysipelas
○ Erythema
○ Bullae
○ Caused by group A streptococci, is
characterized by raised, bright-red plaques
with sharply defined borders
➢ Impetigo Skin and Other Infections
Pseudomonas Infections ➢ Staphylococcus aureus
○ Skin, food poisoning, osteomyelitis, kidney
abscess, endocarditis
➢ Streptococcus pyogenes
○ Skin, pharyngitis and blood strem
➢ Botulinum
○ Wound, food & infant
➢ C. Perfringens
○ Skin and diarrhea
Infections by Pseudomonas ➢ Anthrax
➢ Pseudomonas aeruginosa ○ Cutaneous, respiratory, & GI
○ Gram-negative, aerobic rod
Gas Gangrene (Clostridium Perfringens) ➢ Slow-healing painless ulcer with black eschar
➢ Alpha toxin (phospholipase C) surrounded by edema
○ Zinc metallo phospholipase ➢ Infection may spread- Septicemia- 20% mortality
■ Hemolysis and bleeding
○ Gas formation
➢ Myonecrosis, shock, renal failure and death
Alpha Toxin
➢ Treatment
○ Debridement and excision
○ Antibiotics (prevent further spreading)
○ Hyperbaric oxygen therapy
■ Inhibit or kill the anaerobic bacteria
Epidemiology of Bacillus Anthracis Other Skin and Mucous Membrane Infections
➢ Rare in the US (1974-1990, 17 cases reported by
➢ Staphylococcus epidermidis
CDC)
○ Catheters and prostheses
➢ Enzootic in certain foreign countries (eg. Turkey,
➢ Vibrio vulnificus
Iran, Pakistan, and Sudan)
○ From shellfish and salt water
➢ Anthrax spores infectious for decades
➢ Obligate anaerobes (usually polymicrobial and foul
○ Biologic welfare experiments (annual tests
smelling)
for 20years)
○ Puncture wounds
➢ Three well-defined cycles
○ Deep wounds
○ Survival of spores in the soil
○ Impaired blood supply
○ Animal infection
➢ Gram negative bacteria
○ o Infection in humans
○ Decubitus ulcer (bed sores)
○ After intestinal “spill”
➢ Primarily a disease of herbivorous animals
➢ Pseudomonas aeruginosa
○ Most commonly transmitted to humans by
○ Catheters and prostheses
direct contact with animal products (eg.
○ Burns and surgical wounds
Wool and hair)
Eye Infection
➢ Also acquired via inhalation & ingestion
○ Increased mortality with these portals of Bacterial Infection
entry

➢ Still poses a threat

○ Importing materials contaminated with
spores from these countries (e.g bones,
hides, and other materials)
○ Usually encountered as an occupational
disease
○ Veterinarians, agricultural workers
Cutaneous Anthrax
➢ Bacillus anthracis
○ G+ and spore forming
○ Farm animals are major reservoir
○ Inhalation, GI, cutaneous
➢ Virulence factors:
○ Capsules
○ Edema factor
○ Lethal factor
➢ Vaccine
Bacterial Diseases of the Eye
○ Toxoid (protective antigen)
○ Effective in short term but not long term ➢ Conjunctivitis (Pinkeye)
○ Haemophilus influenzae
Clinical Presentation of Anthrax ○ Various microbes
➢ 95% human cases are cutaneous infections 1 to 5 ○ Associated with unsanitary contact lenses
days after contact ➢ Neonatal Gonorrheal Ophthalmia
➢ Small, pruritic, non-painful papule ○ Neisseria gonorrhoeae
➢ Hemorrhagic vesicle & ruptures ○ Transmitted to a newborn’s eyes during
passage through the birth canal
 ○ Prevented by treatment of a newborn’s
eyes with antibiotics
Bacterial Infection
Bacterial Diseases of the Eye
➢ Chlamydia Trachomatis
○ Inclusion to conjunctivitis
■ Transmitted to a newborn’s eyes
during passage through the birth
canal
■ Spread through swimming pool
water
■ Treated with tetracycline
➢ Trachoma
○ Leading cause of blindness worldwide
○ Infection causes permanent scarring: scars
abrade the cornea leading to blindness
○ Chronic inflammation of the eyelid
Viral Diseases of the Eye
➢ Conjunctivitis
○ Adenoviruses
➢ Herpetic Keratitis
○ Herpes simplex virus 1 (HHV-1)
○ Infects cornea and may cause blindness
○ Treated with trifluridine
Viral Infection
Protozoan Disease of the Eye
➢ Acanthamoeba Keratitis
○ Transmitted from water
○ Associated with unsanitary contact lenses
Protozoan Infection
➢ Guinea Worm
What is MRSA?
➢ Methicillin-resistant Staphylococcus aureus (MRSA)
➢ Easily transmitted and drug resistant, MRSA can
survive on hands, clothing, environmental surfaces,
and equipment.
➢ About 126,000 hospitalized patients develop MRSA
infections each year
➢ Over 5,000 of those patients die
➢ Staphylococcus aureus is commonly carried on
healthy people’s skin, nares, and perineum.
➢ It may cause superficial skin infections treatable with
beta-lactam inhibitors (such as methicillin).
➢ Over time, some strains have become resistant.
➢ First cases of MRSA in the United States occurred in
the 1960s.
➢ Today, 46 out of 1,000 patients have MRSA.
Controlling the spread of MRSA in the health care facility
➢ Improve hand hygiene
➢ Make fastidious environmental cleaning and
disinfection a priority
➢ Consider performing active surveillance cultures
➢ Identify colonized patients and implement contact
precautions
➢ Implement and perform all interventions from the
central line bundle and the ventilator bundle
Stopping Antimicrobial Drug Resistance
➢ Using antibiotics appropriately is key.
➢ Encourage cultures before antibiotics are started,
and, if necessary, narrow the spectrum of antibiotics
based on culture results.
➢ Review all culture reports to ensure that bacteria are
sensitive to the prescribed antibiotics.
➢ Teach the patient how to use antibiotics:
○ Take as prescribed
○ Finish the course of treatment
○ Don’t take someone else’s prescribed
medication
Two Types of MRSA
➢ Community-associated MRSA (CA-MRSA)
○ Causes skin and soft-tissue infections, such
as boils, blisters, abscesses, folliculitis, and
carbuncles
○ Also, fever and local warmth, swelling, pain,
and purulent drainage
➢ Health-care associated MRSA
○ more highly drug resistant
○ causes more invasive infections, such as
surgical site infection, endocarditis,
osteomyelitis, bacteremia, pneumonia
★ “According to the Centers for Disease Control and
Prevention definition, a diagnosis of CA-MRSA
requires that the patient have no medical history of
MRSA or colonization and no risk factors associated
with healthcare–associated MRSA.”
MRSA Transmission
➢ CA-MRSA
○ Person-to-person by sharing personal items
(clothing and towels)
○ Close contact
➢ Health care-associated MRSA
○ Contaminated environmental surfaces
○ Staff members
CNS & PNS INFECTION
How Microbes Enter the Nervous System
● Skull or backbone fractures
● Medical procedures
● Along peripheral nerves
● Blood or lymph
Microbial Diseases of the Nervous System
● Bacteria can grow in the cerebrospinal fluid in the
subarachnoid space of the CNS
● The blood brain barrier (capillaries) prevents passage of
some materials (such as antimicrobial drugs) into the
CNS
● Meningitis: Inflammation of meninges
● Encephalitis: Inflammation of the brain
Bacterial Meningitis
● Fever, headache, and stiff neck
● Followed nausea and vomiting
● May progress to convulsions and coma
● Diagnosis by gram stain or latex agglutination of CSF
● Treated with cephalosporins
● Symptoms (meningeal symptoms)
o High fever
o Head ache
o Stiff neck
o Irritability (children)
o Neurologic dysfunction
🗶 Lethargy
🗶 Confusion
o Uncharacteristic sleepiness
o Vomiting
Agents: vary depending on the age of the patient
1. Newborns/Neonates
● Group B streptococci
● E. Coli K1
● Listeria Monocytogenes
2. Infants and children up to 24 months old
● Streptococcus pneumoniae
● Neisseria meningitidis
● (Haemophilus influenzae type B- vaccine/self study)
3. Adults
● Streptococcus pneumoniae
● Neisseria meningitidis
Neisseria Meningitis, Meningococcal Meningitis
● N. Meningitidis
o Gram-negative aerobic cocci, capsule
o 10% of people are healthy nasopharyngeal carriers
o Begins as throat infection, rash
o Serotype B is most common in the United States
o Vaccination recommended for college students
o N. Meningitidis causes meningococcal meningitis. This
bacterium is found in the throats of healthy carriers
o The bacteria probably gain access to the meninges
through the bloodstream. The bacteria may be found in
leukocytes in CSF
o Symptoms are due to endotoxin. The disease occurs
most often in young children
o Purified capsular polysaccharide vaccine against
serotypes A, C, Y, and W-135 is available
Neisseria Associated Diseases
o Neisseria meningitidis in Cerebrospinal fluid
Epidemiology of Meningococcal Disease
● Humans only natural hosts
● Person-to-person transmission by aerosolization of
respiratory tract secretions in crowded conditions
● Close contact with infectious person (e.g family
members, day care centers, military barracks, prisons,
and other institutional settings
● Highest incidence in children younger than 5 years and
particularly those younger than 1 year of age as passive
maternal antibody declines and as infants immune
system matures
● Commonly colonize nasopharynx of healthy individuals;
highest oral and nasopharyngeal carriage rates in
school-age children, young-adults and lower
socioeconomic groups

Pathogenesis of Meningococcal Disease

● Specific receptors (GD1 ganglioside) for bacterial

Differential Characteristics
Neisseria Spp
fimbriae on non-ciliated columnar epithelial cells in
of Commonly Isolated nasopharynx of host
● Organisms are internalized into phagocytic vacuoles,
avoid intracellular killing
● Replicate intracellularly and migrate to subepithelial
space

Pathogenesis

● Hyperproduction of endotoxin and blebbing into

surrounding environment (e.g subepithelial spaces,
bloodstream)
● Most clinical manifestations including:
Neisseria Meningitidis o Diffuse vascular damage
o Vasculitis
● Encapsulated small, gram-negative diplococci o Thrombosis
● Second most common cause (behind S. Pneumoniae) of o Disseminated intravascular coagulation
community-acquired meningitis in previously healthy
adults Note: Petechiae have coalesced into hemorrhagic bullae
● Swift progression from good health to life-threatening
disease Immunogenicity
● Pathogenicity:
● Following colonization of the nasopharynx, protective
o Pili-mediated, receptor-specific colonization of
humoral immunity develops against the same or closely
nonciliated cells of nasopharynx
related to organisms of the same group
o Antiphagocytic polysaccharide capsule
● Complement system is required for clearance of the
o Hyperproduction of lipooligosaccharide
organisms
Diseases Associated with Neisseria Meningitidis ● Cross-reactive protective immunity acquired with
colonization by closely related antigenic strains (E.g E.
● Following dissemination of virulent organisms from the Coli K1)
nasopharynx:
o Meningitis Laboratory
o Septicemia (meningococcemia) with or without
● Large numbers of encapsulated small, gram-negative
meningitis
diplococci and PMN seen in cerebrospinal fluid
o Meningoencephalitis
● Transparent, non-pigmented non-hemolytic colonies on
o Pneumonia
chocolate blood agar with enhanced growth in moist
o Arthritis
atmosphere with 5% CO2
o Urethritis
● Oxidase-positive
● Acid production from glucose and maltose
Prevention and Treatment
● Penicillin is drug of choice for treatment in adjunct with
supportive therapy for meningeal symptoms
● Chemoprophylaxis of close contacts with rifampin or
sulfadiazine (if susceptible)
● Polyvalent vaccine is effective in people older than 2
years of age adjunct to chemoprophylaxis
Haemophilus Influenzae Meningitis
● Occurs mostly in children (6 months to 4 years)
● Gram-negative aerobic bacteria, normal throat microbiota
● Capsule antigen type B
● Prevented by HIB vaccine
● H. Influenzae requires blood factors for growth
o There are six types of H. Influenzae based on capsule
differences
● H. Influenzae type B
o The most common cause of meningitis in children under
4 years old
● A conjugated vaccine directed against the capsular
polysaccharide antigen in available
Differential Characteristics
Haemophilus
● Gram-negative bacilli liking blood (as per genus name)
● Obligate parasites of man and animals
● Major pathogens for which humans are natural hosts
o Haemophilus influenzae
🗶 Acute pyogenic, normally invasive infections
🗶 Chronic infections with H. Influenzae as 2o pathogen
o Haemophilus Ducreyi
🗶 True pathogen (i.e not found in healthy individuals)
🗶 STD; soft chancre (chancroid)
Haemophilus Diseases
HIB Vaccine
● Humoral IgG to capsule prevents systemic infection by
opsonisation
● New vaccine composed of type B carbohydrate coupled
to protein has drastically reduced meningitis by HIB
● The vaccine is now part of the standard infant/childhood
regimen
Streptococcus Pneumoniae Meningitis, Pneumococcal
Meningitis
● Gram-positive diplococcic
● 70% of people are healthy nasopharyngeal carriers
● Most common in children (1 month to 4 years)
● Mortality: 30% in children, 80% in elderly
● Prevented by vaccination
● Hospitalized patients and young children are most
susceptible to S. Pneumoniae meningitis
● It is rare but has a high mortality rate
● A conjugated vaccine is available
Listeriosis
● Listeria monocytogenes
● Gram-negative aerobic rod
● Usually foodborne; it can be transmitted to fetus
● Reproduce in phagocytes
● Causes meningitis in newborns, the immune-suppressed,
pregnant women, and cancer patients.
● Acquired by ingestion of contaminated food, it may be
asymptomatic in healthy adults.
● L. monocytogenes can cross the placenta and cause
spontaneous abortion and stillbirth.
● Neonates, elderly & immunocompromised
● Granulomatosis infantiseptica
o Transmitted to fetus transplacentally
o Early septicemic form: 1-5 days post-partum
o Delayed meningitic form: 10-20 days following birth
● Intracellular pathogen
o Cell-mediated and humoral immunity develop
o Only cell-mediated immunity is protective
Listeria Monocytogenes
● Gram-positive beta-hemolytic bacillus
● Multiply at refrigerator temperatures (4oC)
● Tumbling motility at room temperature
● CAMP Test positive (like Group B Streptococcus)
Where do we find Listeria?
● Intestinal tract of mammals & birds (especially chickens)
● Persists in soil
● Soft cheeses & unwashed raw vegetables
● Raw or undercooked food of animal origin
o Luncheon meats
o Hot dogs
● Large scale food recalls have become common
Epidemiology o Spore formation
o Tetanospasmin (heat-labile neurotoxin; blocks release of
● Disease/Bacterial Factors neurotransmitters [i.e gamma-aminobutryic acid,
o Organism can grow in macrophages and epithelial cells glycine] for inhibitory synapses)
o Asymptomatic carriage is possible o Tetanolysin (heat-stable hemolysin of unknown
o Virulent strains produce listeriolysin O significance)
o Can grow in cold temperatures (refrigerators) ● Epidemiology
● Transmission o Ubiquitous; spores are found in most soils and can
o Ingestion of contaminated food products colonize gastrointestinal tract of humans and animals
o Transplacentral o Exposure to spores is common, but disease is
● Who is at risk? uncommon except in underdeveloped countries, where
o Neonates there is poor vaccination compliance and medical care
o Elderly is inadequate
o Pregnant women o Risk is greatest for people with inadequate
o Immunocompromised patients vaccine-induced immunity; disease does not induce
● Geography/Season immunity
o Ubiquitous and worldwide ● Diseases
o Sporadic, with peak occurrence in the warmer months o Generalized tetanus (most common form)
● Modes of Control o Cephalic tetanus (high mortality)
o Penicillin or ampicillin, alone or combination with an o Localized or wound tetanus (good prognosis)
aminoglycoside o Neonatal tetanus (high mortality)
o People at high risk should avoid eating raw or partially ● Diagnosis
cooked food of animal origin; soft cheese, and o Diagnosis is based on clinical presentation
unwashed raw vegetables o Microscopy and culture with poor sensitivity
o Neither tetanus toxin nor antibodies are typically
Tetanus detected
● Treatment, Prevention, and Control
● Clostridium tetani
o Treatment requires debridement, antibiotic therapy
● Gram-positive, endosporeforming, obligate anaerobe
(metronidazole), passive immunization with antitoxin
● Grows in deep wounds.
globulin, and vaccination with tetanus toxoid
● Tetanospasmin released from dead cells blocks
o Prevention through use of vaccination, consisting of
relaxation pathway in muscles.
three doses of tetanus toxoid followed by boosters every
● Prevention by vaccination with tetanus toxoid (DTP) and
10 years.
booster (dT).
● Treatment with tetanus immune globulin. Clinical Forms of Tetanus
● Produces the neurotoxin tetanospasmin, which causes
the symptoms of tetanus:
o Spasms
o Contraction of muscles controlling the jaw
o Death resulting from spasms of respiratory muscles.
● Grow in deep, unclean wounds and wounds with little
bleeding.
o Acquired immunity results from DPT immunization that
includes tetanus toxoid.
o Following an injury, an immunized person may receive a
booster of tetanus toxoid.
o An unimmunized person may receive (human) tetanus
immune globulin.
o Debridement (removal of tissue) and antibiotics may be
used to control the infection.

