PATHOLOGY

Infectious Diseases ii:

BACTERIAL INFECTIONS
Dr. Arlene Santos August 11, 2011

11. Enterotoxin
GRAM-POSITIVE BACTERIAL INFECTIONS - Another superantigen
1. Staphylococcal infections
- Causes food poisoning (Acute self-limited diarrhea)
2. Streptococcal & Enterococcal infections
- Stimulates vomiting center in the CNS ENS
3. Diphtheria
Emesis
4. Listeriosis
5. Anthrax (discussed in Bioterrorism)
6. Nocardia
Staphylococcal Infections
Gram-positive cocci in clusters (grapelike)
Produce disease by:
1. Multiplication & spread in the tissues
2. Production of toxins & enzymes
Note:
Cause myriad of skin lesions: boils, carbuncles, furuncles,
SSS (Scalded Skin Syndrome), TSS (Toxic Shock Syndrome),
abscess formation, endocarditis, food poisoning, osteomyelitis
Toxins and Enzymes of Staphylococci
1. Catalase
Fig. Consequences of Staphylococcal Infection
- Positive (+) Bubble formation when H2O2 is added
2. Coagulase Pathologic Findings
- Synonymous with invasive pathogenic potential 1. Furuncle/boil
3. Hyaluronidase - Focal suppurative inflammation of skin & subcutaneous
- Hydrolyses hyaluronic acid in the connective tissue tissue
Facilitates spread of infection - Frequently seen in moist/hairy areas (Face, axillae, groin,
4. Staphylokinase legs and submammary folds)
- Results in fibrinolysis - Starts in a single hair follicle Develops into a growing &
5. Proteinases deepening abscess
6. Lipases 2. Carbuncle
- Degrades lipids on skin surface - Involves a deeper suppuration, spreading laterally beneath
- Enables it to produce boils or carbuncles the deep subcutaneous fascia (Upper back and posterior
7. Exotoxins neck) Burrows superficially to erupt in multiple adjacent
- -toxin skin sinuses
A hemolysin 3. Hidradenitis: Chronic suppurative infection of apocrine
Damages platelets glands most often in axilla
Lethal & dermonecrotic factor 4. Paronychia: Nail bed infection
Acts on vascular smooth muscle 5. Felons: Infection on palmar side of fingertips
- -toxin 6. Lung abscess
Sphingomyelinase - S. aureus lung infections
Toxic for many kinds of cells including RBCs - Extensive neutrophilic infiltrate within the alveoli
- -toxin - Destruction of the alveoli
Detergent-like peptide
- -Toxin Note:
A hemolysin (Lyses RBC and phagocytic cells) Staphylococcus infection in general:
8. Leukocidin Histologically, there is separation and production of
- Lyses phagocytic cells purulent exudate
9. Exfoliative toxin Marked tissue destruction
- Causes Scalded Skin syndrome (SSS) /Ritter disease
- & toxins split the skin by cleaving the protein
desmoglein 1
Keeps keratinocytes and epithelial cells intact
Part of desmosomes that hold epidermal cells
- This leads to loss in barrier function Infection
- SSS affects granulosa layer which can be distinguished
from Toxic Epidermolysis Necrosis (TEN)
Furuncle/boil Carbuncle
10. Toxic Shock Syndrome Toxin (TSS)
- The prototype of a superantigen
- Associated with fever, shock (hypotension) &
multisystem involvement

