HS 202: Biopsychosocial Dimensions of Illness EXAM

INTRODUCTION TO INFECTIOUS DISEASES (BACTERIAL)

LECTURE 2 15 June 2011 Dr. Nelson Geraldino 1
• Entry into macrophages is receptor dependent – must be eaten
OUTLINE
I. Introduction
by a macrophage/ must recognize antibodies or complement
II. Mechanisms of Bacteria-Induced Injury of the surface of bacteria.
III. Host Response to Injury • Entry into epithelial cells is also receptor dependent –
IV. Megatable of Bacterial Infectious Diseases stimulates host signaling pathways and cytoskeletal
rearrangement.
I. INTRODUCTION
4. Bacterial Endotoxin
Three most common causes of mortality due to infectious diseases:
• The lipopolysaccharide in the cell wall of Gram (-) bacteria
1. Pneumonia – 5th most common
consists of a fatty acid (lipid A) and a core sugar chain (LIPO =
2. Tuberculosis – 6th most common
lipid, SACCHARIDE = sugar)
3. Malaria
• Attached to the core sugar is a variable carbohydrate chain
(O antigen) used to serotype bacteria
Two related aspects in studying diseases:
• Lipid A + sugar - responsible for most biologic activities of
 Specific properties of organisms causing the infection
lipopolysaccharide (fever, macrophage activation, B-cell
 Host’s response to the infectious agent mitogenicity, all cytokine-mediated)
When studying pathology, four aspects should be in mind, always: Recent studies show that Gram positive bacteria and fungi can
 Etiologic agent also produce endotoxins.
 Pathogenesis Gram (-) bacteria may cause septic shock due to endotoxins.
 Morphology Application: Chemotherapy will be detrimental to patient if the
 Clinical significance microorganism will be lysed since more endotoxins will be
produced.
II. MECHANISMS OF BACTERIA-INDUCED INJURY
1. Bacterial Virulence – measure of pathogenicity. Virulence genes 5. Bacterial Exotoxin
govern the following abilities of bacteria that are used • Bacterial enzymes – role in human diseases is still presumptive
to damage host tissue: • Bacterial toxins – role in human disease well established,
 Adhere to host cells molecular mechanisms known
 Invade cells and tissues Examples: diphtheria toxin, enterotoxins of V. cholerae and
 Deliver toxic moieties E.coli, alpha toxin of C. perfringens, anthrax toxin
Virulence genes encode proteins necessary for nutrient
assimilation, toxin transport, gene regulation, host recognition and III. HOST RESPONSE TO INJURY
invasion.
Some examples of bacterial virulence genes: 1. Diagnostic Techniques
 “Housekeeping” virulence genes of Salmonella typhi and
Escherichia coli TECHNIQUE INFECTIOUS AGENT
 Genes for host recognition and invasion of Salmonella and Gram stain Most bacteria
Shigella (pathogenicity islands). These are absent in Acid fast stain Mycobacteria, nocardiae
avirulent E. coli Silver stains Fungi, legionellae, pneumocystis
 Vibrio cholerae adherence and toxin genes – induced Periodic Acid-Schiff Fungi, amebae
together by iron deprivation. Mucicarmine Cryptococci
 Sets of Salmonella genes – coordinately expressed when Giemsa Campylobacteria, leishmaniae,
the bacterium enters the acidic environment within the malaria parasites, herpes
macrophage phagosome.
Antibody probes Viruses, rickettsiae
 Cag, a pathogenicity island encodes a vacuolating toxin (done using ELISA)
(most important)
that converts Heliobacter pylori from a commensal to a
Culture (can be used for All classes
gastritis-producing pathogen.
anything)
DNA probes Viruses, bacteria, protozoa
2. Bacterial Adhesins - bind bacteria to host cell. They are limited in
type but broad range of host cell specificity.
Examples:
 Fibrillae – on Gram + cocci, with lipoteichoic acids and 2. Inflammatory Response
M protein. a. Suppurative Inflammation – neutrophilic attraction to the site of
infection in response to chemoattractants (neutrophilia in the blood
Lipoteichoic acid – hydrophobic; bind to surface of all is indicative of bacteria in the blood even without Gram staining)
eukaryotic cells, higher affinity for certain receptors, on b. Mononuclear and Granulomatous Inflammation – cell-mediated
blood cells and oral epithelial cells. response of the host -- lymphocytes and macrophages; viruses,
intracellular bacteria and parasites, spirochetes and helminths.
 Fimbriae or pili – on Gram – rods and cocci, mediates binding c. Cytopathic-Cytoproliferative Inflammation – absent host
or adherence and found in most hospital acquired infections inflammatory response, virus-mediated damage to host cells.
like Vibrio cholera and Neisseria gonorrhea. d. Necrotizing Inflammation – Various classes of organisms with
powerful toxins that cause extensive tissue damage (abcess). This
3. Intracellular Bacteria – facultative; infection mainly of epithelial also indicates destruciton of the underlying tissues.
cells (Shigella, E.coli) or macrophages (M. tuberculosis) or e. Chronic Inflammation and Scarring – end-stage of many
both (S. typhi, Listeria) infections.