Summary of C. Tetani Infections

● Physiology and Structure

o Gram-positive bacilli with prominent terminal spores
(drumstick appearance)
o Strict anaerobe (vegetative cells are extremely oxygen
sensitive) Botulism
o Difficult to isolate from clinical specimens
● Virulence ● Clostridium botulinum
● Gram-positive, endospore-forming, obligate anaerobe
● Intoxication comes from ingesting botulinal toxin.
● Botulinal toxin blocks release of neurotransmitter causing
flaccid paralysis.
● Prevention
o Proper canning
o Nitrites prevent endospore germination in sausages.
● Botulism is caused by an exotoxin produced by C.
botulinum growing in foods.
● Serological types of botulinum toxin vary in virulence,
with type A being the most virulent.
● The toxin is a neurotoxin that inhibits the transmission of
nerve impulses.
● Type A
o 60-70% fatality, most heat resistant and proteolytic
o Found in CA, WA, CO, OR, NM
● Type B
o 25% fatality; proteolytic and non-proteolytic
o Europe and Eastern United States
● Type E
o Found in marine and lake sediments
o Pacific Northwest, Alaska, Great Lakes Area
o Non-proteolytic grow in ref temperature and less
anaerobic condition
● Blurred vision occurs in 1 to 2 days
● Progressive flaccid paralysis follows for 1 to 10 days
● Possibly resulting in death from respiratory and cardiac
failure
● C. botulinum will not grow in acidic foods or in an aerobic
environment.
● Endospores are killed by proper canning. The addition of
nitrites to foods inhibits growth after endospore
germination.
● The toxin is heat labile and is destroyed by boiling
(100°C) for 5 minutes
● Treatment: Supportive care and antitoxin.
● Infant botulism results from C. botulinum growing in
intestines.
● Wound botulism results from growth of C. botulinum in
wounds.
● For diagnosis, mice protected with antitoxin are
inoculated with toxin from the patient or foods.
Summary of C. Botulinum Infections
● Physiology and Structure
o Gram-positive, spore-forming bacillus
o Strict anaerobe (vegetative cells extremely
oxygen-sensitive)
o Fastidious growth requirements
o Can produce one of seven distinct botulinum toxins
(A-G)
o Strains associated with human disease produce lipase,
digest milk proteins, hydrolyze gelatine, and ferment
glucose
● Virulence
o Spore formation
o Botulinum toxin (prevents release of neurotransmitter
acetylcholine)
o Binary toxin
● Epidemiology
o Ubiquitous; C. Botulinum spores are found in soil
worldwide
o Human diseases associated with toxins A, B, E and F
o Relatively few cases of botulism in the United States
o Infant botulism more common than other forms
● Diseases
o Foodborne botulism
o Infant botulism
o Wound botulism
● Diagnosis
o Botulism confirmed by isolating the organism or
detecting the toxin in food products or the patient’s feces
or serum
● Treatment, Prevention, and Control
o Treatment involves administration of metronidazole or
penicillin, trivalent botulinum antitoxin, and ventilator
support
o Spore germination in foods prevented by maintaining
food in an acid pH, by high sugar content (e.g fruit
preserves), or by storing the foods at 4oC or colder
o Toxin is hear-labile so can be destroyed by heating of
food for 20 minutes at 80oC
o Infant botulism is associated with consumption of
contaminated foods (particularly honey). Infants younger
than 1 year should not be given honey or foods
containing it.
Diagnosis
Leprosy
● Mycobacterium leprae
● Causes leprosy, or Hansen’s disease.
● Acid-fast rod that grows best at 30°C.
● Grows in peripheral nerves and skin cells.
● Transmission requires prolonged contact with an infected
person.
● Leprosy is not highly contagious and is spread by
prolonged contact with exudates.
● Untreated individuals often die of secondary bacterial
complications, such as tuberculosis.
● Patients with leprosy are made noncontagious within 4 to
5 days with sulfone drugs and then treated as
outpatients.
● Leprosy occurs primarily in the tropics.
● Laboratory diagnosis is based on observations of
acid-fast rods in lesions or fluids and the lepromin test
Mycobacterial Clinical Symptoms
Mycobacterium Leprae Infections
● Diseases
o Tuberculosis form of Leprosy
o Lepromatous form of leprosy
o Intermediate forms of leprosy
● Diagnosis
o Microscopy is sensitive for the lepromatous form but not
the tuberculoid form
o Skin testing required to confirm tuberculoid leprosy
o Culture cannot be used
● Treatment, Prevention and Control
o Dapsone with or without rifampin is used to treat the
tuberculoid form of disease; clofazimine is added for the
treatment of lepromatous form. Therapy is prolonged
o Dapsone is recommended for long-term prophylaxis in
treated patient
o Disease is controlled through the prompt recognition
and treatment of infected people
Tuberculoid vs. Lepromatous Leprosy
Clinical Manifestations and Immunogenicity
Poliomyelitis
● Poliovirus
● Transmitted by ingestion.
● Initial symptoms: Sore throat and nausea
● Viremia may occur; if persistent, virus can enter the CNS;
destruction of motor cells and paralysis occurs in <1% of
cases
● Prevention is by vaccination (enhanced-inactivated polio
vaccine)
● The symptoms of poliomyelitis
o Headache
o Sore throat
o Fever
o Stiffness of the back and neck
o Occasionally paralysis (fewer than 1% of cases)
● Poliovirus is transmitted by the ingestion of water
contaminated with feces
● Poliovirus first invades lymph nodes of the neck and
small intestine.
● Viremia and spinal cord involvement may follow.
● Diagnosis is based on isolation of the virus from feces
and throat secretions
● The Salk vaccine (an inactivated polio vaccine, or IPV)
o Involves the injection of formalininactivated viruses and
boosters every few years
● The Sabin vaccine (an oral polio vaccine, or OPV)
o Contains three live, attenuated strains of poliovirus and
is administered orally.
● Polio is a good candidate for elimination through
vaccination.
Rabies Virus (Rhabdovirus)
● Transmitted by animal bite.
● Virus multiplies in skeletal muscles, then brain cells
causing encephalitis.
● Initial symptoms may include muscle spasms of the
mouth and pharynx and hydrophobia.
● Furious rabies: Animals are restless then highly
excitable.
● Paralytic rabies: Animals seem unaware of surroundings.
● Pre-exposure prophylaxis: Infection of human diploid
cells vaccine.
● Post-exposure treatment: Vaccine plus immune globulin.
● Rabies virus (a rhabdovirus) causes an acute, usually Stages:
fatal, encephalitis called rabies.
o Rabies may be contracted through bite of a rabid animal ● Contamination
o By inhalation of aerosols o In almost all cases: Is due to a bite, scratch or even lick
o Invasion through minute skin abrasions on mucus membrane from animals (dogs) whose saliva
● The virus multiplies in skeletal muscle and connective contains the virus
tissue. o In very exceptional cases: By inhaling virulent aerosol
● Encephalitis occurs when the virus moves along (laboratory experiment, exploration of enclosed caves
peripheral nerves to the CNS. inhabited by infected bats)
● Symptoms of rabies include o In very exceptional cases: by transmission: man to man
o Spasms of mouth and throat muscles followed by 🗶 Indirectly: transplantation of infected cornea
extensive brain and spinal cord damage 🗶 Directly: from a bite or through saliva of an infected
o Death person
● Laboratory diagnosis may be made by direct FA tests of ● Incubation Period
saliva, serum, and CSF or brain smears. o Extraordinarily variable from 4 days to 7 years after
● Reservoirs for rabies in the United States include exposure
skunks, bats, foxes, and raccoons. Domestic cattle, dogs, o Generally 20-90 days
and cats may get rabies. Rodents and rabbits seldom get o Major influencing factors
rabies. 🗶 The virus load
● Current post-exposure treatment includes administration 🗶 The virus strain
of human rabies immune globulin (RIG) along with 🗶 The severity of exposure
multiple intramuscular injections of vaccine. 🗶 The localization of the exposure
● Pre-exposure treatment consists of vaccination. ● Prodrome
● Other genotypes of Lyssavirus cause rabies-like o Last from 2 to 10 days
diseases. o Non-specific symptoms
🗶 Malaise
How Rabies is Transmitted? 🗶 Fatigue
🗶 Headache
● Virus transmitted by infected saliva through bite or wound 🗶 Fever
🗶 Pain or paresthesia close to the site of exposure
● Clinical symptoms (Acute Neurologic Phase)
o Last 2 to 12 days
o Two clinical forms:
🗶 Encephalitic (furious) rabies, 80% of cases
▪ Fluctuating consciousness (agitation, depression,
aggressiveness)
▪ Phobic spasms (hydrophobia)
▪ Autonomic dysfunction (fixed dilated pupils)
▪ Paralysis
🗶 Paralytic (dumb) rabies, 20% of cases
▪ Guillain-Barre-like syndrome (with fever)
▪ Complete paralysis
Course of the virus in the Body ● Coma and Death
o Both clinical forms of rabies will progress to coma and
death
o Within 2-12 days, coma begins
o Death is inevitable and due to complications of
cardiorespiratory failure

Treatment & Prophylaxis

● Post-exposure (PET)
● Pre-exposure Prophylaxis (PEP)

Clinical Manifestations in Humans

Note: Once the first clinical symptoms appear, rabies is nearly

always fatal
Principle for Post-Exposure Treatment
Guidelines of Post-Exposure Treatment Steps
PET-Local Wound Treatment
● Aims to remove as much of the virus possible from the
site of inoculation by:
o Physically removing virus particles
o Further inactivation of the remaining virions by chemical
disruption
● Immediately: Vigorous washing and flushing of wound(s)
with water and soap or detergent
● Then: application of virucidal treatment such as alcohol
(70%), tincture or iodine solution
DOH Guidelines for Post-Exposure Treatment
Category I
Category II
Category III
Pre-Exposure Prophylaxis
Arboviral Encephalitis
● Arboviruses are arthropodborne viruses that belong to
several families
● Prevention is by controlling mosquitoes
● Symptoms of encephalitis are
o Chills
o Headache
o Fever
o Coma
● Many types of viruses (called arboviruses) transmitted by
mosquitoes caused by encephalitis
● The incidence of arboviral encephalitis increases in the
summer months, when mosquitoes are most numerous.
● Notifiable arboviral infections are
o Eastern equine encephalitis (EEE),
o Western equine encephalitis (WEE),
o St. Louis encephalitis (SLE),
o California encephalitis (CE),
o West Nile virus (WNV)
● Diagnosis is based on serological tests
● Control of the mosquito vector is the most effective way
to control encephalitis
Cryptococcus Neoformans Meningitis (Cryptococcosis)

● Soil fungus associated with pigeon and chicken

droppings.
● Transmitted by the respiratory route; spreads through
blood to the CNS.
● Mortality up to 30%.
● Treatment: Amphotericin B and flucytosine.
● Cryptococcus neoformans is an encapsulated yeastlike
fungus that causes cryptococcosis.
● The disease may be contracted by inhalation of dried
infected pigeon or chicken droppings.
● The disease begins as a lung infection and may spread
to the brain and meninges Naegleria Fowleri
● Cryptococcal Meningitis- a horizontal section of the brain
● Protozoan infects nasal mucosa from swimming water.
● Immunosuppressed individuals are most susceptible to
● Encephalitis caused by the protozoan Naegleria fowleri is
Cryptococcus neoformans meningitis.
almost always fatal.
● Diagnosis is based on latex agglutination tests for
● Granulomatous amebic encephalitis, caused by
cryptococcal antigens in serum or CSF.
Acanthamoeba spp. and Balamuthia mandrillaris, is a
African Trypanosomiasis chronic disease.
● N. fowleri trophozoites cultured from cerebrospinal fluid:
● Trypanosoma brucei gambiense infection is chronic (2 to cells have characteristically large nuclei, with a large,
4 years). dark staining karyosome. The amebae are very active
● T. b. rhodesiense infection is more acute (few months). and extend and retract broad pseudopods. Trichrome
● Transmitted from animals to humans by tsetse fly. stain.
● Prevention: Elimination of the vector. ● Naegleria spp.: trophozoite stained with Greenstein’s five
● Treatment: Eflornithine blocks an enzyme necessary for dye stain and observed under dark field microscope.
the parasite.
● Parasite evades the antibodies through antigenic Protozoa from Other Body Sites
variation.
Free Living Amebae
● African trypanosomiasis is caused by the protozoa
Trypanosoma brucei gambiense and T. b. rhodesiense
● Disease
and transmitted by the bite of the tsetse fly.
o Naegleria: Primary Amebic Meningoencephalitis (PAM)
● The disease affects the nervous system of the human
o Acanthamoeba: Chronic Granulomatous Amebic
host, causing lethargy and eventually coma. It is
Encephalitis and keratitis
commonly called sleeping sickness.
● Lab Dx:
● Vaccine development is hindered by the protozoan’s
o Direct microscopic exam (Wheatley’s trichrome stain);
ability to change its surface antigens.
culture of organism by inoculation of sample onto
nonnutritive agar seeded w/ E. coli or E. aerogenes
Trypanosoma Brucei
● Portal of Entry:
o Naegleria: nose
o Acanthamoeba: respiratory tract or ulcers in skin or
mucosa / direct invasion of eye
● Source of Infection:
o Naegleria: warm lakes, streams, ponds or inadequately
chlorinated swimming pools
o Acanthamoeba: immunocompromised or debilitated
host

● Lab Dx: Giemsa stained thick and thin blood smears or
lymph exudate (early stage); Giemsa stained smears of
CSF (late stage)
● Dividing forms are seen in African trypanosomiasis, but
not in American trypanosomiasis (Chagas' disease)
● Ramana’s Sign: Unilateral Conjunctivitis and orbital
edema
Prions
● Diseases of the CNS that progress slowly and cause
spongiform degeneration are caused by prions.
● Sheep scrapie and bovine spongiform encephalopathy
(BSE) are examples of diseases caused by prions that
are transferable from one animal to another.
● Creutzfeldt -Jakob disease and kuru are human diseases
similar to scrapie. They are transmitted between humans.
● Prions are self -replicating proteins with no detectable CARDIOVASCULAR AND LYMPHATIC DISEASE
nucleic acid.
Cardiovascular and Lymphatic System
Transmissible Spongiform Encephalopathies
● Blood: transports nutrients to and wastes from cells
● Caused by prions ● WBCs: Defend against infection
o Sheep scrapie ● Lymphatic: transport interstitial fluid to blood
o Creutzfeldt-Jakob disease ● Lymph nodes: contain fixed macrophages
o Kuru
o Bovine spongiform encephalopathy Sepsis and Septic Shock
● Transmitted by ingestion or transplant or inherited
● Chronic and fatal ● Sepsis: bacteria growing in the blood
● Severe sepsis: decrease in blood pressure
● Septic shock: low blood pressure cannot be controlled

Sepsis

● Gram-negative Sepsis
o Endotoxins caused blood pressure decrease
o Antibiotics can worsen condition by killing bacteria
● Gram-positive Sepsis
o Nosocomial Infections
🗶 Staphylococcus aureus
🗶 Streptococcus pyogenes
🗶 Group B streptococcus
🗶 Enterococcus faecium and E. Faecalis

Sepsis

● Puerperal sepsis (childbirth fever)

o Streptococcus pyogenes
o Transmitted to mother during childbirth by attending
physicians and midwives.

Bacterial Infections of the Heart

● Endocarditis: Inflammation of the endocardium

● Subacute bacterial endocarditis: Alpha - hemolytic
streptococci from mouth
● Acute bacterial endocarditis: Staphylococcus aureus from
mouth
● Pericarditis: Streptococci

Rheumatic Fever

● Inflammation of heart valves

● Autoimmune complication of Streptococcus pyogenes
infections
● RF is characterized by a constellation of findings
● Major Manifestations
o Migratory polyarthritis of the large joints
o Carditis
o Subcutaneous nodules
o Erythema marginatum of the skin
o Sydenham chorea, a neurologic disorder with
involuntary purposeless, rapid movements
● Minor manifestations (nonspecific signs and symptoms)
o fever, arthralgia
o elevated blood levels of acute phase reactants CRP,
ESR, ASO
 o The diagnosis is established by the so - called Jones ● 1972: International agreement to not possess biological
criteria: weapons.
🗶 Evidence of a preceding group A streptococcal ● 1979: B. anthracis weapons plant explosion in the Soviet
infection, with the presence of two of the major Union.
manifestations listed above or one major and two ● 1984: S. enterica used against the people of The Dalles.
minor manifestations ● 2001: B. anthracis distributed in the United States
● After an initial attack, there is increased vulnerability to
reactivation of the disease with subsequent pharyngeal Gangrene
infections, and the same manifestations are likely to
appear with each recurrent attack.
● Carditis is likely to worsen with each recurrence, and
damage is cumulative.
● Valvular disease
o Cardiac murmurs, cardiac hypertrophy and dilation, and
heart failure, arrhythmias (particularly atrial fibrillation in
the setting of mitral stenosis), thromboembolic
complications, and infective endocarditis.

Tularemia

● Francisella tularensis, gram-negative rod

● Transmitted from rabbits and deer by deer flies.
● Bacteria reproduce in phagocytes.

Brucellosis (Undulant Fever)

● Brucella, gram-negative rods that grow in phagocytes.

● B. abortus (elk, bison, cows)
● B. suis (swine)
● B. melitensis (goats, sheep, camels)
● Undulating fever that spikes to 40°C each evening.
● Transmitted via milk from infected animals or contact with
infected animals. ● Ischemia: Loss of blood supply to tissue.
● Necrosis: Death of tissue.
Anthrax
● Gangrene: Death of soft tissue.
● Gas gangrene
● Bacillus anthracis, gram-positive, endospore-forming
o Clostridium perfringens, gram positive,
aerobic rod
endospore-forming anaerobic rod, grows in necrotic
● Is found in soil.
tissue • Treatment includes surgical removal of necrotic
● Cattle are routinely vaccinated.
tissue and/or hyperbaric chamber
● Treated with ciprofloxacin or doxycycline.
● Cutaneous anthrax
Animal Bites and Scratches
o Endospores enter through minor cut
o 20% mortality ● Pasteurella multocida
● Gastrointestinal anthrax ● Clostridium
o Ingestion of undercooked food contaminated food ● Bacteroides
o 50% mortality. ● Fusobacterium
● Inhalational anthrax ● Bartonella hensellae: Cat-scratch disease
o Inhalation of endospores.
o 100% mortality Plague

Biological Weapons ● Yersinia pestis, gram-negative rod

● Reservoir: Rats, ground squirrels, and prairie dogs
● 1346: Plague-ridden bodies used by Tartar army against ● Vector: Xenopsylla cheopsis
Kaffa. ● Bubonic plague: Bacterial growth in blood and lymph
● 1925: Plaque-carrying flea bombs used in the ● Septicemia plague: Septic shock
Sino-Japanese War. ● Pneumonic plague: Bacteria in the lungs
● 1950s: U.S. Army spraying of S. marcescens to test
weapons dispersal.
Relapsing Fever ● Cytomegalovirus (Human herpesvirus 5)
● Infected cells swell (cyto-, mega-)
● Borrelia spp., spirochete ● Latent in white blood cells
● Reservoir: Rodents ● May be asymptomatic or mild
● Vector: Ticks ● Transmitted across the placenta; may cause mental
● Successive relapses are less severe retardation
● Transmitted sexually, by blood, or by transplanted tissue
Lyme Disease
Viral Hemorrhagic Fevers
● Borrelia burgdorferi
● Reservoir: Deer
● Vector: Ticks
● First symptom: Bull's eye rash
● Second phase: Irregular heartbeat, encephalitis
● Third phase: Arthritis

Ehrlichiosis

● Ehrlichia, gram-negative, obligately intracellular (in white

blood cells) American Trypanosomiasis (Chaga’s Disease)
● Reservoir: Deer, rodents
● Vector: Ticks ● Trypanosoma cruzi
● Reservoir: Rodents, opossums, armadillos
Typhus ● Vector: Reduviid bug

● Epidemic typhus Toxoplasmosis

o Rickettsia prowazekii
o Reservoir: Rodents ● Toxoplasma Gondii
o Vector: Pediculus humanus corporis
Malaria
o Transmitted when louse feces rubbed into bite wound
● Epidemic murine typhus:
● Plasmodium vivax, P. ovale, P. malariae, P. falciparum
o Rickettsia typhi
● Anopheles mosquito
o Reservoir: Rodents
o Vector: Xenopsylla cheopsi Other Protozoa