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 3. Streptococcus mutans
- Metabolize sucrose to lactic acid Enamel
demineralization
- Secret glucans that promote aggregation of bacteria and
plaque formation
4. Streptococcus pyogenes
- Scarlet fever assoc with pharyngitis
Histopathology of Streptococcal Infections
- Neutrophilic infiltration of tissues with edema
Fig. Lung abscess: Showing neutrophil infiltration with congested vessels
- Minimal tissue destruction (In contrast to Staph infections)
- Abscess formation minimal
Streptococcal and Enterococcal Infections
Gram-positive cocci in pairs or chains Diptheria
Corynebacterium diptheriae
Virulent factors & toxins: Gram (+) rod
1. Capsule Resist phagocytosis Colonizes the oropharynx
2. M protein Antiphagocytic Transmission: Aerosols or skin shedding
3. Complement C5a peptidase Degrades C5a (chemotactic Exotoxin (Phage encoded A-B) blocking of protein synthesis
peptide) via inhibition of EF-2 function essential for mRNA translation
4. Pyrogenic toxin Cause fever & rash in scarlet fever to protein
5. Pneumolysin - Causes tissue damage and reduces Exotoxin causes necrosis of epithelium Fibrino-suppurative
complement available for opsonization of bacteria membrane Formation of pseudomembranes causes
6. HMW glucans Promote aggregation of bacteria & plaque inflammation of bronchus
formation (Streptococcus mutans Dental carries) Tough pharyngeal membrane & toxin-mediated damage in
Notes: the heart
Cause myriad of suppurative infection: Skin, oropharynx, Bacterial invasion remain localized but may cause several
lungs, heartvalves symptoms as a result of entry of soluble exotoxin into the
Cause: Post-Strep GN (Glomerulonephritis), Rheumatoid blood.
Heart Fever and Erythema nodosa Note:
Can be flesh eating bacteria Causing rapidly progressive Inclusion of diphtheria toxoid in the childhood vaccine (DPT)
necrolytizing fascisitis does not prevent the colonization of C. diphtheriae but protects
Table 1. Common & Important Diseases caused by Streptococci immunized children from the lethal effect of the toxin
Infectious Agent Disease/s Pathogenesis
Pharyngitis, Impetigo, Rheumatic Corynebacterium diptheriae
Streptococcus pyogenes
fever, Glomerulonephritis, erysipelas,
(Group A strep)
Scarlet fever, TSS

Streptococcus agalactiae Releases an exotoxin
(Group B strep)
Neonatal sepsis & Meningitis
Enterococcus faecalis & Abdominal abscess, Urinary tract Causes necrosis of epithelium
other enterococci infection, Endocarditis Outpouring of a dense fibrinosuppurative exudate
Viridans streptococci S. mutans - Dental caries;
(multiple species) Endocarditis, Abscesses Coagulation of exudate on ulcerated necrotic surface
Streptococcus pneumoniae
Pneumonia, Meningitis, Endocarditis
(-hemolytic strep) A tough, dirty gray to black superficial membrane

Pathologic Findings Pathologic Findings

1. Streptoccocal erysipelas Membrane of diptheria lying within a transverse bronchus
- Cutaneous erythematous swelling Pseudomembranous inflammation of the bronchus
- Boarders are hardly demarcated Fibrinosuppurative exudates with aggregates of neutrophils
- Exotoxin released from group A & C Streptococci mixed with edema fluid and fibrin
- Rapidly spreading erythematous cutaneous swelling with Diptheritic Myocarditis
well-demarcated, serpigenous borders o Interstitial Mononuclear Inflammation
- Pathologic Findings in Streptococcal Infection o Necrosis of myocardial fibers with mononuclear
- Butterfly distribution inflammatory cells in between
2. Streptococcal pharyngitis
- Epiglottic swelling and punctuate abscesses of the
tonsillar crypts
- Minimal tissue destruction
- Major antecedent of post-strep GN