Vida, Ria, Anna One Pride, One Five! UPCM 2015 Page 1 of 12
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY PATHOGENESIS
BACTERIUM
Leptospirosis is
Leptospira sp. characterized by the
development of vasculitis,
endothelial damage, and
inflammatory infiltrates
(monocytic cells, plasma
cells, histiocytes, and
neutrophils)
Petechial hemorrhages are
common on gross exam
Organs are often
discolored depending on
degree of icterus.
Histopathology is most
marked in the liver,
kidneys, heart, and lungs.
Liver involvement is
usually through
intrahepatic cholestasis
rather than actual necrosis
of individual hepatocytes
(this is why liver function
normalizes after recovery).
Hepatocytes contain large
amounts of bilirubin.
There are scattered
lymphocytes and
numerous irregularly-
shaped nuclear fragments.
Vida, Ria, Anna
MEGATABLE OF BACTERIAL INFETIOUS DISEASES
MORPHOLOGY CLINICAL SIGNIFICANCE/FEATURES EPIDEMIOLOGY NOTES
Phases of Leptospirosis: Most widespread ICTERIC LEPTOSPIROSIS
1. acute or septicemic phase- lasts about a zoonosis in the world (icteric- yellowing)
week,
2. immune phase-characterized by antibody Ranges from subclinical a much more severe disease,often
production and excretion of leptospires in the infection to a severe very rapidly progressive
urine syndrome of multiorgan
infection with high Severe cases often present late in the
Most complications are associated with mortality course of the disease, and contributes
localization of leptospires within the tissues to the high mortality rate (5-15%)
during the second week of the illness (immune Source of infection in
phase). humans is usually either Jaundice occurring in leptospirosis is
direct or indirect not associated with hepatocellular
Symptoms: chills, headache, myalgia, abdominal contact with the urine necrosis,
pain, conjunctival suffusion, a transient skin of an infected animal
rash (e.g. rodents) Complications emphasize
multisystemic nature of the disease
Anicteric syndrome usually lasts about a week Higher incidence in
and its resolution coincides with the appearance warm climate countries Common cause of acute renal failure
of antibodies. due to longer survival of (ARF), which occurs in 16 to 40% of
leptospires in the env’t cases
Severe headache with retro-orbital pain and
photophobia Usual port of entry is Complications: Pulmonary
through abrasions or hemorrhage, myocarditis, myositis,
Myalgia (muscle pain) affecting the lower back, cuts in the skin or via conjunctival suffusion, uveitis
thighs, and calves is often intense. the conjunctiva
Infection may take
place via intact skin
after prolonged
immersion in water, but
this usually occurs when
abrasions are likely to
occur and is thus
difficult to substantiate
May be acquired
through occupational,
recreational or
avocational exposures.
One Pride, One Five! UPCM 2015 Page 2 of 12
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY PATHOGENESIS MORPHOLOGY CLINICAL SIGNIFICANCE/FEATURES EPIDEMIOLOGY NOTES
BACTERIUM
Non-motile gram positive Virulence factors: In any organ - pyogenic/suppurative inflammation with marked tissue destruction Causes numerous skin lesions aside
Staphylococcus cocci 1. surface proteins for (suppurative- forming or discharging pus) from upper and lower respiratory
aureus adherence tract infections, endocarditis, burn
Have large numbers of 2. secreted enzymes for In the skin - centered on the hair follicles and surgical wound infections,
plasmids - encode for degrading proteins  Furuncle or boil - Focal suppurative inflammation of the skin and subcutaneous hospital-acquired infections, food
enzymes involved in 3. secreted toxins that tissue; solitary or multiple, or recurrent in successive crops; most frequent in poisoning, toxic shock syndrome
antibiotic resistance and damage the host cell moist hairy areas; from a single hair follicle --> deepening abscess --> thinning
other virulence factors and rupture of skin Methicillin-resistant S. aureus (MRSA)
Binding - mediated by  Carbuncle - Deeper suppuration  spread laterally beneath the deep > constitute 20-55% of clinical isolates
receptors for fibrinogen, subcutaneous fascia  erupt in multiple adjacent skin sinuses; found typically in Europe and the US, and 60% in
fibronectin, and in fascial planes favoring their spread (skin of upper back and posterior neck) PGH.
vitronectin - used as  Folliculitis - small red raised lesions, each associated with a hair follicle > mediated by mecA genes which
bridges to bind to host  Hydradenitis suppurativa - persistent abscess formation of the apocrine glands, code for the modified penicillin
endothelial cells often in the axilla protein (2a) PBP 2a to be tested in
 Bullous impetigo - lesions on finger and wrist usually found in children the lab.
Other virulence factors -  Impetigo- often characterized by yellow to brown crusts; restricted to the > mecA is carried on a mobile genetic
laminin receptor, lipase, superficial epidermis element, the staphylococcal cassette
protein A, hemolysins,  Paronychia- nail bed infection chromosome
enterotoxins, exfoliative  Felon- Infection on the palmar sides of the fingertips mec (SCCmec)
toxins, TSST-1
Lung infections caused are frequently opportunistic/secondary; infiltrate similar to Patients with S. aureus pneumonia
that of pneumococcus but more tissue destruction is seen. usually have brain abscesses.