Spotted Fevers (Rocky Mountain Spotted Fever) BLOOD and TISSUE PROTOZOA

● Rickettsia rickettsii ● Plasmodium

● Measles-like rash except that the rash appears on palms ● Babesia
and soles too ● Trypanosoma brucei
● Trypanosoma cruzi
Human Herpesvirus 4 Infections
● Toxoplasma gondii
● Leishmania
Ebstein Barr Virus EBV
Protozoa from other Body Sites
● Infectious Mononucleosis
● Childhood infections are asymptomatic.
● Free-living Amebae
● Transmitted via saliva
o Naegleria
● Characterized by proliferation of monocytes
o Acanthamoeba
● Trichomonas vaginalis
Burkitt’s lymphoma
Plasmodium
● Nasopharyngeal carcinoma
● Cancer in immunosuppressed individuals, and malaria
● Disease: Malaria
and AIDS patients
o P. vivax: Benign tertian malaria
o P. malariae: Quartan malaria
Cytomegalovirus Infections
o P. falciparum: Malignant tertian malaria
 o P. ovale: Ovale tertian malaria
● Lab Dx: Giemsa stained thick and thin blood smears; IFA;
PCR
● Infected RBC:
o P. vivax and P. ovale: reticulocytes
o P. malariae: senescent erythrocytes
o P. falciparum: erythrocytes of all ages
● Cyclic paroxysm of fever:
o P. vivax and P. ovale: every 48 hours
o P. malariae: every 72 hours
o P. falciparum: every 36-48 hours
Note: Gametocytes of P. falciparum in thin blood smears.
Note the presence of a “Laveran’s bib”, which is not always
visible.
Trypanosoma Brucei
● Disease: African trypanosomiasis
o T. b. gambiense: Gambian trypanosomiasis, West &
Mid-African sleeping sickness
o T. b. rhodesiense: Rhodesian trypanosomiasis, East
African sleeping sickness
● Lab Dx: Giemsa stained thick and thin blood smears or
lymph exudate (early stage); Giemsa stained smears of
CSF (late stage)
● Site in host: lymph glands, blood stream, brain
● Portal of entry: skin
● Source of infection: tsetse fly
● Winterbottom’s sign: enlargement of posterior cervical
LNs
Trypanosoma Cruzi
● Disease: American trypanosomiasis, Chagas disease
● Lab Dx: Giemsa stained thick and thin blood smears for
the trypomastigote; histopath exam for the amastigote
● Site in host: Tissues – heart; blood
● Portal of entry: skin
● Source of infection: Kissing bug Triatomidae
● Trypomastigote: shape is short & stubby to long &
slender; in Giemsa stained blood films – C or U shaped;
kinetoplast is large, oval & located posterior to the
nucleus; anterior long free flagellum
● Riduviid bug: the vector of American trypanosomiasis
Ramana’s Sign
● Unilateral conjunctivitis and orbital edema
Toxoplasma Gondii
● Disease: Toxoplasmosis
● Site in host: All organs
● Portal of entry:
o Ingestion of oocyst contaminated water
o Aerosolization of oocyst contaminated dust or litter
o Consumption of raw or undercooked cyst infected meat
o Transplacental passage of the tachyzoite
● Definitive host: domestic cats
● Intermediate host: infected rodents
● Accidental intermediate host: humans
● Lab Dx: IFAT and ELISA; Giemsa-stained smears of
exudates, aspirates or tissues
Note: T. gondii tachyzoites: crescentic to pyriform shaped
with a prominent, centrally placed nucleus.
Leishmania
● Disease
o L. tropica complex: Old Word Cutaneous leishmaniasis
(oriental sore, Aleppo boil, Delhi ulcer, Baghdad boil)
o L. mexicana complex: New Word Cutaneous
leishmaniasis (chiclero ulcer, bay sore)
o L. braziliensis complex: Mucocutaneous leishmaniasis
(espundia, uta)
o L. donovani: Visceral leishmaniasis (kala-azar or black
disease, Dumdum fever)
● Lab Dx: Giemsa stained tissue sections or impression
smears
● Site in host: Monocytes/macrophages of skin & mucosa
● Portal of entry: Skin
● Source of infection: Phlebotomus or Lutzomyia fly
Note: L. tropica amastigotes: ovoid in shape; large &
eccentric nucleus; small, rodlike kinetoplast positioned
opposite the nucleus; rodlike axoneme perpendicular to the
kinetoplast
Babesia
● Disease: Babesiosis
● Lab Dx: Giemsa stained thick and thin blood smears
● Babesia microti infection, Giemsa stained thin smear.
The organisms resemble P. falciparum; however Babesia
parasites present several distinguishing features: they
vary more in shape and in size; and they do not produce
pigment
Schistosomiasis
● Tissue damage (granulomas) in response to eggs lodging
in tissues
 Microfi Lariae

Wuchereria Bancrofti

● Disease: Bancroftian filariasis, wuchereriasis

● Site in host: Lymphatics
● Portal of entry: Skin
● Definitive Host: human
● Intermediate Host: mosquito (Culex, Aedes, Anopheles
species)
Schistosoma Mansoni ● Sources of infection: Mosquitoes
● Lab Dx: Blood smear
● Disease: Schistosomiasis, intestinal schistosomiasis, ● Periodic form: between 10 am and 2am
bilharziasis “snail fever” ● Subperiodic form: between 2 and 5 pm
● Site in host: veins of LI ● Microfilariae: sheathed; nuclei do not extend to tip of tail
● Portal of entry: skin
● Definitive host: humans, baboons & rodents Note: Brugia malayi /Wuchereria bancrofti: B.malayi is
-Intermediate host: snail (Biomphalaria sp & Tropicorbis transmitted by mosquitoes of the genus Mansonia, Anopheles
sp) and Aedes. W.bancrofti is transmitted by mosquitoes of the
● Infective stage: cercariae genus Culex, Anopheles and Aedes.
● Lab Dx: eggs in stool; rectal or liver biopsy
Note: Microfilaria of Wuchereria bancrofti: sheathed, its body
Note: Schistosoma mansoni eggs: large (length 114 to 180 is gently curved, and the tail is tapered to a point. The nuclear
µm) and have a characteristic shape, with a prominent lateral column (the cells that constitute the body of themicrofilaria) is
spine near the posterior end. The anterior end is tapered and loosely packed, the cells can be visualized individually and do
slightly curved. When the eggs are excreted, they contain a not extend to the tip of the tail.
mature miracidium
Brugiya Malayi
Schistosomia Haematobium
● Disease: Malayan filariasis
● Disease: Urinary schistosomiasis, schistosomal ● Site in host: Lymphatics
hematuria, urinary bilharziasis ● Portal of entry: Skin
● Site in host: veins of urinary bladder ● Definitive Host: human, monkey & cat
● Portal of entry: skin ● Intermediate Host: mosquito (Mansonia, Aedes,
● Definitive host: humans, monkeys & baboons Anopheles species)
● Intermediate host: snail (Bulinus, Physopsis, and ● Sources of infection: Mosquitoes
Biomphalaria sp ● Lab Dx: Blood smear Periodic (nocturnal) form: between
● Infective stage: cercariae 10 am and 2am
● Lab Dx: eggs in stool; cystoscopy ● Subperiodic form: between 9 and 11 pm
● Microfilariae: sheathed; nuclei exted to tip of tail w/ 2
Note: S. haematobium eggs: large and have a prominent separated & swollen terminal nuclei
terminal spine at the posterior end

Schistosomia Japonicum
● Disease: Schistosomiasis, Katayama fever
● Site in host: veins of SI
● Portal of entry: skin
● Definitive host: humans, dogs, cats, horses, pigs, cattle,
deer, caribou & rodents
● Intermediate host: snail (Oncomelania)
● Infective stage: cercariae
● Lab Dx: eggs in stool; liver biopsy
Note: S. japonicum egg: typically oval or subspherical, and
has a vestigial spine (smaller than those of the other species)
Loa Loa
● Disease: Loiasis, eye worm, fugitive swellings, Calabar
swellings
● Site in host: Subcutaneous
● Portal of entry: Skin - Definitive Host: human and monkey
● Intermediate Host: fly (Chrysops)
● Sources of infection: fly
● Lab Dx: Blood smear Diurnal periodicity: between 11 am
and 1 pm
● Microfilariae: sheathed; nuclei extend to tip of tail
Manzonella Ozzardi and Manzonella Perstans ● Microbes usually enter the urinary system through
the urethra
● Disease: Ozzardi filariasis/Perstan filariasis ● Microbes usually enter the reproductive system
● Site in host: body cavities through vagina (females) or urethra (males)
● Portal of entry: Skin
● Definitive Host: human Normal Microbiota
● Intermediate Host: midge (Culicoides & Simulium) -
Sources of infection: midge ● Urinary bladder and upper urinary tract sterile
● Lab Dx: Blood smear
● Lactobacilli predominant in the vagina
● Microfilariae found in blood: No periodicity; unsheathed;
● >1,000 bacteria/ml or 100 coliforms/ml of urine
nuclei do not extend to tip of tail (M. ozzardi)/extend to tip
indicates infection
of tail (M. perstan)

Manzonella Streptocerca Cystitis

● Disease: Ozzardi filariasis/Perstan filariasis ● Usually caused by

● Site in host: body cavities o E. coli
● Portal of entry: Skin o S. saprophyticus
● Definitive Host: human ● May also be caused by
● Intermediate Host: midge (Culicoides & Simulium) o Proteus
● Sources of infection: midge - Lab Dx: Blood smear
o Klebsiella
● Microfilariae found in skin: No periodicity; unsheathed;
o Enterococcus
nuclei extend to tip of tail
o Pseudomonas
Onchocerca Volvulus ● E. coli usually causes pyelonephritis.
● Antibiotic-sensitivity tests may be required before
● Disease: Onchocerciasis, onchocercosis, river blindness, treatment.
“Sowda”
● Site in host: Subcutaneous UTI
● Portal of entry: Skin
● Definitive Host: human ● Ureteritis
● Intermediate Host: fly (Simulium) o Inflammation of ureter (maybe caused by stone in
● Sources of infection: fly the ureter)
● Lab Dx: skin biopsy or snips, nodule aspirate
● Cystitis
● Microfilariae found in skin: No periodicity; unsheathed;
o Inflammation of bladder (caused by ascending
nuclei do not extend to tip of tail
bacterial infection usually E. coli)
Dracunculus Medinensis, The Guinea Worm ● Urethritis
o Inflammation of urethra (may lead to prostatitis
● Disease: Dracontiasis, dracunculosis, guinea worm and epididymitis)
disease
● Site in host: Subcutaneous Factors that Contribute to UTI
● Portal of entry: Mouth
● Definitive Host: human & domesticated and wild fur ● Female (proximity to the anus, shorter urethra)
bearing animals ● Poor hygiene
● Intermediate Host: water flea (Cyclops)
● Unsafe sexual practices
● Sources of infection: fly
● Back to front stroke
● Lab Dx: skin biopsy or snips, nodule aspirate
● Microfilariae found in skin: No periodicity ● High pH
● Urinary stasis
Note: D. medinensis worm wound around matchstick.This ● Kidney stones
helminth is gradually withdrawn from the body by winding the ● Obstruction of urine outflow
stick.
S/Sx:
GENITOURINARY INFECTION
GENITOURINARY INFECTION ● Pain assessment
● Pain during and after urination= cystitis
Microbial Diseases of the Urinary and Reproductive ● Pain after urination= urethritis
Systems
● Inguinal pain= ureteritis
● Flank pain= pyelonephritis ● Characterized by an acute febrile jaundice &
● Inflammatory manifestations fever and chills immune complex glomerulonephritis
● Incubation period usually 10-12 days with
Cx: flu-like illness usually progressing through two
clinical stages:
● Ascending Infection ● Leptospiremia develops rapidly after infection
● Obstruction (usually lasts about 7 days) without local lesion
(stones/calculi) o Infects the kidneys and organisms are shed
Management in the urine (leptospiruria) with renal failure
● E. Coli (most common C.A) and death not uncommon
● Increase fluids ● Hepatic injury & meningeal irritation is common
Clinical Progression of Icteric (Weil’s Disease) and
● Warm sitz bath
Anticteric Leptospirosis
● Empty the bladder
● Good hygiene
● Observe safe sexual practice
● Front to back stroke
● Acidify urine (cranberry juice, prune, plums)
● C/S test before giving antibiotics
● For urosepsis, give aminoglycosides
● Observe complications

Leptospirosis

● Leptospira interrogans
● Reservoir: Dogs and rats
● Transmitted by skin/mucosal contact from
urine- contaminated water
● Diagnosis: Isolating bacteria or serological tests
Silver Stain of Leptospira Interrogans serotype
icterohaemorrhagiae
● Obligate Aerobes: Characteristic hooked ends
(like a question mark, thus the species
epithet-interrogans)
Epidemiology of Leptospirosis
● Mainly a zoonotic diseases
● Transmitted through breaks in the skin or
intact mucus membranes
● Indirect contact (soil, water, food) with infected
urine from an animal with leptospiruria
● Occupational disease of animal handling
Comparison of Diagnostic Tests for Leptospirosis

Leptospirosis Clinical Syndromes

● Mild virus-like syndrome

● (Anicteric leptospirosis) Systemic with aseptic
meningitis
● (Icteric leptospirosis) Overwhelming disease
(Weil’s disease)
o Vascular collapse
o Thrombocytopenia
o Hemorrhage
o Hepatic and renal dysfunction
● NOTE: Icteric refers to jaundice (yellowing of Sexually Transmitted Diseases (STDs)
skin and mucus membranes by deposition of
bile) and liver involvement ● Prevented by condoms
● Treated with antibiotics
Pathogenesis of Icteric Leptospirosis
Gonorrhea
● Leptospirosis, also called Weil’s disease in humans
● Direct invasion and replication in tissues ● Neisseria gonorrhoeae
 ● Attaches to oral or urogenital mucosa by fimbriae.
● Females may be asymptomatic; males have
painful urination and pus discharge.
● Treatment is with antibiotics.
● If left untreated, may result in
o Endocarditis
o Meningitis
o Arthritis
o Ophthalmia neonatorum
Pelvic Inflammatory Disease
● Gram stain
● Culture
● Nucleic acid probes
Management
● Ceftriaxone (Rocephin) 250 mg lM
● Ofloxacin (Floxin) 400 mg orally
● Treat concurrently with Doxycycline or Azithromycin
for 50% infected with Chlamydia
Complication

● N Gonorrhoeae ○ PID
● C. trachomatis ○ Ectopic pregnancy and infertility
● Can block uterine tubes ○ Peritonitis
● Chronic abdominal pain ○ Perihepatitis
● Neisseria gonorrhea, gram positive diplococci (IP: ○ Ophthalmia neonatorum
3-7 days) ○ Sepsis
○ Arthritis
Signs and Symptoms
○ Infertility

● Females usually asymptomatic or minimal urethral

Gonorrhea Treatment
discharge with lower abdominal pain
● Male mucopurulent discharge, painful urination
○ Patient and partner should be treated
○ Drugs of choice:
Gonorrhea Manifestations in Men
■ Ceftriaxone
● Urethritis ■ Quinolone
● Epididymitis
Nongonococcal Urethritis
● Proctitis
● Pharyngitis
○ Chlamydia Trachomatis
■ May be transmitted to a newborn’s eye
Gonorrhea Manifestations in Women
■ Painful urination and watery discharge
● Urethritis ○ Mycoplasma hominis
● Endocervicitis ○ Ureaplasma urealyticum
● Proctitis ○ Chlamydia Trachomatis, Gram negative (IP. 2-10
Days)
● PID
● Pharyngitis
Signs and Symptoms

Gonorrhea Disseminated Infection

○ Maybe asymptomatic
○ Gray white discharge, burning and itchiness at the
● Arthritis
urethral openin
● Dermatitis
DX:
● Pericarditis and endocarditis
● Meningitis ○ Gram stain
● Perihepatitis ○ Antigen detection test on cervical smear
○ Urinalysis
Diagnosis
Chlamydia Manifestations in Men
● GSCS of cervical secretions on Thayer Martin
Medium ○ Urethritis
○ Proctitis
Gonorrhea Diagnosis
○ Epididymitis
● Clinical examination
Chlamydia Manifestation in Women Syphilis Frequency

○ Urethritis ○ Incidence has increased, especially in females

○ Endocervicitis aged 15-24 years
○ Proctitis ○ Highest prevalence- urban blacks and Hispanics
○ PID
Syphilis Classification
○ Perihepatitis

Management
○ Doxycycline or Azithromycin
○ Erythromycin and Ofloxacin
CX:
○ PID
○ Ectopic Pregnancy
○ Fetus Transmittal (vaginal birth)
Syphilis
○ Treponema pallidum
○ Invades mucosa or through skin breaks
○ Direct diagnosis
■ Darkfield microscopic identification of bacteria
■ Staining with fluorescent-labeled,
monoclonal antibodies
○ Indirect, serological diagnosis
■ VDRL, RPR, ELISA test for reagin-type
antibodies using cardiolipid (Ag)
■ FTA-ABS test for anti-treponemal antibodies
○ Primary Stage: Chancre at site of infection
○ Secondary: Skin and mucosal rashes
○ Latent period: No symptoms
○ Tertiary: Gummas on many organs
○ Congenital: Neurological Damage
○ Primary and Secondary Stages treated with
penicillin
○ Treponema Pallidum Spirochete (IP. 10-90 Days)
Virulence Factors of T. Pallidum
○ Outer membrane proteins promote adherence
○ Hyaluronidase may facilitate perivascular infiltration
○ Antiphagocytic coating of fibronectin
○ Tissue destruction and lesions are primarily
results of host’s immune response
(immunopathology)
Syphilis Mechanisms of Transmissions
○ Sexual contact
○ Perinatal
○ Primary
○ Secondary
○ Latent
■ Early
■ Late
○ Tertiary
Signs and Symptoms
○ Primary (3-6 weeks after contact)
■ Non-tender lymphadenopathy and chancre; most
infectious, resolves 4-6 weeks
● Secondary
■ Systemic, generalized macular popular rash
including palms and soles and painless wartlike
lesions in vulva or scrotum (condylomata lata)
and lymphadenopathy
○ Tertiary
■ 6-40 years. Neurosyphilis/permanent damage
(insanity); gumma (necrotic granulomatous
lesions), aortic aneurysm
Pathogenesis of T. Pallidum Primary Syphilis
○ Primary disease process involves invasion of
mucus membranes, rapid multiplication & wide
dissemination through perivascular lymphatics and
systemic circulation
■ Occurs prior to development of primary lesion
○ 10-90 days (usually 3-4 weeks) after initial contact
the host mounts an inflammatory response at the
site of inoculation resulting in hallmark syphilitic
lesions, called the chancre (usually painless)
■ Chancre changes from hard to ulcerative with
profuse shedding of spirochetes
■ Swelling of capillary walls & regional lymph
nodes w/ draining
■ Primary lesion heals spontaneously by fibrotic
walling-off within two months, leading to false
sense of relief
Pathogenesis of T. Pallidum Secondary Syphilis
○ Secondary disease 2-10 weeks after primary lesion
○ Widely disseminated mucocutaneous rash
○ Secondary lesions of the skin and mucus
membranes are highly contagious
○ Generalized immunological response
Late Stage Syphilis Principal Clinical Manifestations Syphilis Diagnosis