Pseudomembranous inflammation of the Diptheritic Myocarditis

bronchus

Fig. Pharynx showing streptococcal infection

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 Listeriosis GRAM-NEGATIVE BACTERIAL INFECTIONS
Listeria monocytogenes Gram (+) bacillus 1. Neisserial infections
Table 2. Infection or Diseases Caused by L. monocytogenes 2. Whooping cough
Population at Risk Infection/Disease 3. Pseudomonas infection
People who consume dairy
4. Plague not discussed in lecture but included in ppt
Food-borne infection 5. Chanchroid (soft chancre)
products, chicken or hotdogs
Pregnant women Amnionitis 6. Granuloma inguinale
Neonates Granulomatosis infantiseptica
Neisserial Infections
Neonates;
Immunosuppressed
Disseminated listeriosis; Neisseria species
individuals
Meningitis Gram (-) diplococci, usually occuring in pairs with or inside
WBCs
Pathologic Findings Neisseria meningitidis Attach to epithelial cells of the
Histologic finding: Exudative inflammation (Neutrophilic nasopharynx
infiltration of tissues) Neisseria gonorrheae Attach to epithelial cells of mucous
Meningitis membranes of GUT, eye, rectum & throat
o Gross finding: Purulent exudate within the leptomeninges Antigenic variation Mode to escape the immune response
o Histological finding: Neutrophils within subarachnoid Determinants of Pathogenicity
space & around leptomeningeal vessels N.meningitidis
o CSF: Gram (+), intracellular bacilli 1. Capsular polysaccharides
In neonates & immunosuppressed individuals: Abscesses - Inhibit phagocytosis
alternate with grayish or yellow nodules 2. Pili
Neonates with L. monocytogenes sepsis: Red papular rash - Enhance attachment to host cells
over extremities & abscesses in the placenta - Adhesion
Nocardia 3. Class 1,2 & 3 proteins
Nocardiosis - For pore formation in cell wall
Gram-positive bacilli 4. Class 5 protein (Opa protein)
Cause opportunistic infections in immunocompromised - For adhesion to host cells
patients 5. Lipooligosaccharide
- Has endotoxic effects
Table 3. Diseases caused by Nocardia species
Infectious Agent Disease/s N. gonorrheae
nd
- 2 leading cause of bacterial STD in States
Nocardia asteroides Respiratory Infections Brain abscess
(May be mistaken to be Tuberculosis 1. Long Pili
because of similar symptoms) - Enhance attachment to CD46 in epithelial cells
Nocardia brasiliensis Skin infections - Enhance resistance to phagocytosis
2. Protein I (Por protein)
Pathologic Findings - For pore formation
Gram-stain of a sputum: 3. Protein II (Opa protein)
o Smear-beaded - For adhesion of gonococci w/in colonies
o Branched chains - For attachment to host cells
o Gram (+) organisms - Associates w/ Por protein in pore formation
o Found with WBCs 6. 4.Lipooligosaccharide
(+) Acid fast along with TB and M. leprae - Has endotoxic effects
7. Other proteins:
- Lip protein: Heat modifiable protein
- Iron-binding protein
- IGA 1 protease-inactivates IGA1, a major mucosal Ig
Table 4. Infections & Diseases caused by Nesseria sp.
Infectious Agent Infection/s
Neisseria Bacterial meningitis
meningitidis Meningococcemia
Male Urethritis

Fig. Gram stain showing Nocardia species Female Mostly asymptomatic but infection is
present in endocervix Spread to vagina
Suppurative inflammation Fallopian tube Obliteration Infertility
Granulation tissue formation & fibrosis in the surrounding area
Granulomas do not form Children Gonococcal ophthalmia
neonatorum; during passage in birth canal
Neisseria
conjunctivitis
gonorrheae
Individuals who lack the complement protein
that form the membrane attack complex
Disseminated gonococcal disease
(gonococcal arthritis-dermatitis syndrome)

Uncommon: Meningitis & Eye infections in

adults

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 Pathologic Findings: N. meningitidis Whooping Cough
Meningococcal Infection Bordatella pertussis
- Overwhelming septicemic infection Gram (-) coccobacilli
- Rapidly progressing decreased BP Shock Paroxysmal stage - Cough develops its explosive character &
- Spread to subarachnoid space Meningitis (In children & characteristic whoop upon inhalation
adults)
WaterhouseFriderichsen syndrome Fulminant form of Determinants of Pathogenicity of B. pertussis
meningococcemia associated with bilateral adrenal 1. Pili
hemorrhage 2. Virulence factors
Meningococcal meningitis 3. Filamentous agglutinin
- Polymorphonuclear infiltration of meninges 4. Pertussis toxin
- Aggregates of polymorpholeukocytes (Neutrophils) 8. Adenyl cyclase toxin
9. Dermonecrotic toxin
10. Hemolysin
11. Tracheal cytotoxin
12. Lipopolysaccharide
Pathogenesis of Whooping Cough
B. pertussis