Staphylococcal Scalded Skin Syndrome

- Ritter disease
- caused by the exfoliative A and B toxins
- an exfoliative dermatitis that most frequently occur in children with
Staphylococcal infections of the nasopharynx or skin
- rash, bullae, partial or total skin loss
- skin is split in the granulose layer

Toxic Epidermal Necrolysis (Lyell’s Disease)

- Secondary to drug hypersensitivity
- Desquamation of the skin at the epidermal-dermal junction

Toxic Shock Syndrome (TSS)

- mediated by one or more of the exotoxins produced by S. aureus
- occurs predominantly in menstruating females using tampons (the
Staphylococcus colonizes the vagina or cervix - the tampon probably promotes
superficial ulceration and easy entry for the toxin)
- rash is a diffuse, blanching, macular erythema particularly affecting the hands and
feet, which desquamates 1-2 weeks after it appears.

Vida, Ria, Anna One Pride, One Five! UPCM 2015 Page 3 of 12
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY PATHOGENESIS MORPHOLOGY CLINICAL SIGNIFICANCE/FEATURES EPIDEMIOLOGY NOTES
BACTERIUM
Facultative anaerobic gram Different species: Diffuse interstitial neutrophilic Ecthyma Cause suppurative infections of the
Streptococcus positive cocci 1. produce many virulence infiltrates with minimal - Occurs when Group A streptococci infection skin, oropharynx, heart valves
factors and toxins destructions of host tissues spreads through the epidermis to cause
Most are beta-hemolytic 2. have capsules that resist `punched out' ulcers that extend into the dermis Post-streptococcal syndromes include
(able to lyse cells in blood phagocytosis rheumatic fever, immune complex
agar) 3. express M protein, a Cellulitis glomerulonephritis, erythema
surface protein that - Spreading superficial infection of the skin nodosum
prevents bacteria from occuring at any age
being phagocytosed - often develops at a site of previous trauma or S. pyogenes (group A) causes
skin lesion pharyngitis, scarlet fever, erysipelas,
- abrupt onset of malaise, fever, chills and impetigo, rheumatic fever, TSS, and
headache and the involved skin becomes glomerulonephritis.
tender, red, warm and swollen
- occasionally bullous; inflammation spreads S. agalactiae (group B) colonizes the
with poorly defined margins (as compared to female genital tract and causes sepsis
erysipelas) and meningitis in neonates and
- found in lower extremities chorioamnionitis in pregnancy.

Erysipelas S. pneumonia- common cause of

- a characteristic variant of cellulitis, almost community-acquired pneumonia and
always caused exclusively by S. Pyogenes meningitis in adults.
- painful, bright red, shiny lesion with a raised,
sharply demarcated, advancing edge (“butterfly- The viridans group streptococci-
wing rash” with erythema and induration) common cause of endocarditis.
- common in the legs and face
S. mutans- major cause of dental
Scarlet fever caries
- Some group A haemolytic streptococci
produce an erythrogenic toxin causing the The skin lesions caused by
characteristic rash (punctate erythema) streptococci (furuncles, carbuncles,
- Infection is usually of the pharynx or tonsils. and impetigo) resemble those of
- Hair follicles often with slight prominence staphylococci, although streptococci
-erythema accentuated in the creases of the are less likely to cause the formation
elbows, groin and axillary folds (Pastia's lines) of discrete abscesses
- rash blanches upon pressure
- tongue is at first furred with prominent
papillae (the `white strawberry' tongue)
- extensive desquamation of the skin after 4
days which may continue for 2 weeks or more
- desquamation of the tongue leaves a raw, red
tongue with prominent papillae (`red-
strawberry' tongue)