○ Destructive gummas ○ Clinical examination

○ Aortic valve injury ○ Darkfield microscopy
○ CNS manifestations ○ Serology
■ Dementia ■ VDRL – screening test
■ Tabes dorsalis ■ MHA or FTA – confirmatory test
■ Pupillary abnormalities
Diagnosis
Pathogenesis of T. Pallidum Latent Stage Syphilis
○ Dark-field examination of lesion
○ Following secondary disease, host enters latent ○ 1st and 2nd stage Non specific VDRL and RPR
period ○ FTA-ABS
■ First 4 years = early latent
■ Subsequent period = late latent Management
○ About 40% of late latent patients progress to late
tertiary syphilitic disease ○ Primary and secondary - Pen G
○ Tertiary - IV Pen G
Pathogenesis of T. Pallidum Tertiary Syphilis Diagnostic Tests for Syphilis

○ Tertiary syphilis characterized by localized

granulomatous dermal lesions (gummas) in which
few organisms are present
○ Granulomas reflect containment by the
immunologic reaction of the host to chronic
infection
○ Late neurosyphilis develops in about 1/6
untreated cases, usually more than 5 years
after initial infection
■ Central nervous system and spinal cord
involvement
■ Dementia, seizures, wasting, etc. Note: Treponemal antigen tests indicate experience with a
○ Cardiovascular involvement appears 10-40 treponemal infection, but cross-react with antigens other than
years after initial infection with resulting T. pallidum ssp. pallidum. Since pinta and yaws are rare in
myocardial insufficiency and death USA, positive treponemal antigen tests are usually indicative
of syphilitic infection.
Congenital Syphilis Clinical Manifestations
Syphilis Treatment
○ Fetal death
○ Growth restriction ○ Patient and sexual partner(s) should be treated
○ Multiple anomalies ○ Antibiotic therapy
■ Immediately apparent at birth ■ Penicillin – preferred in pregnancy
■ Delayed appearance ■ Doxycycline
■ Tetracycline
Pathogenesis of T. Pallidum Congenital Syphilis
Prevention & Treatment of Syphilis
○ Congenital syphilis results from transplacental
infection ○ Penicillin remains drug of choice
○ T. pallidum septicemia in the developing fetus ■ WHO monitors treatment recommendations
and widespread dissemination ■ 7-10 days continuously for early stage
○ Abortion, neonatal mortality, and late mental or ■ At least 21 days continuously beyond the early
physical problems resulting from scars from the stage
active disease and progression of the active ○ Prevention with barrier methods (e.g., condoms)
disease state
○ Prophylactic treatment of contacts identified
through epidemiological tracing
Lymphogranuloma Venereum (LGV)
○ Chlamydia trachomatis
○ Initial lesion on genitals heals
○ Bacteria spread through lymph
enlargement of lymph nodes
○ Treatment: Doxycycline
Chlamydia LGV
○ STD caused by serovars L1, L2, L3
○ Common in Asia, Africa, South America, and the
Caribbean
○ Incubation period 3 days to 3 weeks
○ Painless vesicle→ regional lymphatics→ inguinal
and femoral adenitis and proctitis
Chancroid (Soft Chancre)
○ Haemophilus ducreyi
○ Ulcer on genitalia
○ May break through surface
○ Infection of lymph nodes
○ Treatment: Erythromycin and ceftriaxone
Bacterial Vaginosis
○ Gardnerella vaginalis
○ Diagnosis by clue cells
○ Treatment: Metronidazole
Diagnosis
○ Viral culture
○ Pap smear (shows cellular changes)
○ Tzanck smear (scraping of ulcer for staining)
Management
○ Anti viral – acyclovir (zovirax)
CX:
○ Meningitis – mild and self limiting
○ Neonatal infection (vaginal birth)
■ Disseminated with liver involvement
■ Encephalitis
■ Skin, eyes, mouth
Genital Herpes
○ Herpes simplex virus 2 (Human herpesvirus 2
or HHV–2)
○ Neonatal herpes transmitted to fetus or newborns
○ Recurrences from viruses latent in nerves
○ Suppression: Acyclovir or valacyclovir
○ HSV 2
○ Envelop, icosahedral, dsDNA
○ Latent – sacral nerve ganglia
Signs and Symptoms
causing ○ Painful sexual intercourse
○ Painful vesicular lesions (cervix, vagina,
perineum, glans penis)
Genital Warts
○ Human papillomaviruses
○ Treatment: Imiquimod to stimulate interferon
○ HPV 16 causes cervical cancer and cancer of
the penis.
○ DNA test is needed to detect cancer-causing
strains.
○ Vaccination against HPV strains
○ Condyloma Acuminatum
○ HPV type 6 & 11, papilloma virus
Signs and Symptoms
○ Single or multiple soft, fleshy painless growth
of the vulva, vagina, cervix, urethra, or anal
area, Vaginal bleeding, discharge, odor and
dyspareunia
DX:
○ Pap smear-shows cellular changes (koilocytosis)
○ Acetic acid swabbing (will whiten lesion)
Management
○ Laser treatment is more effective
CX:
○ Neoplasia
○ Neonatal laryngeal papillomatosis (vaginal birth)
Candidiasis
○ Candida albicans
○ Grows on mucosa of mouth, intestinal tract, and
genitourinary tract.
○ NGU in males
○ Vulvovaginal candidiasis
○ Diagnosis is by microscopic identification and
culture of yeast.
○ Treatment: Clotrimazole or miconazole.
○ Moniliasis (oral candidiasis)
○ Vulvovaginal candidiasis
○ Candida albicans (Yeast or fungus)
Signs and Symptoms Vaginosis

○ Cheesy white discharge 1. Bacterial Vaginosis

○ Extreme itchiness o Few or No lactobacilli
o Many Coccobacillary Orgs.
DX: 🗶 Garbage
o Clue Cells
○ KOH (wet smear indicate positive result)
🗶 Cell Edge
o Few WBCs
Management:
o Mobilluncous=motile
○ Imidazole, Monistat, Diflucan 2. Cytolytic Vaginosis
o “Lactobacillus Overgrowth Syndrome”
CX: o Many Lactobacilli
o 5 to 15 µ
○ Oral thrush to baby (vaginal birth) 3. Lactobacillosis/Leptothrix
o Long lactobacilli
Trichomoniasis o 40 to 70 µ

○ Trichomonas vaginalis Vaginitis

○ Found in semen or urine of male carriers
○ Vaginal infection causes irritation and profuse 1. Trichomonas
discharge. 2. Candidiasis/Yeast
○ Diagnosis is by microscopic o Candida Albicans “Candidiasis”
identification of protozoan. 🗶 Blastospores
○ Treatment: Metronidazole.
🗶 Budding yeast
○ Trichomonas vaginalis
🗶 Pseudohyphae
○ Parasite
o Candida Glabrata (Torulopsis G.) “Yeast”
🗶 Blastospores
Signs and Symptoms
🗶 Budding yeast
○ Females: itching, burning on urination, yellow gray ○ Grow is clusters = Cumuli>
frothy malodorous vaginal discharge, foul smelling ○ Normal epithelial cells with sharp borders
○ Males: usually asymptomatic ○ Normal lactobacilli- 5 to 15 µ (note size relative
DX: to cell nucleus)

○ Microscopic exam of vaginal discharge HIV and AIDS

Management ○ Retrovirus (HIV1 & HIV2)

○ Attacks and kills CD4+ lymphocytes (T-helper)
○ Metronidazole (Flagyl) ○ Capable of replicating in the lymphocytes
○ Include partners undetected by the immune system
CX: ○ Immunity declines and opportunistic microbes set
in
○ PROM ○ No known cure
Mode of Transmission
Vaginitis and Vaginosis
● Sexual intercourse (oral, vaginal and anal)
● Exposure to contaminated blood, semen, breast milk
and other body fluids
● Blood Transfusion
● IV drug use
● Transplacental
● Needle stick injuries
 High Risk Group NNRTI
○ Ritonavir (Norvir)
● Homosexual or bisexual ● Prevention of spread (safe sex)
● Intravenous drug users ● Universal precautions
● BT recipients before 1985 ● Symptomatic intervention and treatment of
● Sexual contact with HIV+ opportunistic infections
● Babies of mother who are HIV+ ● Vaccines (influenza and hepa B)
Risk Factors:
● People who share needles
● Health workers who are exposed to infected blood GASTROINTESTINAL INFECTION
Possible Symptoms:
● Disease of the digestive system are the second most
● Pain in the upper right quadrant of abdomen
common illnesses in the United States
● Nausea and vomiting
● Loss of appetite Microbial Diseases of the Digestive System
● Jaundice
● Transmitted in food and water
● Fatigue
● Fecal-oral cycle can be broken by:
● Itching
o Proper sewage disposal
Signs and Symptoms o Disinfection of drinking water
o Proper food preparation and storage
● Acute viral illness
○ (1 month after initial exposure) – fever, malaise, Structure and Function of the Digestive System
lymphadenopathy
● Clinical latency ● The gastrointestinal (GI) tract, or alimentary canal,
consists of the mouth, pharynx, esophagus, stomach,
○ 8 yrs w/ no sex; towards end, bacterial and skin
small intestine, and large intestine.
infections and constitutional sex – AIDS related
● In the GI tract, with mechanical and chemical help from
complex; CD4 counts 400-200
the accessory structures, large food molecules are
● AIDS
broken down into smaller molecules that can be
○ 2 yrs; CD4 T lymphocyte < 200 w/ (+) ELISA or
transported by blood or lymph to cells.
Western Blot and opportunistic infections
● Feces, the solids resulting from digestion, are eliminated
Diagnosis through the anus
● HIV
○ Two consecutive positive ELISA and Normal Microbiota
○ One positive Western Blot Test
● AIDS+ ● >700 species in mouth
● Large numbers in large intestine including:
○ HIV+
o Bacteroides
○ CD4+ count below 200/ml Signs and Symptoms
o E.Coli
● Extreme fatigue o Enterobacter
● Intermittent fever o Klebsiella
● Night sweats o Lactobacillus
● Chill o Proteus
● Lymphadenopathy
Normal Microbiota of the Digestive System
● Enlarged spleen
● Anorexia ● Large numbers of bacteria colonize the mouth.
● Weight loss ● The stomach and small intestine have few resident
● Severe diarrhea microorganisms.
● Bacteria in the large intestine assist in degrading food
● Apathy and depression
and synthesizing vitamins.
● PTB
● Up to 40% of fecal mass is microbial cells.
● Kaposis sarcoma
● Pneumocystis carinii Protective
● AIDS dementia
● Waldeyer’s ring
Management
● Mucus lining and high acid (stomach)
● Nucleoside Reverse Transcriptase Inhibitors NRTIs
● Paneth cells (small intestine)
○ Zidovudine (AZT) – limit viral growth
o Phagocyte
● Non-nucleoside Reverse Transcriptase Inhibitors
 o Release defensin and lysozymes
● Normal microbiota (large intestine)
Dental Caries (Tooth Decay)
● Dental caries begin when tooth enamel and dentin are
eroded and the pulp is exposed to bacterial infection.
● Streptococcus mutans-uses sucrose to form dextran from
glucose and lactic acid from fructose.
● Bacteria adhere to teeth and produce sticky dextran,
forming dental plaque.
● Acid produced during carbohydrate fermentation destroys
tooth enamel at the site of the plaque.
● Gram -positive rods and filamentous bacteria
(Actinomycosis) can penetrate into dentin and pulp.
● Carbohydrates such as starch, mannitol, sorbitol, and
xylitol are not used by cariogenic bacteria to produce
dextran and do not promote tooth decay.
● Caries are prevented by restricting the ingestion of
sucrose and by the physical removal of plaque.
Periodontal Disease
● Caries of the cementum and gingivitis are caused by
streptococci, actinomycetes, and anaerobic gram
negative bacteria.
● Chronic gum disease (periodontitis) can cause bone
destruction and tooth loss; periodontitis is due to an
inflammatory response to a variety of bacteria growing on
the gums.
● Acute necrotizing ulcerative gingivitis is often caused by
Prevotella intermedia
Bacterial Diseases of the Lower Digestive System
● A gastrointestinal infection is caused by the growth of
pathogen in the intestines
● Incubation times range from 12 hours to 2 weeks.
Symptoms of infection generally include a fever
● A bacterial intoxication results from the ingestion of
preformed bacterial toxins.
● Symptoms appear 1–48 hours after ingestion of the toxin.
Fever is not usually a symptom of intoxication.
● Infections and intoxications cause diarrhea, dysentery, or
gastroenteritis.
● These conditions are usually treated with fluid and
electrolyte replacement.
Staphylococcal Food Poisoning (Staphylococcal
Enterotoxicosis)
● Ingestion of an enterotoxin (improperly stored foods)
● Bacteria grow and produce enterotoxin (room
temperature)
● Heat stable, 30 minutes of boiling
● Temperature abuse
● Foods with high osmotic pressure and those not cooked
immediately before consumption (most common often
source)
● Higher osmotic pressure/ low moisture food (cream pies,
custard and hams).
● Refrigeration is important (prevention)
● 1million bacteria/gram of food
● Diagnosis is based on symptoms. Nausea, vomiting, and
diarrhea begin 1–6 hours after eating and last about 24
hours.
● Laboratory identification of S. aureus isolated from foods
is used to trace the source of contamination.
● Serological tests are available to detect toxins in foods.
Note: Staphylococcus aureus enterotoxin is a superantigen
Shigellosis (Bacillary Dysentery)
● Shigella Spp. Gram negative facultative bacilli producing
Shiga toxin
● Shiga toxin causes inflammation and bleeding
● Families, day care facilities
● Shigellosis is caused by any of four species of Shigella.
● Shigella sonnei- most common in US, mild dysentery,
traveler’s diarrhea
● Symptoms severe dysentery and prostration
● Blood and mucus in stools, abdominal cramps, and fever.
Infections by S. dysenteriae result in ulceration of the
intestinal mucosa. With “Shiga toxin)
● Shigellosis is diagnosed by isolating and identifying the
bacteria from rectal swabs
● Shiga bacillus: dysenteriae (fatal), flexneri (Philippines),
boydii, sonnei; gram (-)
● Shiga toxin destroys intestinal mucosa
● Humans are the only hosts
● Not part of normal intestinal flora
● IP: 1-7 Days
Mode of Transmission
● Oral fecal route
Signs and Symptoms
● Fever
● Abdominal pain
● Diarrhea is watery to bloody with pus
● Tenesmus
Diagnosis
● Stool culture
Management
● Oresol
● Ampicillin
● Trimethoprim-Sulfamethoxazole, Chloramphenicol,
Tetracycline, Ciprofloxacin
● Fluoroquinolones
Salmonellosis (Salmonella Gastroenteritis)
● Salmonella enteric serovars such as S. Typhimurium
● Mortality (<1%) due to septic shock cause by endotoxin Signs and Symptoms
● Salmonellosis, or Salmonella gastroenteritis, is caused
by many Salmonella enterica serovars. ● Rose spot (abdominal rashes), Step ladder fever 40-41
● Symptoms include nausea, abdominal pain, and diarrhea deg, headache, abdominal pain, constipation (adults),
and begin 12–36 hours after eating large numbers of mild diarrhea (children)
Salmonella.
● Septic shock can occur in infants and in the elderly. Pathophysiology
● Fever might be caused by endotoxin.
● Mortality is lower than 1%, and recovery can result in a
carrier state.
● Cooking food will usually kill Salmonella.
● Laboratory diagnosis is based on isolating and identifying
Salmonella from feces and foods.