Enters through the respiratory tract

Maculopapular rashes in N. meningitides Bilateral adrenal hemorrhage: Adhesion & Multiplication on epithelial surface of trachea &
infection Waterhouse-Friderischen syndrome
bronchi
Interference with ciliary action (Paralysis of cilia)

Release of toxins & substances w/c irritate surface cells

Coughing & Lymphocytosis

Focal necrosis of the epithelium
Polymorphonuclear infiltration
Peribronchial inflammation
Neutrophilic infiltration around the meninges and its vessels
Interstitial pneumonia
Gonorrhea
Caused by Neisseria gonorrhea Obstruction of smaller bronchioles by mucus plugs (Mucosal
Adolescent are at high risk erosion)
Often asymptomatic, may lead to pelvic inflammatory disease,
infertility and ectopic pregnancy Atelectasis
Transmitted by oral, anal or vaginal intercourse Decreased oxygenation of blood
Perinatal transmission
S/S: Urethral infection, vaginal discharge, Morning drop Convulsions in infants w/ whooping cough
Dx: Gram stain, culture Note:
DNA screening There is Lymphocytosis not Neutrophilia even though this
Pathologic Findings is a bacterial infection
Pathologic Findings
Bacilli entangled with cilia of the bronchial epithelial cells:

Fig. Urethral discharge in gonorrhoeal infection: Morning drop

Acute suppuration Fig. Bacilli caught by the cilia of bronchial epithelium

Chronic inflammation Pseudomonas Infection
Fibrosis Pseudomonas aeruginosa
Gram-negative bacillus
Causes opportunistic infections in the following settings:
1. Disruption of skin & mucosa
2. Use of intravenous or urinary catheters
3. Neutropenia (Example: During cancer chemotherapy)
Note:
Common in hospital acquired infection and is actually the
number 1 cause of nosocomial infection

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 Determinants of Pathogenicity of P. aeruginosa
1. Pili
2. Adherence proteins
3. Lipolysaccharide
4. Alginate Prevents antibodies, antibiotics and
complements from acting to Pseudomonas due to biofilm
formation
5. Exotoxin A Inhibits protein synthesis
6. Exoenzyme S
7. G proteins Fig. Chancroid Manifestation
8. Phospholipase C Lyse RBC and pulmonary surfactant
9. Elastase Degrades IgG and ECM proteins Granuloma Inguinale (Donovanosis)
10. Iron-containing compounds Toxic to endothelial cells Sexually transmitted disease
Vascular lesions Caused by Klebsiella granulomaris (Formerly called
11. Mucoid exopolysaccharide called alginate forming a slimy Calymmatobacterium donovani)
biofilm that protects bacteria from antibodies Coccobacillus
Mode of transmission: Sexual contact
Infections and Diseases caused by P. aeruginosa
1. Infection of wounds & burns (Source of sepsis)
Pathology of Granuloma Inguinale
2. Meningitis Caused by Calymmatobacterium donovani
3. Necrotizing pneumonia Gross: Painless genital ulcers w/ rolled borders & a friable
4. Otitis externa (Swimmers ear) base
5. Eye infection Surrounding granulation tissue soft and sharply demarcated
6. Ecthyma gangrenosum (Lesions in patient with skin burns) Single or several
- In skin burns, it proliferates widely, penetrating deeply into Soft, sharply demarcated areas of granulation tissue that
veins and spreads hematogenously bleeds easily
- Skin lesions in sepsis
- Necrotic & hemorrhagic oval skin lesions
Pathologic Findings in Necrotizing Pneumonia
Organisms forming a perivascular blue haze in blood vessel
walls +Thrombosis + Hemorrhage Highly suggestive of P.
aeruginosa infection