Vida, Ria, Anna One Pride, One Five! UPCM 2015 Page 4 of 12
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY
BACTERIUM
Pleiomorphic, gram-
Haemophilus negative ubiquitous
influenzae colonizer of the pharynx
Both encapsulated and
unencapsulated forms may
cause disease
Of the serotypes a-f, type B
is the most usual cause of
disease
pili mediate adherence to
respiratory epithelium, also
a factor that disorganizes
ciliary beating, protease
that degrades IgA, capsule
Capsule prevents
opsonization by
complement and
phagocytosis by host cells
Aerobic, non-spore
Mycobacterium forming, non-motile bacilli
tuberculosis with a waxy coat that
causes them to retain the
red dye when treated with
acid in acid-fast stains
Grow 20 to 100 times
slower than most other
bacteria
With unique waxy cell wall
composed of mycolic
contains:
1. Cord factor- a surface
glycolipid causing it to grow
in serpentine cords in vitro
2. Lipoarabinomannan
(LAM)- a
Vida, Ria, Anna
PATHOGENESIS
Pathogenicity is related to
its ability to escape killing
by macrophages and
induce delayed type IV
hypersensitivity. This
hypersensitivity probably
explains the
destructiveness and
emergence of resistant
strains of the organism.
Bacteria reside in
phagosomes, which are
not acidified into
lysosomes, perhaps due to
organisms secretion of
urease and uptake of
bacteria by complement-
or mannose-binding
receptors rather than Fc
MORPHOLOGY
Histological appearance:
1. submucosal infiltration with
acute inflammatory cells
2. desquamation of the ciliated
epithelium
3. intrabronchial exudate of
fibrin, pus cells and blood
Secondary lesion usually begins
as a small focus of
consolidation
Coalescent granulomas,
epitheloid cells, fibroblasts, and
lymphocytes
Tubercles coalesce to form
bigger granulomas
Caseous necrosis and cavities
may rupture into blood vessels,
causing hemoptysis
One Pride, One Five! UPCM 2015
CLINICAL SIGNIFICANCE/FEATURES
Cause lower respiratory tract infections and
meningitis in young children
Pneumonia- Great triad: Fever, cough, and
dyspnea (since there is low oxygen exchange
that will occur in portions of the lung where
alveolar spaces are filled with exudates)
Meningitis- endotoxin induces inflammation,
cell wal peptidoglycan damages endothelium
and disrupts blood brain barrier
Mild to severe involvement of the pharynx,
middle ear, sinuses, tonsils, epiglottis, larynx,
trachea, bronchi, as well as lower respiratory
tract, also the conjunctiva
In predisposed older patients: septicemia,
endocarditis, pyelonephritis, cholecyctitis,
suppurative arthritis
Diagnosis confirmed by special staining, smears,
and cultures of the organism
Secondary lesion may lead to:
a. Cavitary fibrocaseous tuberculosis- within the
lung, large confluent granuloma
b. Miliary tuberculosis- favoured areas of spread
are bone marrow, liver, spleen, retina
c.Tuberculous bronchopneumonia
Page 5 of 12
EPIDEMIOLOGY NOTES
Very hard to culture in the
Philippines.
Cigarette smokers are likely to suffer
from acute bronchitis because of the
excessive amounts of bronchial
mucus that they produce since:
1. ciliary action is abnormal
2.Part of the normal mucus-secreting
bronchial epithelium has undergone
squamous metaplasia
Anticapsular antibodies protect
against infection
Capsular polysaccharide b is
incorporated into the vaccine
Infects about 1/3 of the Two species cause tuberculosis in
world’s population and humans: M. tuberculosis and M. Bovis
kills about 3 million
patients each year In most people primary tuberculosis
is asymptomatic, although it may
Single most important cause fever and pleural effusion.
cause of death in
humans All symptomatic cases in adults are
likely to be reactivation type of illness
(occurring especially when immune
defenses are lowered).
The elderly and profoundly
immunosuppressed persons may lose
their immunity to M. tuberculosis and
so may develop primary tuberculosis
more than once.
Tuberculin test: Erythema and
induration at site of intradermal
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY
BACTERIUM
lipopolysaccharide,
(continued…..) inhibiting macrophage
Mycobacterium activation by interferon
tuberculosis gamma and inducing
macrophages to secrete IFN
gamma and IL10
3. Complement- to
opsonize the organism and
facilitate its uptake by the
macrophage complement
receptor
4. Heat shock proteins- to
induce autoimmune
reactions
Vida, Ria, Anna
PATHOGENESIS MORPHOLOGY CLINICAL SIGNIFICANCE/FEATURES EPIDEMIOLOGY NOTES
receptors injection of 5 tuberculin units in a
child with primary tuberculosis.
Pattern of host cell
response depends on Lupus vulgaris
whether the infection - TB of the skin, characterized by an