Definition of Terms

● Salmonella Enteritis
o Non-invasive salmonella enteritis (caused primarily by
Salmonella enteritidis) in the form of food poisoning with Typhoid Fever
diarrhea and vomiting
● Typhoid Fever ● 1st week
o Infectious invasive enteritis (and rarely, enterocolitis) o Step ladder fever (blood)
caused by Salmonella typhi with systemic organ ● 2nd week
manifestations following hematogenous dissemination. o Rose spot and fastidial
o Typhoid psychosis (urine & stool)
Occurrence: Humans act as reservoirs for the pathogen ● 3rd week
o (complications) intestinal bleeding, perforation,
Typhoid Fever peritonitis, encephalitis
● 4th week
● Salmonella typhi o (lysis) decreasing S/SX
● Frequent cause of death in the world with poor sanitation ● 5th week
● Bacteria are spread throughout body in phagocytes. o (convalescent)
Lysed and released to the bloodstream
● Incubation period of 2-3 weeks
● High grade fever 40C and headache
● Diarrhea and fever decline 2nd or 3rd week
● Severe cases fatal ulceration and perforation of intestine
● 1-3% becomes Chronic carrier (gallbladder)
● 1 to 3% recovered patients become carriers, harboring
Salmonella in their gallbladder
● Salmonella typhi causes typhoid fever; the bacteria are
transmitted by contact with human feces.
● Fever and malaise occur after a 2-week incubation
period. Symptoms last 2–3 weeks.
● S. typhi is harbored in the gallbladder of carriers.
● Typhoid fever is treated with quinolones and
cephalosporins; vaccines are available for highrisk
people.
● Salmonella typhii, gram (-) Diagnosis
● Carried only by humans
● Enteric Fever ● Blood culture (typhi dot)
● Active Immunization ● 1st week Stool and urine culture 2nd week
● Carrier state – harbor in gallbladders ● Widal test (Ab to O and H Ag) – nonspecific
● IP: 1-3 Weeks
Management
Mode of Transmission
● Chloramphenicol, Amoxicillin, Sulfonamides,
● Oral fecal route Ciprofloxacin, Ceftriaxon
Cholera Non-cholera Vibrios

● Vibrio cholerae serotypes that produce cholera toxin. ● Usually from contaminated crustaceans or mollusks
● Toxin causes host cells to secrete Cl– , HCO– , and ● V. cholerae serotypes other than O:1, O:139, and eltor
water. ● V. parahaemolyticus
● Severe diarrhea and violent vomiting with severe ● V. vulnificus
dehydration, no fever ● Ingestion of other V. cholerae serotypes can result in mild
● 12-20 liters (3-5gallons) fluid lostshock, collapse and diarrhea.
death ● Vibrio gastroenteritis can be caused by V.
● Brackish (salty) waters- copepods, algae, aquatic plants parahaemolyticus and V. vulnificus.
and plankton ● These diseases are contracted by eating contaminated
● Sensitive to stomach acid crustaceans or contaminated mollusks.
● Epidemic :
o Serotype O:1 Escherichia Coli Gastroenteritis
o Serotype O:1 Eltor/ El Tor
o Serotype O:139 ● Occurs as traveler's diarrhea and epidemic diarrhea in
o None serotype O:1/ O:139 nurseries.
● 100 million of bactreia per gram of stool ● 50% of feedlot cattle may have enterohemorrhagic
● Tx. Doxycycline strains in their intestines.
● Vibrio cholerae O:1 and O:139 produce an exotoxin that ● Enterohemorrhagic strains such as E. coli O157:H7
alters the membrane permeability of the intestinal produce Shiga toxin.
mucosa; the resulting vomiting and diarrhea cause a loss ● O = cell wall antigen
of body fluids. ● H = flagellar antigen
● The symptoms last for a few days. Untreated cholera has ● Traveler’s diarrhea may be caused by enterotoxigenic or
a 50% mortality rate. enteroinvasive strains of E. coli.
● Fluid and electrolyte replacement provide effective ● The disease is usually self-limiting and does not require
treatment. chemotherapy.
● Vibrio coma (inaba, ogawa, hikojima), vibrio cholerae, ● Enterohemorrhagic E. coli, such as E. coli O157:H7
vibrio el tor; gram (-) o Produces Shiga toxins that cause inflammation and
● Choleragen toxin induces active secretion of NaCl bleeding of the colon, including hemorrhagic colitis and
● Active Immunization hemolytic uremic syndrome.
● IP: few hours to 5 days ● Shiga toxins can affect the kidneys to cause hemolytic
uremic syndrome.
Mode of Transmission
Campylobacter Gastroenteritis
● Oral Fecal Route
● Campylobacter jejuni
Signs and Symptoms ● Campylobacter is the second most common cost of
diarrhea in the United States
● Rice watery stool with flecks of mucus (mucus and ● Usually transmitted in cow’s milk
epithelial cells)
● S/Sx of severe dehydration i.e. Washerwoman’s skin, Helicobacter Peptic Ulcer Disease
poor skin turgor
● Dx: stool culture ● Treated with antibiotics
● H. pylori causes stomach cancer
Management ● Helicobacter pylori produce ammonia, which neutralizes
stomach acid; the bacteria colonize the stomach mucosa
● IV fluids, Tetracycline, Doxycycline, Erythromycin, and cause peptic ulcer disease.
Quinolones, Furazolidone and Sulfonamides (children) ● Bismuth and several antibiotics may be useful in treating
peptic ulcer disease.

Yersinia Gastroenteritis

● Y. enterocolitica and Y. pseudotuberculosis

● Can reproduce at 4°C
● Usually transmitted in meat and milk

Clostridium Infections

● Clostridium perfringens Gastroenteritis

o Grow in intestinal tract, producing exotoxin
● Clostridium difficile–associated diarrhea
o Grow following antibiotic therapy
o Associated with hospitalized patients and nursing home
residents

Clostridium Perfringens Gastroenteritis

● C. perfringens causes a selflimiting gastroenteritis.

● Endospores survive heating and germinate when foods
(usually meats) are stored at room temperature.
● Exotoxin produced when the bacteria grow in the
intestines is responsible for the symptoms. Diarrhea
● Diagnosis is based on isolation and identification of the
bacteria in stool samples. ● The term diarrhea is used if stool has lost its normal firm
consistency. This is usually associated with an increase
Clostridium Difficile- Associated Diarrhea in its weight (in males >235; females >175 g/d) and its
frequency (>2 per day)
● Growth of C. difficile following antibiotic therapy can
result in mild diarrhea or colitis. Assessment of Diarrhea
● The condition is usually associated with hospitalized
patients and nursing home residents

Bacillus Cereus Gastroenteritis

● Ingesting food contaminated with the soil saprophyte

Bacillus cereus can result in diarrhea, nausea, and
vomiting.
● Ingestion of bacterial exotoxin produces mild symptoms.
 ● Mumps virus enters and exits the body through the
respiratory tract.
● About 16–18 days after exposure, the virus causes
inflammation of the parotid glands, fever, and pain during
swallowing. About 4 –7 days later, orchitis may occur.
● After onset of the symptoms, the virus is found in the
blood, saliva, and urine.
● A measles, mumps, rubella (MMR) vaccine is available.
● Diagnosis is based on symptoms or an ELISA test is
performed on viruses cultured in embryonated eggs or
cell culture.
● RNA, Mumps virus
● Mumps vaccine - > 1year old
● MMR – 15 months
● Lifetime Immunity
● IP: 12-16 days

Mode of Transmission

● Droplet, saliva, fomites

Signs and Symptoms

● Unilateral or bilateral parotitis

● Orchitis -sterility if bilateral
● Oophoritis
● Stimulating food cause severe pain
● Aseptic meningitis

DX:

● Serologic testing, ELISA

Management

● Supportive

Hepatitis

● Inflammation of the liver.

● Inflammation of the liver is called hepatitis.
● Symptoms include loss of appetite, malaise, fever, and
jaundice
● Hepatitis may result from drug or chemical toxicity, EB
virus, CMV, or the hepatitis viruses.
● Hepa A – fecal oral route
● Hepa B – body fluids
● Hepa C – non A non B, BT, body fluids
● Hepa D – hypodermic, body fluids
● Hepa E – fecal oral route, fatal and common among
pregnant women
● Hepa G – BT, parenteral

Mumps

● Mumps virus
● Enters through respiratory tract
● Infects parotid glands
● Prevented with MMR vaccine
Hepatitis A ● Blood is tested for HBsAg before being used in
transfusions.
● Hepatitis A virus (HAV) causes hepatitis A; at least 50% ● The average incubation period is 3 months; recovery is
of all cases are subclinical. usually complete, but some patients develop a chronic
● HAV is ingested in contaminated food or water, grows in infection or become carriers.
the cells of the intestinal mucosa, and spreads to the ● A vaccine against HBsAg is available
liver, kidneys, and spleen in the blood. ● Hepatitis B virus (HBV) causes hepatitis B, which is
● The virus is eliminated with feces frequently serious.
● The incubation period is 2–6 weeks; the period of ● HBV is transmitted by blood transfusions, contaminated
disease is 2– 21 days, and recovery is complete in 4–6 syringes, saliva, sweat, breast milk, and semen.
weeks. ● Blood is tested for HBsAg before being used in
● Diagnosis is based on tests for IgM antibodies. transfusions
● A vaccine is available; passive immunization can provide ● DNA, Hepa B virus
temporary protection. ● Serum heap
● RNA, Hepa A virus ● Worldwide distribution
● Infectious hepa ● Main cause of liver cirrhosis and liver cancer
● Poor sanitation ● Blood recipients, hemodialysis, IV drug users, sexually
● Worldwide distribution active homosexual, tattooing and health care workers
● Mortality 1%, with full recovery (high risk)
● IP: 3 - 5 weeks ● Active Immunity (hepavax-B)
● Passive Immunity (HBIg)
Mode of Transmission ● Carrier state
● IP: 2-5 months
● Fecal oral route, food handlers
Mode of Transmission
Signs and Symptoms
● Blood and other body fluids route, percutaneous,
● Flu like symptoms
perinatal, sexual
● Diarrhea, fatigue and abdominal pain
● Loss of appetite Manifestations
● Nausea, diarrhea and fever
● Jaundice and dark colored urine
● Pale stools
● Young children are asymptomatic

Pathogenesis

● Enters and infects the liver, interlobular infiltration with

mononuclear cells
● Necrosis and hyperplasia of kuffer cells
● Period of Communicability – a week before and after the
appearance of symptoms
Diagnosis
Diagnosis
● Elevated AST or SGPT (specific) and ALT or SGOT
● Anti HAV IgM – active infection ● Increased IgM during acute phase
● Anti HAV IgG – old infection; no active disease ● (+) or REACTIVE HBsAg = INFECTED, may be acute,
● Liver function test chronic or carrier
● (+) HBeAg = highly infectious
Management: Supportive ● HBcAg = found only in the liver cells
● (+) Anti-HBc = acute infection
● Active Immunity (Havrix) ● (+) Anti-HBe = reduced infectiousness
● Passive Immunity (HAIg) ● (+) Anti-HBs = with antibodies (from vaccine or disease)
● Blood Chem
Hepatitis B ● Liver biopsy (to detect progression to CA)

● Hepatitis B virus (HBV) causes hepatitis B, which is Management

frequently serious.
● HBV is transmitted by blood transfusions, contaminated ● Prevention of spread – Immunization and Health
syringes, saliva, sweat, breast milk, and semen. Education
● Enteric and Universal precautions
● Assess LOC ● Diagnosed by microscopic examination of stool for ova
● Bed rest and trophozoite
● ADEK deficiency intervention ● Treated with metronidazole
● High CHO, Moderate CHON, Low fat
Cryptosporidiosis
Complication
● Cryptosporidium hominis
● Fulminant Hepatitis – s/sx of encephalopathy ● Transmitted by oocysts in contaminated water
● Chronic Hepatitis - lack of complete resolution of clinical ● Diagnosed by acid-fast staining of stool or presence of
sx and persistence of hepatomegaly antibodies by FA or ELISA
● HBsAg carrier ● Treated with oral rehydration

Hepatitis C Cyclospora Diarrheal Infection

● Hepatitis C virus (HCV) is transmitted via blood. ● Cyclospora cayetanensis

● The incubation period is 2–22 weeks; the disease is ● Transmitted by oocysts in contaminated water
usually mild, but some patients develop chronic hepatitis. ● Diagnosed by microscopic examination for oocysts
● Blood is tested for HCV antibodies before being used in ● Treated with trimethoprim and sulfamethoxazole
transfusions.
Amoebic Dysentery
Other Hepatitis Group
● Entamoeba histolytica
● Hepatitis D (Delta Hepatitis) ● Amoeba feeds on RBCs and GI tract tissues
o Hepatitis D virus (HDV) has a circular strand of RNA ● Diagnosis by observing trophozoites in feces
and uses HBsAg as a coat. ● Treated with metronidazole
● Hepatitis E
o Hepatitis E virus (HEV) is spread by the fecal–oral Helminthic Diseases of the Digestive System
route.
● Other Types of Hepatitis Tapeworms
o There is evidence of the existence of hepatitis types F
● Taenia spp.
and G
● Transmitted as cysticerci in undercooked meat
Viral Gastroenteritis ● Cysticerci may develop in humans
● Diagnosed by observing proglottids and eggs in feces
● Rotavirus: ● Treatment with praziquantel
o 3 million cases annually • ● Neurocysticercosis may require surgery
o 1-2 day incubation; 1 week illness ● Tapeworms are contracted by the consumption of
● Norovirus: undercooked beef, pork, or fish containing encysted
o 50% of U.S. adults have antibodies larvae (cysticerci).
o 1-2 day incubation; 1-3 day illness ● The scolex attaches to the intestinal mucosa of humans
● Treated with rehydration (the definitive host) and matures into an adult tapeworm.
● Eggs are shed in the feces and must be ingested by an
Mycotoxins intermediate host.
● Adult tapeworms can be undiagnosed in a human.
● Mycotoxins are produced by some fungi
o Claviceps purpurea Hydatid Disease
🗶 Grows on grains
🗶 Produces ergot ● Echinococcus granulosus
🗶 Toxin restricts blood flow to limbs; causes hallucination ● Definitive host: Dogs, wolves
o Aspergillus flavus ● Intermediate host: Sheep and other herbivores; humans
🗶 Grows on grains ● Transmitted by ingesting E. granulosis eggs
🗶 Produces aflatoxin ● Treatment is surgical
🗶 Toxin causes liver damage; liver cancer
Pinworms
Giardiasis
● Enterobius vermicularis
● Giardia lamblia ● Definitive host: Humans
● Transmitted by contaminated water ● Transmitted by ingesting Enterobius eggs
● Symptoms of giardiasis are malaise, nausea, flatulence, ● Treatment with pyrantel pamoate or mebendazole
weakness, and abdominal cramps that persist for weeks
Hookworms
● Larvae in soil hatched from eggs shed in feces
● Larvae bore through skin; migrate to intestine
● Treated with mebendazole
Ascariasis
● Ascaris lumbricoides
● Lives in human intestines
● Transmitted by ingesting Ascaris eggs
● Treated with mebendazole
Trichinosis
● Trichinella spiralis
● Larvae encyst in muscles of humans and other mammals
● Transmitted by ingesting larvae in undercooked meat
● Treated with mebendazole to kill adults worms
Trichinellosis
● Trichinella spiralis larvae encyst in muscles of humans
and other mammals to cause trichinellosis.
● The roundworm is contracted by ingesting undercooked
meat containing larvae.
● Adult females mature in the intestine and lay eggs; the
new larvae migrate to invade muscles.
● Symptoms include fever, swelling around the eyes, and
gastrointestinal upset.
● Biopsy specimens and serological tests are used for
diagnosis
RESPIRATORY INFECTION
Upper Respiratory System
● Consists of the nose, pharynx, and associated structures,
such as the middle ear and auditory tubes.
● Coarse hairs in the nose
● Ciliated mucous membranes (nose and throat)
● Lymphoid tissue, tonsils, and adenoids
Lower Respiratory System
● Consists of the larynx, trachea, bronchial tubes, and
alveoli.
● Ciliary escalator
● Alveolar macrophages.
● Respiratory mucus contains IgA antibodies.
Normal Microbiota of the Respiratory System
● The normal microbiota of the nasal cavity and throat can
include pathogenic microorganisms.
● The lower respiratory system is usually sterile because of
the action of the ciliary escalator
Microbial Diseases of the Upper Respiratory System
● Laryngitis: S. pneumoniae, S. pyogenes, viruses
● Tonsillitis: S. pneumoniae, S. pyogenes, viruses
● Sinusitis: Bacteria
● Epiglottitis: H. influenzae Hib vaccine
● These infections may be caused by several bacteria and
viruses, often in combination.
● Most respiratory tract infections are selflimiting.
● H. influenzae type B can cause epiglottitis
Streptococcal Pharyngitis (Strep Throat)
● GAS- Streptococcus pyogenes
● Resistant to phagocytosis
● Streptokinases lyse clots
● Streptolysins are cytotoxic
● Diagnosis by indirect agglutination/ EIA
● Group A beta-hemolytic streptococciStreptococcus
pyogenes.
● Symptoms of this infection are inflammation of the
mucous membrane and fever; tonsillitis and otitis media
may also occur
● Rapid diagnosis is made by enzyme immunoassays.
● Penicillin is used to treat streptococcal pharyngitis.
● Immunity to streptococcal infections is type-specific.
● Strep throat is usually transmitted by droplets.
Scarlet Fever
● Streptococcus pyogenes
● Pharyngitis
● Erythrogenic toxin produced by lysogenized S. pyogenes
by a phage.
● Strep throat, caused by an erythrogenic toxin-producing
S. pyogenes, results in scarlet fever.
● Starts general malaise and swelling of neck
● Symptoms include a red rash, high fever, and a spotted
strawberry -like red, enlarged tongue.
Diphtheria
● Corynebacterium diphtheriae: Gram-positive rod
pleomorphic club shape
● Clinical
o Start as sore throat and fever followed by general
malaise and swelling of neck
o Diphtheria (leather) tough grayish membrane of fibrin,
dead tissue, and bacteria
● Diphtheria toxin produced by lysogenized C. diphtheriae
(highly virulent toxin)
● A membrane can block the passage of air.
● Exotoxin inhibits protein synthesis, and heart, kidney, or
nerve damage may result (fatal)
● Minimal dissemination of the exotoxin in the bloodstream.
● Antitoxin - neutralize the toxin
● Antibiotics- Penicillin and Erythromycin can stop growth
of the bacteria.
● Prevented by DTaP and Td vaccine (Diphtheria toxoid)
● Cutaneous diphtheria: Infected skin wound leads to slow
healing ulcer
Corynebacteria (Genus Corynebacterium)
● Aerobic or facultatively anaerobic
● Small, pleomorphic (club-shaped), grampositive bacilli
short chains (“V” or “Y” configurations) or in clumps
resembling “Chinese letters”
● Cells contain metachromatic granules
● Lipid-rich cell wall contains meso - diaminopimelic acid
● Colds are most often transmitted by indirect contact.
● Rhinoviruses grow best slightly below body temperature.
● The incidence of colds increases during cold weather
● Antibodies are produced against the specific viruses
Microbial Diseases of the Lower Respiratory System
Bacteria, viruses, and fungi cause

Otitis Media ● Bronchitis

● Bronchiolitis
● Infection of the middle ear, primarily in infants and young ● Pneumonia
children
● Three manifestations Pertussis (Whooping Cough)
o Acute otitis media
o Chronic otitis media ● Bordetella pertussis: Gram-negative coccobacillus
o Otitis media with effusion ● Capsule
● Symptoms fever, pain in the ear, dulled hearing. ● Tracheal cytotoxin of cell wall damaged ciliated cells
● S. pneumoniae (35%) ● Pertussis toxin produces systemic disease
● H. influenzae (20-30%) ● Prevented by DTaP vaccine (acellular Pertussis cell
● M. catarrhalis (10-15%) fragments)
● S. pyogenes (8-10%)
Epidemiology of Bordetella Pertussis Infection
● S. aureus (1-2%)
● RSV ● Man is only natural host; obligate parasites of man
o Affects 85% of children before age 3, and estimated 8 ● Disease is highly communicable (highly infectious)
million cases/ year ● Children under one year at highest risk, but prevalence
● Treated with broad-spectrum antibiotics Amoxicillin increasing in older children and adults
● Incidence of S. pneumoniae reduced by vaccine
● Earache, or otitis media, can occur as a complication of Whooping Cough
nose and throat infections.
● Pus accumulation causes pressure on the eardrum ● Symptoms
causes inflammation and pain. o Severe coughing, spasms, inspiratory whoop
● Often in children because of shorter and more horizontal o Lymphocytosis
eustachian tube ● Stages of disease
o Catarrhal -> Paroxysmal -> Convalescent
● Spread--highly contagious
● Diagnosis o Inhalation or direct contact with secretion
o Clinical presentation of fever and pain, especially ● Usually self-limiting
following an URT infection such as a cold o Neurological sequelae
o Otoscopic examination to see inflammation and/or fluid o Secondary respiratory infections
(pus); also loss of mobility with air pressure o Secondary aspiration pneumoniae
● Swelling and blockage 🗶 leading cause of death
● Cyclic pattern of damage ● Ciliary action is compromised. Mucus
● Discomfort - pressure and blocked nasal passages accumulate-desperate attempt to cough out
● Gasping of air between coughs causes the whooping
Common Cold sound (several times a day for 1-6 weeks)
● Infants incapable of coughing produces irreversible brain
● Rhinoviruses (50%) damage
● Coronaviruses (15-20%)
● Any one of approximately 200 different viruses can cause Initial Stage of Pertussis
the common cold; rhinoviruses cause about 50% of all
colds. ● Resembles a cold and is called catarrhal stage
● Immunity is based on the ration of IgA antibodies
● Symptoms Paroxysmal (Second) Stage
o Sneezing
o Nasal secretions ● Accumulation of mucus in trachea and bronchi causes
o Congestion deep coughs
● Sinus infections, lower respiratory tract infections,
laryngitis, and otitis media can occur as complications of
a cold.
Convalescence (Third) Stage Lung Abscess