Fig. Painless ulcer

Histologically:
o Dense dermal inflammatory infiltrate (Histiocytes & plasma
cells) with small abscesses
o Marked epithelial hyperplasia at the border of ulcer:
Pseudoepithelial hyperplasia
Fig. Perivascular blue haze in blood vessels Diagnosis: Donovan bodies Small, round, encapsulated
coccobacilli in macrophages or histiocytes
Note:
It is NOT pathognomonic yet highly suggestive of Pathologic Findings
Pseudomonas infection. There is bronchial obstruction in a cystic Wright stain of a smear of the lesion-Donovan bodies:
fibrosis patient due to alginate production.
Chancroid
Caused by Haemophilus ducreyi
Sexually transmitted
Gram (-) bacillus
One of the most common causes of genital ulcers in Africa &
Southeast Asia
Manifests as a painful genital ulcer in contrast with the genital
ulcer of granuloma inguinale which is painless Fig. Donovan bodies
Called chancroid or soft-chancre in contrast to syphilis which
have hard chancre MYCOBACTERIUM
Ulcer is not indurated (hardened) and multiple lesions may be Acid fast bacteria due to mycolic acid in cell wall
present Obligate aerobes, non-encapsulated, non-spore forming,
If untreated, inflamed and enlarged nodes (buboes) may slowly growing
erode the overlying skin Modes of Transmission
Dx: Culture MTb
Pathologic Findings o Aerosol spread: Droplet formation (Coughing or sneezing)
In males Usually on penis M. bovis
Chancroid in a female o Ingestion (Not common due to pasteurization)
o Starts as an erythematous papule Ulcer (Has a base M. avium
covered by shaggy yellow exudate) o Intracellular complex (MAC) widely disseminated infection
o Ulcerate in skin with draining exudate o AIDS patients Abundant acid-fast bacilli within
o Lesion is on the mons pubis macrophages

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 Tuberculosis
Caused by M. tuberculosis
An acid-fast bacillus
Pathogenesis
- Ability to escape killing by macrophages
- Type 4 hypersensitivity reaction
Cord factor
Lipoarabinomannan (LAM) Inhibits macrophage Fig. Macrophages packed with Mycobacteria
activation Immunosuppressed individuals without cellular immunity do
Secretion of TNF (Fever, tissue damage & weight not form granulomas
loss) No central caseation
Complement activated on the surface of MTb opsonize Instead, foamy macrophages containing mycobacteria are
and facilitate its uptake by MAC Complement receptor found
Fate of Primary Tuberculosis
- Healed and become calcified: 90%
- Progression of TB: Spread by contiguity or by erosion into
bronchi Disseminate
- Miliary TB Hematogenous spread of TB throughout the
body Numerous minute yellow-white foci
Secondary TB

Fig. The Natural History & Spectrum of Tuberculosis Fig. Lungs of a patient with secondary TB
(fig 8-28 p.369 of Robbins). Study this figure.
> 3 weeks
Primary Pulmonary TB Post-primary tuberculosis
0-3 weeks after onset Reactivation of primary tuberculosis or re-infection in a
Pathology of Primary Tuberculosis previously sensitized person
o Presence of TB granuloma/tubercle in lower lobe Granuloma in the apex of lung (due to high O2 content)
o Ghon complex: 2 features: Caseation necrosis & Cavities (cavitation)
Ghon focus (Gray white inflammation) + lymph node Resistant to TB: Heart, striated muscle, thyroid gland &
Ranke complex Ghon complex becomes fibrotic and pancreas
is the radiologically detectable calcification of the Yellow/white areas of consolidation in apex
Ghon complex Presence of cavitation
The focus undergoes caseous necrosis Fate of Secondary Tuberculosis
Histopathology of Tuberculosis - Progressive pulmonary tuberculosis TB erodes bronchi
- A granuloma without central caseation and vessels Hemoptysis
- Acid-fast Stain of Mycobacterium tuberculosis - Miliary Pulmonary Disease TB drains into lymphatics to
- Presence of TB granuloma in lung parenchyma veins and circulate back to the lungs Millet seed
- Presence of epitheloid cells appearance
If epitheloid cells form a horse-shoe pattern, is called - Endobronchial, Endotracheal & laryngeal TB
Langhans Giant Cells - Systemic Miliary TB Ehen it reaches systemic arterial
- At the periphery, lymphocytes are seen system
- Isolated Organ TB May appear in any organ/tissue
(Meninges, kidney, adrenals, bones, fallopian tubes&
vertebrae)
- Lymphadenitis (Occurring in cervical region: Scrofula)
- Intestinal TB