represents a primary first indolent, slowly spreading, reddish-
exposure to the organism brown plaque-like lesion
or a secondary reaction in
an already sensitized host. Tuberculids- regarded as allergic
reactions to tuberculosis elsewhere in
Primary Infection with the body
Tuberculosis
-Inhalation of organism 
phagocytosis of the
organism by alveolar
macrophages transport
to hilar lymph nodes
- naive macrophages not
able to kill the organism -
organisms multiplylyse
the host cell, infect other
macrophages  T cell
mediated immunity after a
few weeks
- Lysed macrophages form
caseating granulomas
Three ways of host and
bacterial interaction:
1. IFN gamma from CD4+
cells activates
macrophages to kill
intracellular mycobacteria
through reactive nitrogen
intermediates.
2.CD8+ cells lyse
macrophages infected with
Mycobacteria
3. CD4-CD8- cells lyse cells
without killing
Mycobacteria
One Pride, One Five! UPCM 2015 Page 6 of 12
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY
BACTERIUM
(continued….)
Mycobacterium
tuberculosis
Acid fast obligate
Mycobacterium intracellular organism that
leprae grows very poorly in culture
Leprosy (Hansen but can be propagated in
disease) armadillo
Slender, aerobic rods that
grow in straight or
branching chains
Affects skin and peripheral
nerves and results in
disabling deformities
Vida, Ria, Anna
PATHOGENESIS
The development of
resistance to the organism
is accompanied by the
appearance of a positive
tuberculin test.
Secondary and
Disseminated
Tuberculosis
- reinfection, reactivation,
or direct progress from
primary disease
-involves apex of the lung
- major cause of organ
damage: granulomas
- caseous necrosis and
cavities: may rupture into
blood vessels or bronchi.
It proliferates best at 32˚ –
34 ˚C, the temperature of
the human skin. It secretes
no toxins, virulence
depends on its cell wall
properties (like M.
tuberculosis)
It is a slowly progressive
infection
It is transmitted from
person to person through
aerosols from lesions in
the respiratory tract
It is taken up by alveolar
macrophages,
disseminates through the
blood, grows only in the
cooler tissues of the
extremities and the skin
MORPHOLOGY
Tuberculoid leprosy begins
with localized flat, red skin
lesion that enlarge and develop
irregular shapes with
indurated, elevated,
hyperpigmented margins, &
depressed pale centers (central
healing)
Lepromatous leprosy involves
the skin, peripheral nerves,
anterior chamber of the eye,
upper airways, testes, hands, &
feet; contain large aggregates
of lipid-laden macrophages
often filled with masses of acid-
fast bacilli
One Pride, One Five! UPCM 2015
CLINICAL SIGNIFICANCE/FEATURES EPIDEMIOLOGY NOTES
Leprosy is a bipolar disease, determined by the Leprosy is an infectious Leonine facies (thickened infiltrated
host cellular immune response disease of low skin, widened nose, and loss of
communicability (for eyebrows) usually found in
M . leprae causes two strikingly different instance, in lepromatous leprosy
patterns of disease: leprosariums, only a
a. Tuberculoid leprosy – have dry, scaly skin minority of the children Nasal passages are the usual location
lesion that lack sensation; have asymptomatic of couples with leprosy of this bacteria
involvement of large peripheral nerves, T-cell are affected by the
mediated immune response, with granuloma disease)
(group of macrophages that have isolated
mycobacterial organisms) formation. In 10-15 million people
tuberculoid leprosy, damage to peripheral living in poor tropical
nerves is mediated by DTH reactions to countries have leprosy
mycobacterial antigens in the sheaths and in the
fibers. Nerves of predilection- ulnar, median, The Philippines has
radial, lateral popliteal, great auricular about ten times more
cases of leprosy as that
b. Lepromatous leprosy (more severe) – diffuse of the United States.
lesions containing foamy macrophages teeming There are leprosariums
with mycobacteria, includes symmetric skin in Iloilo, Antique and
thickening & nodules ; called anergic leprosy Bicol
because of unresponsiveness of the host
immune system. In lepromatous leprosy, there
could be numerous nodular skin lesions and
Page 7 of 12
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY PATHOGENESIS MORPHOLOGY CLINICAL SIGNIFICANCE/FEATURES EPIDEMIOLOGY NOTES
BACTERIUM
thickening of the pinna. Loss of eyebrows,
(continued…..) atrophic rhinitis, testicular atrophy, and ocular
Mycobacterium damage are common in patients with
leprae lepromatous leprosy.
Leprosy (Hansen
disease)
The T-helper lymphocyte response to M. leprae
determines whether an individual has
tuberculoid or lepromatous leprosy