● Can last for months Chronic Pneumonia

Clinical Progression of Pertussis ● Histoplasmosis, Morphology

● Blastomycosis, Morphology
● Coccidioidomycosis, Morphology

Pneumonia in the Immunocompromised Host

Pulmonary Disease in Human Immunodeficiency Virus

Infection

Predisposing Factors

● Loss of cough reflex

● Diminished mucin or cilia function
● Alveolar macrophage interference
● Vascular flow impairments
● Bronchial flow impairments

Laboratory Culture, Prevention & Treatment of Bordetella Note: Although pneumonia is one of the most common
causes of death, it usually does not occur in healthy people
● Nonmotile
spontaneously
● Fastidious and slow-growing
o Requires nicotinamide and charcoal, starch, blood, or Classification of Pneumonias
albumin
o Requires prolonged growth ● Community Acquired
o Isolated on modified Bordet-Gengou agar ● Community Acquired, Atypical
● Treatment with erythromycin ● Nosocomial
● Aspiration
Whooping Cough ● Chronis
● Necrotizing/Abscess formation
● Laboratory diagnosis is based on isolation of the bacteria
● Pneumonias in immunocompromised hosts
on enrichment and selective media, followed by
serological tests. Community Acquired
● Regular immunization for children has decreased the
incidence of pertussis ● Streptococcus pneumonia (i.e, “diplococcus”
● Haemophilus influenzae (H-Flu)
Pulmonary Infections ● Moraxella
● Staphylococcus (Staph)
Community Acquired Bacterial Acute Pneumonias
● Klebsiella Pneumoniae
(Bacterial)
● Pseudomonas Aeruginosa
● Legionella Pneumophilia
● Streptococcus Pneumoniae
● Haemophilus Influenzae
Streptococcus
● Moraxella Catarrhalis
● Staphylococcus Aureus ● The classic LOBAR pneumonia
● Klebsiella Pneumoniae ● Normal flora in 20% of adults
● Pseudomonas Aeruginosa ● Only 20% of victims have + blood cultures
● Legionella Pneumophila ● “Penicillins” are often 100% curative
● Vaccines are often 100% preventive
Community Acquired Atypical (Viral and Mycoplasma)
Pneumonias (Non-Bacterial) Pneumomoccal Pneumonia

● Influenza Infections ● Streptococcus pneumoniae: Gram positive encapsulated

● Severe Acute Respiratory Syndrome (SARS) diplococci
● Diagnosis is by culturing bacteria.
Nosocomial Pneumonia
● Penicillin Fluoroquinolones is drug of choice.
● Susceptible population
Aspiration Pneumonia
o Elderly
 o Previously ill ● Compromised host
o Phagocytic dysfunction (e.g., asplenic, sickle cell) o Alcoholic
● Also cause meningitis, otitis media 🗶 Aspiration
● Sensitive to optichin; autolysis by bile o Chemotherapy
● The bacteria can be identified o Tracheostomy
o Alpha-hemolysins, o Broad spectrum antibiotics that change host flora
o Inhibition by optochin,
o Bile solubility Klebsiella Pneumoniae
o Serological tests.
● Symptoms ● Debilitated Malnourished People
o Fever ● Alcoholics with pneumonia are often thought of as having
o Breathing difficulty Klebsiella until proven otherwise
o Chest pain ● Gram negative rod
o Rust-colored sputum o Very mucoid capsule
● A vaccine consists of purified capsular material from 23 ● Aspiration
serotypes of S. Pneumoniae o Head down in the gutter
● Rusty sputum
Stages of Pathogenesis ● High fever

● Encounter - humans only, by respiratory droplet Pseudomonas Aeruginosa

● Entry - colonization of the oropharynx, aspiration into
lung (pneumonia) ● Usually not community acquired but nosocomial
● Spread (extracellular) ● Cystic fibrosis patients with pneumonia are presumed to
o Pneumonia - blood culture can be positive have pseudomonas until proven otherwise
o Meningitis - penetration of mucous membrane
Legionella (Pneumophila)
o Otitis media- eustachian tube to middle ear
● Multiplication ● Often in OUTBREAKS
o Grows well in serous fluid in alveoli space ● Often LOBAR
● Evade defenses ● Spread by water “droplets”
o Capsule--antiphagocytic ● Often immunosuppressed patient
o sIgA protease
Legionellosis
Haemophilus Influenzae Pneumonia
● The disease is caused by the aerobic gramnegative rod
● Gram-negative coccobacillus Legionella pneumophila.
● Alcoholism, poor nutrition, cancer, or diabetes are ● High fever 40.5C, cough and general pneumonia
predisposing factors. symptoms
● Second-generation cephalosporins ● The bacterium can grow in water, such as
● Commonest in children <2 with otitis, URI, meningitis, air-conditioning cooling towers, and then be disseminated
cellulitis, osteomyelitis in the air.
● Pneumonia in children <2 are often thought as being H
Flu until prove otherwise, otitis, meningitis too Legionnaire’s Disease/Pontiac Fever Legionella
● Most common pneumonia from COPD in adults Pneumophila
● Bactrim (Trimethoprim-Sulfa most common treatment)
● Gram-negative rod
Moraxella Catarrhalis o Stains irregularly
o Silver stain
● 2nd most common COPD pneumonia, after haemophilus ● Disease
● Gram Negative coccobacillus, like H. Flu o Pontiac Fever - flu-like in anyone (1968)
🗶 Fever muscular ache and cough (self limiting)
Staphylococcus Aureus
● Legionnaire's disease - pneumonia
● Most common pneumonia following viral pneumonias o Primarily in middle aged to older men who heavy
● M.R.S.A., of course, is usually NOT “community” smoker and drinker or chronically ill
acquired o 1976 American Legion Convention in Philadelphia (toll
182 cases/29 death)
Gram Negative Bugs
Legionellosis
● Typically from body flora
‘Opportunistic’ infections ● This pneumonia does not appear to be transmitted from
person to person.
● Bacterial culture, FA tests, and DNA probes are used for ● s/sx: fever, headache , chills, some with delirium and
laboratory diagnosis. disorientation
● Prevention : Copper Ionizing procedure ● Commercial bird handlers are most susceptible to this
● Treatment : Erythromycin, some macrolides like disease.
Azithromycin ● The bacteria are isolated in embryonated eggs, mice, or
cell culture; identification is based on FA staining.
Morphology ● Tx: Tetracycline

● Acute Chlamydial Pneumonia

● Organizing
● Chronic ● Chlamydophila pneumoniae causes pneumonia; it is
● Fibrosis vs. Full Resolution transmitted from person to person.
● “Hepatization”, red vs. grey ● Atherosclerosis-deposition of fats on arteries
● Consolidation ● s/sx resemble mycoplasma pneumonia
● Infiltrate, xray vs. histopath ● Tetracycline is used for treatment.
● Loss of crepitance
Q Fever
Community Acquired (Atypical)
● Obligately parasitic, intracellular Coxiella burnetii causes
● Viral (Influenza) Q fever or X fever
● Mycoplasma Pneumoniae (Obligate Intracellular) ● The disease is usually transmitted to humans through
● Not bacterial unpasteurized milk or inhalation of aerosols in dairy
● Cultures not helpful barns, cattle tick bites
● Laboratory diagnosis is made with the culture of bacteria
Mycoplasmal Pneumonia in embryonated eggs or cell culture.
● Wide range of clinical symptoms
● Mycoplasma pneumoniae causes mycoplasmal ● 60% asymptomatic
pneumonia; it is an endemic disease. ● s/sx: High fever, muscle ache, headache and coughing
● Young adults and children ● Hepatitis and endocarditis (persist for months)
● Symptoms persist for 3 weeks and longer (low fever, ● Tx: Doxycycline , Chloroquine
cough and headaches)
● Primary atypical/ walking pneumonia Melioidosis
● M. pneumoniae produces small “friedegg” colonies after
two weeks’ incubation on enriched media containing ● Melioidosis, glanders disease (horses) caused by
horse serum and yeast extract. Burkholderia pseudomallei
● Diagnosis is by PCR or serological tests ● Transmitted by inhalation, ingestion, or through puncture
wounds.
Atypical (walking) Pneumonia ● Symptoms include pneumonia, sepsis, and encephalitis.
● Tx: Ceftazidime
Mycoplasma Pneumonia
CMV Pneumonia
● Lacks peptidoglycan
o β-lactam resistant ● Common virus
● Disease primarily in young adults ● Infant and neonate
● Encounter- inhalation from human ● Immune suppressed
● Entry- restricted to mucosal surface o HIV
o Terminal adhesion protein (P1) o Chemotherapy
● Multiplication- require sterols ● Characteristic inclusion
● Damage
o Inflammation
o Damage and desquamation of ciliated epithelium
● Treatments
o Erythromycin, doxycycline, tetracycline

Psittacosis (Ornithosis)

● Chlamydophila psittaci – gram negative intracellular

bacteria and is transmitted by contact with contaminated
droppings and exudates of fowl.
● Elementary bodies allow the bacteria to survive outside a
host.

Diagnostic
Streptococcus Pneumoniae
Viral Pneumonia
(Frequently “interstitial, not alveolar)
● A number of viruses can cause pneumonia as a
complication of infections such as influenza.
● The etiologies are not usually identified in a clinical
laboratory because of the difficulty in isolating and
identifying viruses
Respiratory Syncytial Virus (RSV)
● RSV is the most common cause of pneumonia in infants
2-6months
● Life threatening- tx Ribavirin and Palizumab
● Coughing, wheezing last more than a week, fever by
bacterial infection
Influenza Serotypes
● A: Causes most epidemics, H3N2, H1N1, H2N2
● B: Moderate, local outbreaks
● C: Mild disease
Influenza Virus
● A, B, C
● 1915, 1918, PAN-demics, type A
● Has mutated throughout history, many strains, avian
swine, etc.
● B and C in children
● Exact strains can be ID’s by PCR
Influenza
● Hemagglutinin (H) spikes used for attachment to host
cells.
● Neuraminidase (N) spikes used to release virus from cell.
● Antigenic Shift
o Changes in H and N spikes
o Probably due to genetic recombination between different
strains infecting the same cell
● Antigenic Drift
o Mutations in genes encoding H or N spikes
o May involve only 1 amino acid.
o Allows virus to avoid mucosal IgA antibodies.
● Deaths during epidemic - secondary bacterial infections.
● Multivalent vaccines for the elderly and other high -risk
groups.
● Amantadine and rimantadine are effective prophylactic
and curative drugs
● Zanamivir and oseltamivir
Coronavirus
● Positive-sense single-stranded RNA (+ssRNA) virus ,
50– 200 nanometres in diameter
● Family of viruses as SARS CoV1, SARS CoV2, and
MERS CoV
● SARS was more deadly but much less infectious than
COVID-19
● Incubation period 1-12.5 (14) days
SARS (Severe Acute Respiratory Syndrome)
● SARS CoV1 Virus
● First appearing in Southern China in November 2002.
● Recognized as a global threat in March 2003
● Like most other NON-bacterial pneumonias confirmed by
PCR
● Like most viral pneumonias, interstitium infiltrated, some
giant cells often present
● Coronavirus
● Severe acute respiratory syndrome IP: 2-7 (14) days
MOT: respiratory droplet/person to person contact
Risk Factors
● history of recent travel to China, Hong Kong, or Taiwan or
close contact w/ ill persons with a hx of recent travel to
such areas, OR
● Is employed in an occupation at particular risk for SARS
exposure, i.e. healthcare worker with direct patient
 contact or a worker in a laboratory that contains live
SARS, OR
● Is part of a cluster of cases of atypical pneumonia without
an alternative diagnosis
Transmission
● Spread is by close person-to-person contact
o Respiratory droplets (droplet spread) coughs or sneezes
(3 feet)
o Person touches a surface or object contaminated with
infectious droplets
o Air (airborne spread)
● “Close contact”
o Cared for or lived with a person known to have SARS
o Having a high likelihood of direct contact with respiratory
secretions and/or body fluids of a patient known to have
SARS.
o Examples --kissing or embracing, sharing eating or
drinking utensils, close conversation (within 3 feet),
physical examination, and any other direct physical
contact between people.
● Outbreak of MERS Arabian Peninsula and Republic of
Korea in 2015.
● Spread from ill people to others through close contact,
such as caring for or living with an infected person.
● Age from younger than 1 to 99 years old.
Signs and Symptoms
● Severe respiratory illness with symptoms of:
o Fever
o Cough
o Shortness of breath
● Some people also had
o Diarrhea and nausea/vomiting
● People with MERS, more severe complications\
o Pneumonia and kidney failure
● 3 or 4 out of every 10 people died
● pre-existing medical condition that weakened their
immune system, or an underlying medical condition that
hadn’t yet been discovered
MERS Complication

Signs and Symptoms ● Pre-existing conditions among people who got MERS
have included:
● Fever, chills, rigors, myalgia, headache, diarrhea, sore o Diabetes
throat, rhinorrhea o Cancer
● 2-7 days after onset of illness - shortness of breath o Chronic lung disease
and/or dry cough o Chronic heart disease
● Begins with a high fever (>100.4°F [>38.0°C]) chills o Chronic kidney disease
● Headache o Some infected people had mild symptoms (such as
● General feeling of discomfort cold-like symptoms) or no symptoms at all.
● Body aches o The symptoms of MERS start to appear about 5 or 6
● Mild respiratory symptoms days after a person is exposed, but can range from 2 to
● Diarrhea 10 percent 14 days.
● After 2 to 7 days, may develop
o Dry, nonproductive cough accompanied by oxygen MERS Transmission
levels in the blood are low (hypoxia)
o 10-20 percent requires mechanical ventilation. ● MERS-CoV likely spreads from an infected person’s
o Most patients develop pneumonia. o Respiratory secretions- coughing.
o Close contact - caring for or living with an infected
Diagnosis person. Infected people have spread MERS-CoV to
others in healthcare settings, such as hospitals.
● Viral culture ● All reported cases
● RT PCR o Lived in the Arabian Peninsula
● Serologic Testing o Recently traveled from the Arabian Peninsula before
● Mgmt: Supportive they became ill-
o Close contact with an infected person who had recently
Middle East Respiratory Syndrome (MERS) traveled from the Arabian Peninsula