Fig. This is an acid fast stain of Mycobacterium tuberculosis (MTB). Note the red
rods--hence the terminology for MTB in histologic sections or smears: Acid fast Fig. Miliary Tuberculosis of the Spleen: Minute yellow/white foci of consolidation
bacilli and inflammation

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Diagnosis of Tuberculosis Pathology of Leprosy
- Clinical history, PE and radiologic findings - Inflammatory infiltrates in the endoneural & epineural
- AFB smears and culture compartments
- Histological findings - Cells within the endoneurium contain acid-fast positive lepra
- PCR Assay (Advanced rapid and sensitive) bacilli
- However culture Gold standard (Testing for drug - Presence of hypopigmented maccule
susceptibility and multiple drug resistance) - Skin nodules coalesce

Mycobacterium avium-intracellulare Complex MAC

MAC is uncommon except among people with AIDS and low
3
numbers of CD4+ lymphocytes (<60 cells/mm )
Hallmark of M. avium infection Abundant acid-fast bacilli
within macrophages
How does TB manifest in HIV patients?
- Patients with CD4+ T-cell count: >300 cells/mm3: Usual
secondary TB Fig. Lepromatous TB. AFB within macrophage: Red-snappers
- Patients with <200 cells/mm3: Primary or progressive TB
- Other features : SPIROCHETES
Increase sputum smear negativity Syphilis
(-) PPD Caused by Treponema pallidum
Absence of granulomas Usual mode of transmission: Sexual intercourse
Pathology of MAC Infection Can be transmitted to the fetus during pregnancy
- The lymph nodes in this mesentery, best seen at the left, are Gross: Painless, shallow ulcer (hard chancre)
enlarged and have cut surfaces that appear yellow-tan Micro: Ulceration, chronic inflammation (Predominance of
- These nodes are filled with sheets of Mycobacterium avium- plasma cells) & vasculitis
complex (MAC) organisms, and the immune response is so Treatment: PCN
poor in this AIDS patient that there is no focal granuloma Diagnosis
formation o Dark-field examination;
o Immunofluorescence techniques
o VDRL (Venereal Disease Research Laboratory test)
o RPR (Rapid Plasma Region)
o Treponema pallidum (Dark field microscopy)

Leprosy (Hansens disease)

M. leprae Delayed hypersensitivity reaction
Tuberculoid Leprosy
o Less severe form, dry scaly lesions with lack of sensation
o Focal areas of skin pallor & anesthesia due to early
involvement of nerves
o Basic lesion is a granuloma just like MTb
o Bacilli are almost never found hence the name
Paucibacillary leprosy
o Strong T cell-immunity (Has TH1 response Production
of IL2 and IFN- as with MTb)
Lepromatous Leprosy Fig. Protean Manifestations of Syphilis
o Severe form, also called anergy leprosy because of
unresponsiveness (anergy) of the host immune system Primary Syphilis
o Present with nodular lesion Spirochetes are found within the chancre (lesion of primary
o Disfiguring nodularity of the skin coalesce Leonine facie syphilis)
o Peripheral nerves affected late Syphilitic chancre in the scrotum
o Skin biopsy will show no granuloma but abundance of Hard chancre
lymphocytes
o Lesions with large aggregates of lepra cells (Lipid laden
macrophages) or globi (Filled with masses of acid-fast
bacilli) hence the name Multibacillary leprosy
o Granuloma formation will not happen because of failure
of TH1 response