CD8+ suppressor T cells at the margins of

lepromatous lesions secrete:
a. IL-10 – inhibit helper T cells and mediate the
anergy seen in lepromatous leprosy

b. IL-4 – induces antibody production by B cells,

these are not protective, but rather form
antigen-antibody complexes that lead to
erythema nodosum leprosum, life-threatening
vasculitis and glomerulonephritis

Borderline tuberculoid (BT) leprosy is difficult

Gram negative facultative Plasmid invasion genes
Shigella sp. anaerobe (like S. typhi)
S. dysenteriae
S. flexneri Only infects humans Escapes from
S. boydi phagolysosome and
S. sonnei A few organisms can cause attacks host cell
symptomatic disease and
invade intestinal mucosal Shiga toxin – binds to
cells globo glycolipids and
blocks protein synthesis by
cleaving 28S rRNA,
endothelial cell damage
leading to hemorrhagic
colitis, haemolytic-uremic
syndrome
In bacillary dysentery, colonic
mucosa hyperemic and
edematous, with hyperplastic
lymphoid follicles that project
into lumen, the
fibrinosuppurative exudates
soon covers the mucosa.
The mucosa becomes soft and
friable (easily crumbles) and
ulcerates.
Exudates on surface,
mononuclear infiltrates in the
lamina propria becomes
granulation tissue, regenerated
epithelial layer
to distinguish from a fungal infection. In BT
leprosy, the lesion is anesthetic.
Bacillary dysentery: diarrhea with blood or Exudate that soon covers the mucosal
mucoid stool with fresh blood (Note that surface (pseudomembrane) is a good
dysentery occurs in both shigellosis and source of specimen for culture
infection with Entamoeba histolytica)
How do you differentiate shigellosis
Reiter syndrome: chronic arthritis in HLA-B27 from infection with Entamoeba
individuals due to S. flexneri, bacterial antigen histolytica?
reacts with the HLA-B27 protein The pseudomembrane and long
segment are apparent in shigellosis
The diarrhea is almost always self-limited while Entamoeba histolytica
infections have focal lesions.

Vida, Ria, Anna One Pride, One Five! UPCM 2015 Page 8 of 12
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY PATHOGENESIS MORPHOLOGY CLINICAL SIGNIFICANCE/FEATURES EPIDEMIOLOGY NOTES
BACTERIUM
Gram negative Damaged intestinal Hyperemia, edema, Invasiveness is strain dependent, depend on In developing countries Before, Campylobacter Was classified
Campylobacter mucosa and lamina neutrophilic and mononuclear host cell signal transduction pathways Up to 40% of children under Vibrio cholerae because both
Campylobacter Comma-shaped, flagellated propria causing ulceration, infiltrates, and even colonic under 2 years may be appear comma-shaped under the
jejuni inflammation, and crypt abscesses Clinical outcomes of infection: diarrhea, infected and the microscope
Flagella for penetrating hemorrhage ; friable and dysentery, enteric fever organism is an
mucus covering of eroded colonic mucosa important cause of
epithelial surfaces Post-infectious complications like Guillain-Barre diarrhea in travellers to
Inflammation of the entire syndrome (an acute inflammatory these countries
From contaminated food gut possible demyelinating polyneuropathy) and reactive
especially undercooked arthritis in HLA-B27 individuals C. jejuni accounts for
meat and unpasteurized more cases of enteric
milk C. jejuni, like the Yersinia species, may produce diseases than
a pseudo-appendicitis syndrome of terminal Salmonella or Shigella
Can be caused by contact ileitis and mesenteric adenitis. Untreated
with infected dogs patients usually excrete the organisms for 2-3
weeks after recovery.
Gram negative Virulence factors: Affects distal ileum and colon, Y. enterocolita, Y. Pseudotuberculosis cause Morphologically indistinguishable
Yersinia sp. Facultative intracellular Invasin pharynx and tonsils ilietis, mesenteric lymphadenitis,autoimmune from Shigella
Y. enterocolita Ail sequelae like arthritis, erythema nodosum, GN
Y. Yop Intestinal ulcers, diffuse
pseudotuberculosis enteritis with villus shortening Yersinosis- presence of necrotic inflammatory
Y. pestes crypt hyperplasia, foci
microabscesses in mucosa and
submucosa
Hyperplasia of lymphoid tissue
in terminal ileum
Gram negative Invasion of epithelial cells Peyer’s patches become Typhoid fever: Non-typhi Salmonellae infect chickens
Salmonella sp. and macrophages by sharply delineated , then 1st wk: protracted disease associated with and cows, humans only host of S.
S. enteritidis Flagellated invasion genes induced by ulcerated in the 2nd week (with bacteremia, fever, chills typhi
S. typhi low oxygen tension in the lymphadenopathy) 2nd wk: RES involvement with rash, abdominal
S. typhimurium gut pain, prostration Salmonella has a predilection for
Splenomegaly, hepatomegaly, 3rd wk: ulceration of Peyer’s Patches, intestinal systemic hyperplasia in lynph nodes
These genes: gallbladder colonization on the bleeding, shock, rupture inside abdominal cavity
a. encode proteins 3rd week Most susceptible location is the ileum
involved in adhesion and Effects of Salmonella infections (not S. typhi: (high number of Peyer’s Patches)
recruitment of host’s Eryhthrophagocytosis by a. Enterocolitis - fever, nausea and vomiting,
cytoskeletal proteins that macrophages, w/ other myalgia and headache followed by diarrhea. Blood culture is still the best way to
internalize bacterium inflammatory cells in different Usually a self-limiting disease lasting 2-3 days. diagnose typhoid fever. Even if ELISA
b. mediate growth within layers of gut could give you the answer in 30
macrophage aided by b. Enteric fever - similar to typhoid fever (fever, minutes, it is just a presumptive
acidic pH inside In typhoid fever, lesions such as muscle aches and headache without diarrhea) diagnosis of typhoid fever and
macrophage lysosome ulcers are oriented but usually milder and of shorter duration. Salmonella IgG and IgM just have a