● Middle East Respiratory Syndrome Coronavirus MERS Prevention

(MERS-CoV).
● Severe respiratory illness with symptoms of fever, cough ● No vaccine to protect people against MERS
and shortness of breath. ● Reduce risk of getting respiratory illnesses.
● 3 or 4 out of every 10 patients reported with MERS have ● Wash your hands often with soap and water for at least
died. 20 seconds or alcohol-based hand sanitizer.
● Saudi Arabia in September 2012. ● Cover your nose and mouth with a tissue when you
● First known cases of MERS occurred in Jordan in April cough or sneeze
2012. ● Avoid touching your eyes, nose, and mouth with
unwashed hands.
● Avoid personal contact, such as kissing, or sharing cups
or eating utensils, with sick people.
● Clean and disinfect frequently touched surfaces and
objects, such as doorknobs.
● If you are caring for or living with a person confirmed to
have, or being evaluated for, MERS-CoV infection
MERS Treatment
● No vaccine to protect people against MERS
● There is no specific antiviral treatment recommended for
MERS-CoV infection
● Receive medical care to help relieve symptoms
● For severe cases, current treatment includes care to
support vital organ functions
Coronavirus Disease 2019 (COVID-19)
What is COVID-19?
● CORONAVIRUS DISEASE 2019 “COVID-19” is a
disease caused by SARS CoV2 Virus.
● Positive-sense single-stranded RNA (+ssRNA) virus ,
50–200 nanometres in diameter
● Formerly referred to as ‘2019 novel coronavirus’ or
‘2019-nCoV.’
● It is a new virus linked to the same family of viruses as
SARS CoV1 and MERS CoV
● SARS was more deadly but much less infectious than
COVID-19
● Incubation period 1-12.5 (14) days
Where did the COVID-19 Originate?
● Last December 2019, a clustering of pneumonia cases of
unknown etiology in Wuhan, China was reported to the
WHO Country office.
● The outbreak was later determinedυ to be caused by a
new coronavirus strain.
● Animal origin are bats andυ domesticated wild animal
sold in marketplace
COVID-19 Variants
● UK variant (B.1.1.7) reported on December 14, 2020,
British-identified variant VOC 202012/01 with a higher
viral load, increased transmission.
● 1st Philippine case ,male resident of Quezon City from
Dubai arrived in the Philippines last Jan. 7
Pathogenesis
● Coronavirus virion structure
o Genome RNA is complexed with
o N protein to form a helical cased within the viral
membrane HE, hemagglutininesterase
o S, spike
o E, small membrane envelope
o M, membrane are all transmembrane proteins
How it spreads?
● When people with COVID-19 breathe out or cough, they
expel tiny droplets that contain the virus.
● These droplets can enter the mouth or noseυ of someone
without the virus, causing an infection to occur.
● The most common way that this illnessυ spreads is
through close contact with someone who has the
infection. Close contact is within around 6 feet
● The disease is most contagious when a person’s
symptoms are at their peak.
● Droplets containing the virus can alsoυ land on nearby
surfaces or objects. Other people can pick up the virus by
touching these surfaces or objects.
● Infection is likely if the person thenυ touches their nose,
eyes, or mouth.
Pathogenesis
● The primary route of transmission of human
coronaviruses is via the respiratory tract, most likely
spread by aerosols and in large droplets (e.g., sneezes).
● Infection with the common-cold coronaviruses leads to
loss of ciliary action (ciliostasis) and degenerative
changes affecting the cilia of epithelial cells of the
respiratory tract
● Infection remains localized to the upper respiratory tract
because the optimum temperature for viral growth is 33°
C to 35° C and may lead to the lower respiratory tract.
● HCoV-OC43 is generally associated with mild upper
respiratory tract infections, although it has been shown to
have neuroinvasive properties.
● The severe symptoms of COVID-19 are associated with
an increasing numbers and rate of fatalities especially in
the epidemic region of China
o On January 22, 2020, the China National Health
Commission reported the details of the first 17 deaths •
o On January 25, 2020 the death cases increased to 56
deaths
o The percentage of death among the reported 2684
cases of COVID-19 was approximately 2.84% as of Jan
25, 2020 and the median age of the deaths was 75
(range 48–89) years
o By March 5, 2020, COVID-19 reached the United States
● Patients infected with COVID-19 showed higher
leukocyte numbers, abnormal respiratory findings, and
increased levels of plasma pro-inflammatory cytokines.
o Leucopenia with leukocyte counts
o C-reactive protein was noted which is above the normal
range
o High erythrocyte sedimentation rate and D-dimer
● Patients infected with COVID-19 showed higher
leukocyte numbers, abnormal respiratory findings, and
increased levels of plasma pro-inflammatory cytokines
● The main pathogenesis of COVID-19 infection as a
respiratory system targeting virus was severe
pneumonia, RNAaemia, combined with the incidence of
ground-glass opacities, and acute cardiac injury
How does COVID-19 spread or transmitted? ● Practice proper cough and etiquette
● Social distancing at least 2 meters (6 feet)
● Droplets ● Wear face mask and face shield
● Contact and Fomites ● Don’t touch your eyes, nose, and mouth
● Airborne ● Stay home if you feel unwell
● If you have fever, cough, and difficulty of breathing, seek
Most Common Symptoms of COVID-19 medical attention
● Regular cleaning and disinfecting
● Fever or chill
● Dry cough Available Testing Methods
● Tiredness/Fatigue
● Shortness of Breath ● Rapid test
● RT-PCR Swab Test
Less Common Symptoms of COVID-19
What to do if you test Positive
● Colds, Sore throat
● Nausea, vomiting & diarrhea ● Tract your symptoms
● Conjunctivitis ● Stay at indoors at all cost
● Head and body pain ● Rest and hydrate
● Loss of taste & smell ● Inform your doctor
● Rash on skin, or discoloration of fingers or toes
Classification of COVID-19 Surveillance System
Severe Symptoms of COVID-19
Suspect
● Shortness of breath and cyanosis
● Chest pain or pressure ● A person who meets the clinical AND epidemiological
● Loss of speech & movement criteria:
● Confusion and excessive drowsiness ● Clinical criteria:
1. Acute onset of fever and cough; OR
Do all individuals infected with COVID-19 present sign & 2. Acute onset of any three or more of the following signs
symptoms? or symptoms:
o Fever, cough, general weakness/fatigue, headache,
● Some people become infected but don’t develop any myalgia, sore throat, coryza, dyspnea,
symptoms and don’t feel unwell (Asymptomatic) anorexia/nausea/vomiting, diarrhea altered mental
status.
Who are most likely to present with severe symptoms?
● Epidemiological Criteria:
● Children & senior citizen 1. Residing or working in an area with high risk of
● Individuals with Health Conditions/Disabilities transmission residential settings and humanitarian
● Pregnant Women settings, such as camp and camp-like settings for
displaced persons, any time within the 14 days prior
Clinical Condition to symptom onset;
2. Residing in or travel to an area with community
● Heart condition transmission anytime within the 14 days prior to
● Chronic kidney disease symptom onset
● COPD (Chronic Obstructive Pulmonary Disease) 3. Working in health setting, including within health
● Cancer facilities and within households, anytime within the
● Smoking 14 days prior to symptom onset.
● Immunocompromised state ● A patient with severe acute respiratory illness (SARI:
● Obesity (body mass index [BMI] of 30 or higher) acute respiratory infection with history of fever or
● Pregnancy measured fever of > 38 C°; and cough; with onset within
● Hypertension the last 10 days; and who requires hospitalization).
● Type 2 diabetes mellitus
● Asthma (moderate to severe) Probable
● Cerebrovascular disease
● Liver disease ● A patient who meets clinical criteria above AND is a
● Blood disorder contact of a probable or confirmed case, or
epidemiologically linked to a cluster of cases which has
Protection and Prevention had at least one confirmed case identified within that
cluster. Epidemiologically linked refers to exposure of a
● Practice frequent & proper handwashing suspect case to a confirmed case which occurred within
 2-14 days prior to the suspect case's onset of illness.
This is based on current available data on COVID-19
incubation period.
● A suspect case (described above) with chest imaging
showing findings suggestive of COVID-19 disease
● Typical chest imaging findings suggestive of COVID19
include the following (Manna 2020):
a) Chest radiography: hazy opacities, often rounded in
morphology, with peripheral and lower lung distribution
b) Chest CT: multiple bilateral ground glass opacities,
often rounded in morphology, with peripheral and lower
lung distribution
c) Lung ultrasound: thickened pleural lines, B lines
(multifocal, discrete, or confluent), consolidative patterns
with or without air bronchograms.
● A person with recent onset of anosmia (loss of smell) or
ageusia (loss of taste) in the absence of any other
identified cause.
● Death, not otherwise explained, in an adult with
respiratory distress preceding death AND who was a
contact of a probable or confirmed case or
epidemiologically linked to a cluster which has had at
least one confirmed case identified within that cluster.
Confirmed Case
● Any individual, irrespective of presence or absence of
clinical signs and symptoms, who was laboratory
confirmed for COVID-19 in a test conducted at the
national reference laboratory, a subnational reference
laboratory, and/or DOH-licensed COVID-19 testing
laboratory;
● Any suspect or probable COVID-19 cases, as defined
above, which tested positive using antigen tests in areas
with outbreaks and/or in remote settings where RT-PCR
is not immediately available; provided that the antigen
tests satisfy the recommended minimum regulatory,
technical and operational specifications set by the Health
Technology Assessment Council.
Vaccination
COVID-19 Vaccines
● They cannot give someone COVID-19.
● mRNA vaccines do not use the live virus that causes
COVID-19.
● They do not affect or interact with our DNA in any way.
● mRNA never enters the nucleus of the cell, which is
where our DNA (genetic material) is kept.
● The cell breaks down and gets rid of the mRNA soon
after it is finished using the instructions.
COVID-19 Viral Vector Vaccines
● Contain a weakened version of a live virus—a different
virus than the one that causes COVID-19
● Genetic material from the virus that causes COVID19
inserted in it (this is called a viral vector).
● Using these instructions, our cells make copies of the
protein= prompts our bodies to build Tlymphocytes and
B-lymphocytes that will remember how to fight that virus
if we are infected in the future.
COVID-19 mRNA Vaccines
● Contain material from the virus that causes COVID-19
that gives our cells instructions for how to make a
harmless protein that is unique to the virus
● After our cells make copies of the protein, they destroy
the genetic material from the vaccine.
● Our bodies recognize =build T-lymphocytes and
B-lymphocytes that will remember how to fight the virus
that causes COVID-19 if we are infected in the future
Protein Subunit Vaccines
● Include harmless pieces (proteins) of the virus that cause
COVID-19 instead of the entire germ
● Our immune system recognizes that the proteins don’t
belong in the body and begins making T-lymphocytes
and antibodies. If we are ever infected in the future,
memory cells will recognize and fight the virus
COVID-19 Vaccines Require > One Show
● All but one of the COVID-19 vaccines that are currently in
Phase 3 clinical trials in the United States use two shots.
o First shot
🗶 Starts building protection
o Second shot
🗶 A few weeks later is needed to get the most protection
the vaccine has to offer.
● One vaccine in Phase 3 clinical trials only needs one shot
When Testing might be performed
● Individuals should be considered for and offered testing if
they:
1. Show signs or symptoms consistent with COVID19
(diagnostic)
2. Have a recent known or suspected exposure to a person
with laboratory-confirmed COVID-19 (diagnostic)
3. Have been asked or referred to get testing by their
healthcare provider or health department (diagnostic)
4. Are part of a cohort for whom testing is recommended (in
the context of an outbreak)
5. Are attending an IHE that requires entry screening (entry
testing as part of screening)
6. Are in a community where public health officials are
recommending expanded testing on a voluntary basis
including testing of a sample of asymptomatic individuals,
especially in areas of moderate to high community
transmission (screening)
7. Volunteer to be tested in order to monitor occurrence of ● Often synonymous with the 4 classic systemic fungal or
cases and positivity rate (surveillance) granulomatous pulmonary infections infections, i.e., TB,
Histo-, Blasto-, Coccidio-
● It is not recommended to retest previously positive
● If you see pulmonary granulomas, think of a chronic
asymptomatic individuals within 3 months of a positive
process, often years
test. Data currently suggest that some individuals test
persistently positive due to residual virus material but are Chronic Pneumonias
unlikely to be infectious
● TB
Note: Methenamine Sliver stain for Pneumocystis carinii ● Histo-Plasmosis
● Blasto-mycosis
Nosocomial
● Coccidio-mycosis
● Acquired in HOSPITALS, also called “hospital acquired”,
Fungal Pneumonias
versus “community acquired” pneumonias.
o Debilitation ● Typically means something wrong with immune system
o Catheters, ventilators ● Histoplasmosis is very common
o Enterobacter, pseudomonas o Ohio River Valley
o Staph (MRSA) o Virtually all of us beat the bug
o MRSA (MR= Methicillin Resistant) ● HIV has changed things a lot
● Other Common causes of Noso. Pneum.
o P. aeruginosa Fungal Diseases of the Lower Respiratory System
o Klebsiella
o E. coli ● Fungal spores are easily inhaled; they may germinate in
o S. pneumoniae the lower respiratory tract.
o H. influenza ● The incidence of fungal diseases has been increasing in
recent years.
Aspiration Pneumonias ● The mycoses in the sections below can be treated with
amphotericin B
● Unconscious patients
● Patients in prolonged bed rest Histoplasmosis
● Lack of ability to swallow or gag
● Usually caused by aspiration of gastric contents ● Dimorphic yeast
● Posterior lobes (gravity dependent) most commonly ● Fungal growth phase
involved, especially the superior segments of the lower ● Oral or pulmonary infection
lobes ● Granulomas
● Often lead to abscesses ● Most people lock it down.
● Forms of the disease:
Lung Abscesses o Pulmonary
o Systemic
● Aspiration ● Resembles Tuberculosis
● Septic Embolization ● Histoplasma capsulatum causes a subclinical respiratory
● Neoplasia infection that only occasionally progresses to a severe,
● From neighboring structures: generalized disease.
o Esophagus ● Transmitted by airborne conidia from soil and thru bird
o Spine droppings
o Pleura ● Diagnosis by culturing fungus
o Diaphragm ● Treatment: Amphotericin B or Itraconizole
● Any pneumonia which is severe and destructive, and ● Spores in bird or bat droppings
untreated enough ● Mimics TB
● Histoplasma Capsulatum
Pulmonary Abscess
● Pulmonary granulomas, often large and calcified
● Staphylococcus ● Tiny organisms live in macrophages
● Aspiration of gastric material ● Ohio, Mississippi valley
● Hole with Air-fluid level ● Many other organ scan be affected

Chronic Pneumonias Blastomycosis

● Usually not persistences of the community or nosocomial ● Spores in soil

bacterial infections, but can be, at least histologically ● Mimics TB, like all the granulomatous lung diseases do.
● Blastomyces dermatidis Granuloma
● Pulmonary granulomas, often large and calcified
● Large distinct SPHERULES (larger than coccidio) ● Compromised hosts
● Ohio, Mississippi valley, Great Lakes, worldwide o Pneumocystis carinii
● Many other organs can be affected, especially skin o Cytomegalovirus (CMV)
o Fungi
Coccidiomycosis
Pneumocystis Carinii
● Spores in soil, Mimics TB
● Coccidioides Immitis ● Immune failure
● Pulmonary granulomas, often large and calcified ● Organism is very common
● Smaller spherules than blasto. ● Immunosuppression
● Tiny organisms live in macrophages o Starvation
● American Southwest o HIV
● Many other organs can be affected o Chemotherapy
● Can’t culture
Coccidioidomycosis ● Bronchial wash
● Stain for the bug
● Valley Fever or San Joaquin Fever
● s/sx- fever, coughing and weight loss Tuberculosis
● Most cases are subclinical, but when there are
predisposing factors such as fatigue and poor nutrition, a ● Leading causes of death world wide
progressive disease resembling tuberculosis can result ● Up to a half of world’s population infected, 95% in
● Transmitted by airborne arthrospores developing countries
● Diagnosis by serological tests or DNA probe ● 8 million people get TB every year
● Treatment: Amphotericin B also Ketoconazole, ● Philippines ranks 4th for # of TB cases worldwide,
Itraconazole highest # per head in SEA
● 2/3 of Filipinos with TB
Pneumocystis Pneumonia
PTB
● Pneumocystis jiroveci (P. carinii) is found in healthy
human lungs. ● Mycobacterium tubercle, acid fast bacilli
● Pneumonia occurs in newly infected infants and ● Airborne/droplets
immunosuppressed individuals. ● Pott’s disease – thoracolumbar
● Treatment: Trimethoprim Sulfamethoxazole ● Milliary TB – kidney, liver, lungs
● P. jiroveci causes disease in immunosuppressed patients.
● Site - lining of alveoli Morphology
● DOC Trimethoprim –Sulfamethoxazole
● Mycobacterium tuberculosis
Blastomycosis ● Thin straight rods, 0.4 x 3 µm
● Acid-fast organisms
● Blastomyces dermatitidis, dimorphic fungus
● Found in soil Mycobacterial Cell Wall Components
● Can cause extensive tissue destruction, cutaneous
● Lipids (mycolic acids)
lesions
● Proteins
● Treatment: Amphotericin B
● Polysaccharides
● The infection begins in the lungs and can spread to
cause extensive abscesses. TB Symptoms
Other Fungi Involved in Respiratory Disease 1. Cough with two weeks or more
2. Sputum expectoration
● Opportunistic fungi can cause respiratory disease in
3. Fever
immunosuppressed hosts, especially when large
4. Significant weight loss
numbers of spores are inhaled
5. Hemoptysis
Opportunistic Fungi Involved in Respiratory Disease 6. Chest and/or back pains
7. Weight loss, night sweats, low fever, non productive to
● Aspergillus productive cough, anorexia, Pleural effusion and
● Rhizopus hypoxemia, cervical lymphadenopathy
● Mucor
Tuberculosis ● Primary infection
o Pulmonary
● Mycobacterium tuberculosis: Acid-fast rod; transmitted o Perhaps goes lymphatics
from human to human. o Hopefully it stops here.
● M. bovis: <1% U.S cases, not transmitted from human to ● Secondary TB
human o Internal reactivation
● M. avium-intracellulare complex infects people with late o Perhaps years later
stage HIV infection o Not all patients

Mycobacterium Tuberculosis Stages of Disease

● Acid fast-lipid, wax ● Primary infection

o Slow growth (nutrient permeability) o Asymptomatic to flu-like
o Resist to detergent and common antibiotics o 3-5% develop TB
● A leading cause of death by infectious disease o Tubercle (granulomatous response)
o 50% population infected, 3m death/yr ● Reactivation (active TB)
o Reemergence in 1980 (AIDS, homeless, immigrants) o Years later, 10% experience
● Diagnosis ● LRT disease (pneumonia)
o PPD test ● Disseminated miliary TB
o Chest X-ray 🗶 Almost everywhere
o Sputum smear (for acid-fast bacilli) 🗶 AIDS and antibiotic resistance
o Sputum culture
o DNA hybridization Stages of Pathogenesis
o Bacteriophage
o PCR (16s rRNA) ● Encounter - respiratory droplet
🗶 Slow, 13 hour generation time, takes weeks ● Entry - direct inhalation into LRT (ID=10)
● Spread - alveoli, but can spread throughout body seeding
PPD-ID many tissues
● Multiplication
o Grows in phagosome of macrophage
o Strict aerobe
o Very slow in culture (24 hr doubling time)
● Evade defenses
o Inhibits phagolysosomal fusion

Tuberculosis

● Tuberculosis is caused by Mycobacterium tuberculosis.

● Large amounts of lipids in the cell wall account for the
bacterium’s acid-fast characteristic as well as its
resistance to drying of disinfectants.
● M. tuberculosis may be ingested by alveolar
macrophages; if not killed, the bacteria reproduce in the
macrophages.
● Lesions formed by M. tuberculosis are called tubercles
● Dead macrophages and bacteria form the caseous lesion
that might calcify and appear in an X ray as a Ghon’s
Diagnosis complex.
● Liquefaction of the caseous lesion results in a
● Chest X-ray cavitary lesion tuberculous cavity in which M. tuberculosis can grow.
● Sputum exam ● New foci of infection can develop when a caseous lesion
● Sputum culture ruptures and releases bacteria into blood or lymph
vessels; this is called miliary tuberculosis.
● Miliary tuberculosis is characterized by weight loss,
coughing, and loss of vigor.
Tuberculosis ● Chemotherapy usually involves 3 or 4 drugs taken for at
least 6 months; multidrug-resistant M. tuberculosis is
● Mycobacterium tuberculosis (most cases)
becoming prevalent.
o Type IV hypersensitivity
o Granuloma
M. Tuberculosis ● Referrals
● Follow-up short course- 6-9 months
● Damage ● Long course- 9-12 months
o Host response to bacteria (cell-mediated immunity) ● Follow up
o Glycolipids (Freund adjuvant) o 2 weekks after medications – non communicable
● Spread to new hosts o 3 successive (-) sputum - non communicable
o Contagious by droplet, resistant to drying o Rifampicin – prophylactic
● Vaccine- BCG
o Causes people to become PPD+, not very effective Categories of TB
o Infect AIDS
● Treatment ● Category I (new PTB)- (+) sputum
o Unusual set of antibiotics (isoniazid, ethambutol, ● Category II (relapse)
rifampin) ● Category III (PTB case)- (-) sputum
o High mutation rate
Treatment
Tuberculosis
● Category I- new PTB, (+) sputum give ripe 2 months,
● Positive tuberculin skin test maintenance of ri 4 months
o An active case of TB prior infection ● Category II- previously treated with relapses. Gives ripes
o Vaccination 1st 2 months, reps 1 month, maintenance rie 5 months
o Immunity to the disease ● Catregory III- new PTB (-) sputum for 2x. Give rip 2
● Induration and reddening at inoculation site within months, maintenance ri 2 months
48hours. ● If resistant to drugs, give additional month/s as
● Most accurate- Mantoux tes prescribed
● Laboratory diagnosis is based on the presence of
acid-fast bacilli and isolation of the bacteria, which MDT Side Effects
requires incubation (3-6weeks) of up to 8 weeks
● R- orange urine
(LowensteinJensen Agar)
● I- neuritis and hepatitis
PPD Tuberculosis Skin Test Criteria ● P- hyperuricemia
● E- impairment of vision
PPD= Purified Protein Derivative from M. Tuberculosis ● S- 8th cranial nerve damage

Sputum Collection Schedule for Diagnosis

Tuberculosis

● Mycobacterium bovis
o Causes bovine tuberculosis
o Transmitted to humans by unpasteurized milk.
o Affect the bones or lymphatic system.
o BCG vaccine -a live, avirulent culture of M. bovis
● M. avium-intracellulare complex infects patients in the
late stages of HIV
Ideal Sputum Specimen
● Treatment of tuberculosis: Prolonged treatment with
multiple antibiotics.
Macroscopic
● Vaccines: BCG, live, avirulent M. bovis; not widely used
in the United States. ● Yellowish
● Mucopurulent
Management
● Cheesy material
● Short course- 6-9 months
Microscopic
● Long course- 9-12 months
● DOTS- directly observed treatment short course ● Greater than 25 WBC/LPO, 5 WBC/OIO
● Case finding ● Presence of alveolar macrophage, dust cells
● Home meds (members of the family)
When to collect another set of 3 sputum specimens?