Fig. LPO - Primary syphilis of the vulva. Note ulceration of epithelium with necrosis,
neutrophil infiltrates. Below epithelium: Mononuclear inflammatory cells,
lymphocytes, plasma cells, histocytes

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 Pathology of Lyme Disease
Erythema chronicum migrans (ECM) Stage 1:
o Expanding area of redness with a pale center

Fig. HPO Primary syphilus of the vulva. Note pressence of gumma in liver, and
marked scarring and fibrosis of gumma
Secondary Syphilis
Mucocutaneous changes Maculopapular, scaly or pustular
Condylomata lata Broad-based elevated plaques
Lymphadenopathy is common in 2 syphilis infection
NOTE:
Much of the pathology associated with B. burgdorferi is
thought to be secondary to the immune response against
the bacteria and the inflammation that accompanies it.
Lyme arthritis: Villous hypertrophy, lining cell hyperplasia
and abundant lympho and plasma cell
Distinctive feature: Onion skin-like lesion resembling in SLE
May have extensive erosion of cartilage

ANAEROBIC BACTERIA
Clostridial Infections
Clostridium perfringens Appear as box-shaped, gram (+)
bacilli
Tertiary Syphilis
3 characteristics: Table. Diseases caused by Clostridium
1. Cardiovascular syphilis Infectious Agent Disease/s
2. Neurosyphilis 1. C. perfringens, Cellulitis
3. Benign syphilis C. septicum Gas gangrene
Ruptured syphilitic aneurysm Aortic arch (Syphilitic aortitis) 2. C. tetani Tetanus
Gumma Granuloma or nodular lesions due to delayed 3. C. botulinum Botulism
hypersensitivity 4. C. difficile Pseudomembranous colitis
Primary and secondary are highly contagious, tertiary is not
Note:
and occur approximately 1 out of 3 untreated patients
C. botulism release neurotoxin which blocks synaptic
release of ACh Paralysis of respiratory and skeletal muscle
Histopathology of Clostridium perfringens
- Gas bubbles are caused by bacterial fermentation
- Gangrenous tissue with C. perfringens
- Presence of gram (+) box shapped bacilli

Congenital Syphilis
Occur during 1 or 2 when spirochetes are most abundant
Saddle nose
Hutchinson teeth
Late stages Triad of Hutchinsons teeth, interstitial keratitis,
eight-nerve deafness H-IK-ED)
Lyme Disease
Caused by Borrelia burgdorferi
Transmitted by tiny Ixodes deer ticks (Babesia & Erlichia)
Major arthropod borne disease in USA, Europe & Japan Cellulitis - Foul odor, thin discoloured Bluish-black friable to semi-fluid tissue
Involving multiple organs exudate which occurs at site of muscle necrosis
Distinctive feature of Lyme arthritis Arteritis with onion-skin-
like lesions OBLIGATE INTRACELLULAR BACTERIA
Late stage: Extensive erosion of cartilage in large joints Chlamydial Infections
Most common bacterial disease in the world
Leading cause of infertility
Leading cause of blindness worldwide
Often asymptomatic
Life cycle: Intracellular 2 forms: Elementary body
(metabolically inactive) & Reticulate body (metabolically
active)
Dx: Amplified DNA and flourescent monoclonal AB screening
C. trachomatis serotype A-C: Trachoma (Blindness),
keratoconjunctivitis
Serotype D-K: Infection and inclusion conjunctivitis
L1-L3 serotype: Lymphogranuloma venereum (Chronic
ulcerative disease)
Fig. Clinical Stages of Lyme Disease

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 Pathologic Findings Pathology
Male: Rash
o Urethritis Eschar Punched out ulcer covered by a black scar
o Epidydimitis Peripheral blood granulocyte (Band neutrophil) containing
o Mucopurulent discharge (Predominance by PMN) Ehrlichia inclusion in the cytoplasm
o Dysuria
o Frequency of urination
Females: Band neutrophil with Ehrlichia
o Trachomatis inclusion(morulae) shaped like
o Urethritis mulberries
o Cervicitis lead to sterility and ectopic pregnancy