Vida, Ria, Anna One Pride, One Five! UPCM 2015 Page 9 of 12
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY PATHOGENESIS MORPHOLOGY CLINICAL SIGNIFICANCE/FEATURES EPIDEMIOLOGY NOTES
BACTERIUM
longitudinally to the lumen Severe intestinal infection may produce positive predictive value of 40-50%.
(continued….) histopathological changes similar to those seen The blood culture may cost 3 times as
Salmonella sp. Mucosa could increase in in typhoid fever much but at least it makes your
S. enteritidis thickness about 4x because of diagnosis more certain and you’ll
S. typhi hyperplasia c. Localized infection - metastatic infection of know what antibiotic to give.
S. typhimurium vascular structures, bone and a wide variety of
In a typhoid ulcer, there could other tissues secondary to bacteremia .
be a transmural inflammatory This type of disease is especially common in
reaction, focal areas of infection due to S. choleraesuis.
necrosis, and fibrinous
exudates on the serosal surface d. Bacteremia with recurrences following
antibiotic therapy in patients with AIDS.

S. typhi shed in feces, urine, vomitus, oral

secretions
In S. typhi, there is proliferation of phagocytes
and systemic lymphadenopathy

S. enteritidis, S. typhimurium- lesions limited to

Gram negative Cholera toxin-similar to E.
Vibrio cholerae coli enterotoxin
Cholera Comma-shaped
There is persistent
140 serotypes; O1 activation of adenylate
classically associated with cyclase, high levels of
cholera intracellular cAMP,
massive secretion of
chloride, sodium, and
water
Minor histopathologic changes
the ileum and colon, erosion and mixed
inflammation
Rice-water diarrhea (a little cloudy) with flecks Most prevalent in Person may lose up to 20 L a day, 100
of mucus; rapid depletion of electrolytes southern Asia L in the duration of the disease (4-7
(Bangladesh) but also days). Note that the circulating blood
If losses are replaced promptly, only other exists along the Coast volume is just about 5 L.
symptoms would be abdominal fullness and and Gulf of Mexico and
hyperperistalsis USA When there is profound watery
diarrhea, patient loses a lot of
With inadequate replacement, hypovolemia Seven great pandemics electrolytes especially K and Na
with shock, altered consciousness, renal failure, from the Ganges valley
hypokalemia, acidosis occur of India and Bangladesh

Organism remains in Mortality rate in

lumen cholera- more than 20%

No bacteremic phase
observed

Neisseria Gram negative Bacterial capsule prevents Intracellular diplococci (one of Gonorrheal urethritis, pharyngitis, proctitis,
gonorrhea phagocytosis w/o anti- the few cocci that is Gram- bacteremia, arthritis-dermatitis syndrome;
Gonorrhea Encapsulated diplococcus gonococcal antibodies negative) conjunctivitis from autoinoculation (rubbing

Vida, Ria, Anna One Pride, One Five! UPCM 2015 Page 10 of 12
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY PATHOGENESIS MORPHOLOGY CLINICAL SIGNIFICANCE/FEATURES EPIDEMIOLOGY NOTES
BACTERIUM
eyes)
(continued.…) Genetically similar to N. Binds and invades Organisms found in
Neisseria meningitides epithelial cells; when neutrophils, not in urethral Gonococcal urethritis- most usual presentation
gonorrhea pathogenic, secretes cells of gonorrhoea, typical purulent meatal
Gonorrhea INTRACELLULAR – found protease that cleaves IgA discharge with inflammation of glans penis;
inside the cytoplasm of Exudative and purulent swelling of shaft due to periurethral abscess;
neutrophils, diagnostic sign Release peptidoglycans reactions form granulation when severe and chronic may lead to sterility
and endotoxins that cause tissue
host to secrete TNFa that Urethritis in females increases chances of
may cause shock and Plasma cell reaction leads to sterility and ectopic pregnancy
multisystem failure, also fibrosis Exudative and purulent reactions lead to
mediate damage to cells formation of granulation tissue and eventually,
lining the fallopian tubes fibrosis