● When the diagnosis for the sputum microscopy

examination is doubtful.
● When the patient fails to complete his sputum collection
within two weeks from the time of the previous collection.

Staining

Fixation

● Fix the smear by passing it through the flame of an Interpretation of Lab Results
alcohol lamp 2 to 3 times, about 2-3 seconds each.
● Heat the back of smeared surface of the slide. Never
scorch the smear.

Initial Staining

● Arrange the slides on the staining bridge consecutively.

● Pour carbol fuchsin solution covering the whole surface
of the slide.

Heating of the Slide

● Heat the slide using alcohol lamp or spirit cotton in a stick

‘till steam comes off from the stain.
● Do not boil and do not allow the stain to dry. Leave it for INTRODUCTION TO VIROLOGY & MYCOLOGY
five minutes.
Fungus “The Fungi”
Washing of the Slides
● Eukaryotic
● Tilt the slide to drain off excess stain.
● Wash the staining solution off with a gentle stream of ● Aerobic or facultatively anaerobic
running water. ● Chemoheterotrophic
● Most are decomposers
Decolourization ● Mycology is the study of fungi

● Tilt the slide to drain off excess rinse water.

Molds
● Cover the whole slide with 3% hydrochloric acid-ethanol
and leave it until solution runs clear
● The fungal thallus consists of hyphae; a mass of
hyphae is a mycelium
Washing of the Slides

● Wash the slide with a gentle stream of running water. Yeasts

● Tilt the slide to drain off excess rinse water.
● Unicellular fungi
Counterstaining ● Fission yeasts divide symmetrically
● Budding yeasts divide asymmetrically
● Pour 0.1% methylene blue to cover the whole surface of
the smear and leave for 5-10 seconds.
Dimorphism
● Tilt the slide to drain off excess methylene blue.
● Pathogenic dimorphic fungi are yeast-like at 37 oC and
Washing and Drying
mold-like at 25 oC
● Wash the slide with a gentle stream of running water.
● Tilt and place the slide on the slide rack to dry in the air. Fungal Diseases (Mycoses)
Don’t place under the sun to dry.
● Systemic mycoses: deep within body
AFB Staining ● Subcutaneous mycoses: beneath the skin
● Cutaneous mycoses: affect hair, skin, and nails
National Standard Reporting Scale (2001)
● Superficial mycoses: localized e.g hair shafts
 ● Opportunistic mycoses: caused by normal microbiota or • rRNA sequencing places most in Ascomycota; a
environmental fungi few are Basidiomycota
• Penicillium
Asexual Spores • Sporothrix (subcutaneous mycoses)
• Stachybotrys, Coccidiodes, Pneumocystis
● Sporangiospore (systemic mycoses)
● Conidiospore • Candida albicans (cutaneous mycoses)
o Arthrospore
o Blastoconidium Economic Effects of Fungi
● Chlamydospore
Lichens
Sexual Reproduction
o Mutualistic combination of an alga (or
● Plasmogamy: haploid donor cell nucleus (+) penetrates cyanobacterium) and fungus
cytoplasm of recipient cell (-) o Alga produces and secretes carbohydrates,
● Karyogamy: + and – nuclei fuse fungus provides holdfast
● Meiosis: diploid nucleus produces haploid nuclei
(sexual spores) The Algae

Sexual Spores o Eukaryotic

o Unicellular, filamentous, or multicellular (thallic)
● Zygospore: fusion of haploid cells produces one o Most are photoautothrops
zygospore Dinoflagellata
● Ascospore: formed in a sac (ascus)
● Basidiospore: formed externally on a ● Dinoflagellates
pedestal (basidium) ● Cellulose in plasma membrane
● Unicellular
Zygomycota
● Chlorophyll a and c, carotene, xanthins
● Store starch
● Conjugation fungi
● Some are symbionts in marine animals
● Coenocytic
● Neurotoxins cause paralytic shellfish poisoning
● Produce sporangiospores and zygospores
• Rhizopus, mucor (opportunistic, systemic mycoses) Virus

Ascomycota ● Contain DNA or RNA

● Contain a protein coat
o Sac fungi
● Some are enclosed by an envelope
o Septate
● Some viruses have spikes
o Produce ascospores and frequently conidiospores
● Most viruses infect only specific types of cells in one
• Aspergillus (opportunistic, systemic mycoses)
host
• Blastomyces dermatitidis, Histoplasma capsulatum ● Host range is determined by specific host attachment
(systemic mycoses) sites and cellular factors
• Microsporum, Trichophyton (cutaneous mycoses)
Viral Taxonomy
Basidiomycota
● Family names end in -viridae.
oClub fungi
● Genus names end in -virus.
oSeptate
● Viral species: A group of viruses sharing the same
oProduce basidiospores and sometimes conidiospores genetic information and ecological niche (host).
• Cryptococcus neoformans (systemic mycosis) Common names are used for species.
Animorphs ● Subspecies are designated by a number.
● Herpesviridae
o Teleomorphic fungi
● Herpesvirus
• Produce sexual and asexual spores
● Human herpes virus HHV-1, HHV-2, HHV-3
o Anamorphic fungi
● Retroviridae
• Produce asexual spores only
● Lentivirus
● Human immunodeficiency virus HIV-1, HIV-2 Cancer

Growing Viruses ● Activated oncogenes transform normal cells into

● Viruses must be grown in living cells
o Bacteriophages form plaques on a lawn of bacteria
● Animal viruses may be grown in living animals or in
embryonated eggs
● Animals and plants viruses may be grown in cell culture
o Continuous cell lines may be maintained indefinitely
cancerous cells.
● Transformed cells have increased growth, loss of
contact inhibition, tumor specific transplant and T
antigens.
● The genetic material of oncogenic viruses
becomes integrated into the host cell's DNA.
Oncogenic DNA Viruses

● Adenoviridae
Virus Identification
● Heresviridae
● Cytopathic effects ● Poxviridae
● Serological effects ● Papovaviridae
o Detect antibodies against viruses in a patient ● Hepadnaviridae
o Use antibodies to identify viruses in neutralization
tests, viral hemagglutination, and Western blot Oncogenic RNA Viruses
● Nucleic acids
o RFLPs ● Retroviridae
o PCR ● Viral RNA is transcribed to DNA which can
integrate into host DNA
Multiplication of Bacteriophages (Lytic Cycle) ● HTLV 1
● HTLV 2
● Attachment: Phage attaches by tail fibers to host cell.
● Penetration: Phage lysozyme opens cell wall, tail Latent Viral Infections
sheath contracts to force tail core and DNA into cell.
● Biosynthesis: Production of phage DNA and proteins. ● Virus remains in asymptomatic host cell for long
periods.
● Maturation: Assembly of phage particles.
● Cold sores, shingles
● Release: Phage lysozyme breaks cell wall.
Persistent Viral Infection
Lytic Cycle: Phage causes lysis and death of host
cell Lysogenic Cycle: Prophage DNA incorporated in ● Disease processes occurs over a long period; generally
host DNA Multiplication of Animal Viruses is fatal.
● Attachment: viruses attach to cell membrane ● Subacute sclerosing panencephalitis (measles virus)
● Penetration by endocytosis or fusion
Prions
● Uncoating by viral or host enzymes
● Biosynthesis: production of nucleic acid and proteins
● Infectious proteins
● Maturation: nucleic acid and capsid proteins assemble
● Inherited and transmissible by ingestion, transplant,
● Release by budding (enveloped viruses) or rupture and surgical instruments
● Spongiform encephalopathies: Sheep scrapie,
DNA and RNA Viruses Compared Creutzfeldt-Jakob disease, GerstmannSträussler-
Scheinker syndrome, fatal familial insomnia, mad cow
● DNA: Cellular enzyme transcribes viral DNA in nucleus. disease
● DNA, reverse transcriptase: Cellular enzyme ● PrPC : Normal cellular prion protein, on cell surface
transcribes viral DNA in nucleus; reverse ● PrPSc: Scrapie protein; accumulates in brain cells
transcriptase copies mRNA to make viral DNA. forming plaques
● RNA, + strand: Viral RNA is a template for
synthesis of RNA polymerase. Virus Families (DNA)
● RNA – strand: Viral enzyme copies viral RNA to
make mRNA in cytoplasm. ● Single Stranded DNA, non-enveloped viruses
● RNA, double-stranded: Viral enzyme copies –
o Parvoviridae
strand RNA to make mRNA in cytoplasm.
🗶 Human parvovirus
● RNA, reverse transcriptase: Viral enzyme copes
🗶 Fifth disease
viral RNA to make DNA in cytoplasm
🗶 Anemia in immunocompromised patients
● Double Stranded DNA, non-enveloped viruses
 o Adenoviridae 🗶 Lyssavirus (rabies virus)
🗶 Mastadenovirus 🗶 Cause numerous animal diseases
🗶 Respiratory infections in humans o Filoviridae
🗶 Tumors in animals 🗶Filovirus
o Papovaviridae 🗶 Enveloped, helical viruses
🗶 Papillomavirus (human wart virus) 🗶 Ebola and Marburg viruses
🗶
Polyomavirus (cause tumors; some cause cancer) o Paramyxoviridae
● Double Stranded DNA, Enveloped viruses 🗶 Paramyxovirus
o Poxviridae 🗶 Morbillivirus
🗶 Orthopoxvirus (vaccinia and smallpox viruses) 🗶 Parainfluenza
🗶 Molluscipoxvirus (smallpox, molluscum contagiosum, 🗶 Mumps
cowpox) 🗶Newcastle disease
o Herpesviridae o Deltaviridae
🗶 Simplexvirus (HHV1 and HHV 2) 🗶 Hepatitis D virus
🗶 Varicellavirus (HHV 3) 🗶 Depends on coinfection with Hepadnavirus
🗶 Lymphocryptovirus (HHV 4) ● Single Stranded RNA- Strand, Multiple RNA Strands
🗶 Cytomegalovirus (HHV 5) o Orthomyxoviridae
🗶 Roseolovirus (HHV 6) 🗶 Influenzavirus (Influenza viruses A and B)
🗶 HHV 7 🗶 Influenza C virus
🗶 Kaposi's sarcoma (HHV 8) 🗶 Envelope spikes can agglutinate RBCs
🗶 Some herpesviruses can remain latent in host cells. o Bunyaviridae
o Hepadnaviridae 🗶 Bunyavirus (CE Virus)
🗶 Hepadnavirus (Hepatitis B virus) 🗶 Hantavirus
🗶 Use reverse transcriptase to produce DNA from o Arenaviridae
mRNA 🗶 Arena virus
🗶 Helical capsids contain RNA-containing granules
Virus Families (RNA)
🗶 Lymphocytic choriomeningitis
● Singe-Stranded RNA + Strand, Non-enveloped 🗶
VEE and Lassa Fever
o Picornavirida o Retroviridae
e 🗶 Lentivirus (HIV)
🗶 Enterovirus 🗶 Oncogenic viruses
🗶 Rhinovirus 🗶Use reverse transcriptase to produce DNA
🗶 Hepatitis A virus from viral genome
🗶 Includes all RNA tumor viruses
o Caliciviridae
🗶 Hepatitis E virus ● Double-Stranded RNA, Non-Enveloped
🗶 Norovirus causes gastroenteritis o Reovirus (Respiratory Enteric Orphan)
o Rotavirus (Mild respiratory infections
🗶 Use reverse transcriptase to produce DNA from
and gastroenteritis)
mRNA
o Colorado tick fever
● Single-Stranded RNA + Strand, Enveloped
● Single-stranded RNA + Strand, Enveloped
o Coronavrius
o Togaviridae
🗶 SARSCOV1: Severe Acute Respiratory Syndrome
🗶
Alphavirus (transmitted by arthropods; include
🗶 SARSCOV2: COVID19 Coronavirus Disease 2019
EEE, WEE
🗶 MERSCOV: Middle East Respiratory Syndrome
🗶 Rubivirus (rubella virus)
o Flaviviridae
🗶 Arboviruses can replicated in arthropods;
include yellow fever, dengue, SLE, and West
Nile viruses
🗶 Hepatitis C virus
● Single Stranded RNA- Strand One RNA Strand
o Rhabdoviridae
🗶
Vesiculovirus
Viral Skin Infection Distinguishing features of Smallpox from other
Warts rashes
Papillomaviruses
o Treatment
Removal
► Imiquimod (stimulates interferon production)
► Interferon

● Note in this slide that the density of the rash is

greater on the face than on the body
● Pocks are usually present on the palms of the hands
and on the soles of the feet
Monkeypox- an indigenous virus of equatorial Africa
● Although not a virus of humans, the clinical
symptoms are indistinguishable from small pox
● Lethality is only slightly less than smallpox
● Although not as efficient as smallpox, human to
human transmission has been well documented
● Monkeypox should perhaps be considered as
bioterrorist agent
HPV and Skin Warts

Poxviruses
Smallpox (variola)
o Smallpox virus (orthopox virus)
o Variola major has 20% mortality
o Variola minor has <1% mortality
Monkeypox
o Prevention by smallpox vaccination
● In smallpox, fever is present for 2 to 4 days before
Smallpox the rash begins, while with chickenpox, fever and
rash develop at the same time. All the pocks of the
smallpox rash are in the same stage of development
on any given part of the body and develop slowly. In
chickenpox, the rash develops more rapidly, and
vesicles, pustules, and scabs may be seen at the
same time.
Herpes Viruses
● Herpes simplex I & II (cold sores, genital herpes)
● Varicella zoster (chicken pox, shingles)
● Cytomegalovirus (microcephaly, infectious mono)
● Epstein-Barr Virus (mononucleosis, Burkitt’s
lymphoma)
● Human herpes virus 6 & 7 (Roseola)
● Human herpes virus 8 (Kaposi’s sarcoma)
● Varicella-zoster virus (human herpes virus 3)
 ● Transmitted by the respiratory route
● Causes pus-filled vesicles
● Virus may remain latent in dorsal root ganglia
Chickenpox (Varicella)
Varicella Vaccine
● Prevents 40-70% of chickenpox occurrence
● Greatly reduces the severity in the rest
● Attenuated virus
● Can still establish latency and reactivate
Shingles (Herpes Zoster)
● Reactivation of latent HHV-3 releases viruses that
move along peripheral nerves to skin
Human Herpes Viruses
Herpes Simplex 1 and Herpes Simplex 2
● Human herpes virus 1 and HHV-2
● Cold sores or fever blisters (vesicles on lips)
● Herpes gladiatorum (vesicles on skin)
● Herpes whitlow (vesicles on fingers)
● Herpes encephalitis (HHV-2 has up to a 70% fatality
rate)
● HHV-1 can remain latent in trigeminal nerve ganglia
● HHV-2 can remain latent in sacral nerve ganglia
● Acyclovir may lessen symptoms
Tissue Tropism of HSV-1 and HSV-2
● HSV-1:
● Causes 95% of orofacial herpes (remainder caused
by HSV-2)
● Causes 10-30% of primary genital herpes (but
seldom recurs there)
HSV-2:
● Causes primary and recurrent genital herpes
infections
● May cause primary oral herpes but, like HSV-1 in
genital area, it seldom recurs there
Herpes Simplex Infection
Herpes Simplex Virus Type 2
● Infects the genital tract
● Is sexually transmitted
● Complicates childbirth
Roseola
 Measles (Rubeola) Measles Time Course
● Measles virus
● Transmitted by respiratory route
● Macular rash and Koplik’s spots
● Prevented by vaccination
● Encephalitis in 1 in 1,000 cases
● Subacute sclerosing panencephalitis in 1 in
1,000,000 cases

● Time course of measles virus infection.

Characteristic prodrome symptoms are cough,
conjunctivitis, coryza, and photophobia (CCC and P),
Measles Induced Syncytia followed by the appearance of Koplik’s spots and
● Formation of giant cells (syncytia) in measles rash. SSPE, subacute sclerosing panencephalitis
pneumonia. Notice the eosinophilic inclusions in both Koplik’s Spots
the cytoplasm and nuclei ● Koplik’s spots in the mouth and exanthem. Koplik’s
Measles Pathogenesis spots usually precede the measles rash and may be
seen for the first day or two after the rash appears.
Rubella (German measles)
● Rubella virus
● Macular rash and fever
● Congenital rubella syndrome causes severe fetal
damage
● Prevented by vaccination
German Measles (Rubella)

● Mechanisms of spread of the measles virus within

the body and the pathogenesis of measles. CMI,
cell-mediated immunity; CNS, central nervous
system
Rubella Virus
Pathogenesis
o Respiratory transmission
o Replication in cytoplasm; budding
o Viremia
o Mild rash in adults; congenital rubella syndrome (CRS) after
infection in first trimester when virus passes the placenta and
infects fetus
o CRS- deafness, blindness, mental retardation
Rubella Pathophysiology
● Transmission is by respiratory droplets
● Respiratory tract- cervical lymph nodes-
hematogenous dissemination
● Incubation period is 2 to 3 weeks
Rubella Clinical Manifestations
● Malaise Hand and Mouth Disease
● Headache
● Coxsackie Viral Infection
● Myalgias and arthralgias
● Post-auricular adenopathy
● Conjunctivitis
● Non-pruritic, erythematous, maculopapular rash
A 1905 list of skin rashes included:
1. Measles
2. Scarlet fever
3. Rubella
4. Filatow-dukes (mild scarlet fever)
5. Fifth disease: Erythema infectiosum. Human parvovirus
B19 produces milk flu-like symptoms and facial rash
Roseola
Human herpesvirus 6 causes a high fever and rash, lasting
for 1-2 days
Parvovirus
● Structure
o Small (5 kb) linear ssDNA genome, naked capsid
Pathogenesis
o Respiratory transmission
o Replication in nucleus, very host dependent, needs S phase
cells or helper virus
o Viremia
o Antibody important in immunity
o Targets erythroid lineage cells; fifth disease (symptoms
immunological); transient aplastic crisis; hydrops fetalis
● Diagnosis
o Serology, viral nucleic acid
Treatment/Prevention
o None

Fifth Disease (Erythema Infectiosum)