Typhus nodule in the brain-

composed of focal microglial
proliferation with an inflammatory
infiltrate of T lymphocytes &
macrophages

Fig. Chlamydia urethrittis. Note mucupurulent discharge like gonorrhea

Rocky Mountain Spotted Fever with
Lymphogranulma venereum a thrombosed vessel & vasculitis:
Caused by Chlamydia serotypes L1, L2 & L3 Thrombus formation with vasculitis
It is a chronic ulcerative dx Inflammation infiltrate within
Often confused w/ syphilis, herpes or chancroid vascular wall
Mainly affects lymphoid tissue
Initial ulcer ordinarily pass away unnoticed Note:
Initial clinical manifestation: Swelling of the inguinal lymph RMSF Hemorrhagic rash that extends over entire body, increase
node due to stellate abscesses surrounded by epithelioid cells palms and soles is hallmark of RMSF
Extensive scarring Fistulas & strictures REFERENCES
Diagnostic tests:
1. Robbins Pathologic Basis of Disease (IMPORTANT!!)
o Frei test
2. Lecture of Dr. Arlene Santos
o Tissue culture
3. Powerpoint and Recording of the lecture
o Monoclonal antibody test
Rayney: 11 cases of SCCA on lymphogranulomatous REVIEW QUESTIONS
strictures 1. What organism causes Skin Scalded Syndrome
Pathologic findings in Lymphogranuloma venereum 2. The no. 1 cause of nosocomial infection
- Enlarged lymph nodes in both groins 3. Ghon complex becomes fibrotic and is the radiologically
- Groove Sign detectable calcification of the Ghon complex
Shallow depression, linear fibrotic lesion parallel to 4. Chancroid is the manifestation of this organism
inguinal ligamement 5. Aside from Mycobacterium species, this family is also an
Deen in ingunal area in males and in pararectal region acid fast bacilli
in females 6. Chlamydia serotype L1-L3 can cause this disease
7. At what stage of Lyme disease can chronic arthritis be
Rickettsial Infections manifested?
Most Rickettsial are transmitted by insect vectors 8. Lymphocytosis is manifested in this bacterial infection
o Q fever Aerosols 9. Fulminant form of meningococcemia
o Rickettsia prowazekii Epidemic typhus: Lice 10. What organism can cause Rocky Mountain Spotted Fever?
o Rickettsia rickettsii and others - RMSF Ticks
o Orienta tsutsugamushi Scrub typhus Mites ANSWERS
o Mnemonics: Smell feet SMEL FT 1. Staphylococcus aureus
Tropism: Endothelial cells in blood vessels Rashes 2. Pseudomonas aeruginosa
Predominantly infect endothelial cells & vascular smooth 3. Ranke Complex
muscle cells Vasculitis and disruption Vascular leakage 4. Haemophilus ducreyi
Hypovolemic shock 5. Nocardia species
Rickettisal Enter skin or with scratching of the skin covered 6. Chronic Lymphogranuloma venerum
with insect feces Vholesterol containing receptor 7. Stage 3
Endocytosed into phagolysosomes Escapes into cytosol 8. Pertussis/Whooping Cough
Vauses cell lysis or infects other cells 9. Waterhouse-Friderichsen Syndrome
Eschar Hemorrhagic rash 10. Rickettsia rickettsii
Microscopically thrombosed vessels Vasculitis
Dx: Immunostaining & antibody detection REMARKS
Tip: Study/Correlate/Integrate it with the lectures we had
Note:
in Microbiology especially this trans so that youll be able to finish
They lyse endothelial cell in typhus group or spread from cell faster. We didnt explain the virulence factors/toxins in full detail
to cell in spotted fever group
because it was already in Micro-trans. Be responsible to read it.
Hope that this can really help. God Bless!! =)

SECTION B UERMMMC Class 2014 Pathology 9 | 9