In males – urethral strictures, chronic infection

Vitronectin and syndecan of the epididymis, prostate, and seminal
– cell binding sites vesicles, urethral discharge in 2 to 7 days in
men, posterior urethra, epididymis, prostate,
Binding – through seminal vesicles affected, and in chronic cases,
adehesins or pili urethral strictures and sterility. The most
common presenting symptom in male is staining
of the underwear, tingling and hot sensation
and dysuria. This is because pain is felt when
urine flows through a section of the urethra that
is acutely inflamed.

In females –urethritis in women not as

prominent. There could be abscesses that cause
bulging of the Bartholin and Skeene glands ,
salpingitis that seal off ends of fallopian tubes.
Such are called tuboovarian abscesses. Females
are more asymptomatic than males.
Flagellated microaerophilic Endarteritis: spirochetes Histological hallmark – Affectation more superficial than herpes, less Known as “The Great Impostor.” In
Treponema spirochete bind to endothelial cells obliterative endarteritis and painful since nerves are not hacked the Philippines, the great impostor is
pallidum inflammation of arterial plasma cell-rich mononuclear Mycobacterium tuberculosis
Syphilis Cannot be cultured but can endothelial layer infiltrates a. Primary syphilis-chancre that erodes into an
be demonstrated by silver immunologic response ulcer that is shallow (vs. deep in Herpes); Show me where the lesion is, that’s
stains, dark field called Monos a. Primary SY – chancre - plasma cell infiltrates with few macrophages where it was inoculated.
examinations, slightly elevated firm reddened and lymphocytes, appears 3 weeks after Epidermispoint of contact
immunofluorescent papule up to several cms. in contact, heals without treatment in a few weeks
techniques diameter, erodes into a shallow Spirochetes appear in primary and
ulcer on microscopy – plasma b. Secondary-widespread mucocutaneous secondary stages only; tertiary no

Vida, Ria, Anna One Pride, One Five! UPCM 2015 Page 11 of 12
 HS 202 VIRAL INFECTIOUS DISEASES
CHARACTERISTICS OF
ETIOLOGY PATHOGENESIS MORPHOLOGY CLINICAL SIGNIFICANCE/FEATURES EPIDEMIOLOGY NOTES
BACTERIUM
A common STD cell infiltrates, with a few lesions; condyloma lata: papular lesions in the more spirochetes, not infectious
(continued…) macrophages and lymphocytes penis and vulva, 2 to 10 weeks after chancre,
Treponema sole and palm rash with fever, Spirochete –specific antibodies basis
pallidum b. Secondary SY – widespread lymphadenopathy, headache and arthritis; for diagnosis using serologic tests
Syphilis mucocutaneous lesions resolves spontaneously
(macular, condyloma lata
involving the oral cavity, palms c. Tertiary- years after; active inflammatory Related treponemes – T. pertenue
and soles) lesions of the heart, aorta, CNS; gummas in (yaws), T. carateum (pinta), T.
liver, bones, skin denticola (periodontal disease)
Condyloma lata – papular
elsions in the penis or vulva, 2- Congenital- most severe when mom’s is more Syphilic gummas are rare
3 cm. elevated red-brown recent; can lead to late abortion, stillbirth,
plaques death soon after birth; if not, there’s still The bacteria exhibits almost no
(not to be confused with interstitial keratitis, Hutchinson’s teeth, eight resistance to penicillin
condyloma acuminata which is nerve deafness
due to HPV)
Aortitis -infllammatory scarring of the media 
aneurysm

Neurosyphilis – meningovascular syphilis, tabes

dorsalis, general paresis

Syphilitic gummas – in skin, sct, bone, joints

Greetings:
Vida: Thanks sa lahat ng tumulong sa FOP! Cheers and confetti for Krisha and Nikoz, FOP Core Group and for the whole class of 2015! What a way to start our year!  Thanks Patrick and Ste for the new trans guidelines! Hello< Hygeia!

Ria: Hello 2015! Hello to new transmate ennuh and old transmate joebuh! Ang saya saya talaga magtrans ng toxic! Woohoo! First day pa lang, mukhang marami nang aaralin. Good luck to our first LU4 exam! Here’s to a great year
ahead!

Anna: Welcome back, Class 2015! All the best for LU 4! Looking forward to another great year with you guys.  Be informed! www.upmedics.com.

Vida, Ria, Anna One Pride, One Five! UPCM 2015 Page 12 of 12