1. Bacterial Infections
GRAM-POSITIVE BACTERIAL INFECTIONS :
Staphylococcal Infections:
 Staphylococcus aureus : are pyogenic, nonmotile,
Gram-positive cocci that form grapelike clusters.
cause skin lesions (boils, carbuncles, impetigo, and
scalded skin) and also cause osteomyelitis, pneumonia,
endocarditis, food poisoning, and toxic shock syndrome .
 Staphylococcus epidermidis : causes opportunistic
infections in catheterized patients, patients with
prosthetic cardiac valves, and drug addicts.
 Staphylococcus saprophyticus : causes urinary tract
infections in young women.

2. Pathogenesis:
S. aureus and other virulent staphylococci possess
a multitude of virulence factors, which include:
 surface proteins involved in adherence.
secreted enzymes that degrade proteins.
 secreted toxins that damage host cells.
Morphology:
Whether the lesion is located in
skin, lungs, bones, or heart valves, S. aureus causes
pyogenic inflammation that is distinctive for its local
destructiveness.

4. Streptococcal Infections:
Streptococci are facultative or obligate anaerobic Gram
positive cocci that grow in pairs or chains :
 β-hemolytic streptococci : are typed according to their
surface carbohydrate (Lancefield) antigens.
• Streptococcus pyogenes (group A) : causes pharyngitis,
scarlet fever, erysipelas, impetigo, rheumatic fever,
toxic shock syndrome, and glomerulonephritis.
• Streptococcus agalactiae (group B) : colonizes female
genital tract and causes sepsis and meningitis in
neonates and chorioamnionitis in pregnancy.

5.  α-hemolytic streptococcus :
• Streptococcus pneumoniae : cause community-acquired
pneumonia and meningitis in adults.
• Streptococcus viridans : normal oral flora but also cause
endocarditis.
• Streptococcus mutans : cause dental caries.
Pathogenesis:
 different species of streptococci produce many
virulence factors and toxins.
 Many streptococci, including S. pyogenes and
S. pneumoniae have capsules that resist phagocytosis.

6.  S. pyogenes also expresses M protein, a surface protein
that prevents bacteria from being phagocytosed.
 Poststreptococcal acute rheumatic fever is autoimmune
disease caused by anti streptococcal M protein
antibodies that cross-react with cardiac myosin.
Morphology:
Streptococcal infections are characterized by
diffuse interstitial neutrophilic infiltrates with
minimal destruction of host tissues.

7. Diphtheria:
 Diphtheria is caused by a slender Gram-positive rod with
clubbed ends, Corynebacterium diphtheriae, which is
passed from person to person through aerosols or
skin shedding.
 C. diphtheriae causes a range of illnesses:
asymptomatic carriage ; skin lesions in neglected
wounds; and a life-threatening syndrome that includes
formation of a tough pharyngeal pseudomembrane ;
and toxin-mediated damage to heart, nerves, and other
organs.
 C. diphtheriae has only one toxin which blocks host cell
protein synthesis.

8. Morphology:
 Inhaled C. diphtheriae proliferate at site of
attachment on mucosa of nasopharynx, oropharynx,
larynx, or trachea.
 Release of exotoxin causes necrosis of epithelium,
accompanied by an outpouring of a dense
fibrino suppurative exudate.
 The coagulation of this exudate on ulcerated
necrotic surface creates a tough, dirty gray to black,
superficial pseudomembrane.
 Neutrophilic infiltration in underlying tissues is
intense and is accompanied by marked vascular
congestion, interstitial edema, and fibrin exudation.

10. Anthrax :
 Bacillus anthracis is a large, spore-forming Gram-positive
rod-shaped bacterium.
 acquired through exposure to animals or animal
products.
 three major anthrax syndromes: cutaneous, inhalational,
and gastrointestinal.
 Cutaneous anthrax:
• painless, pruritic papule that develops into a vesicle
within 2 days, and regional lymphadenopathy.
• After vesicle ruptures, the remaining ulcer becomes
covered with a characteristic black scar.
• Bacteremia is rare with cutaneous anthrax.

11.  Inhalational anthrax:
• occurs when spores are inhaled, causes hemorrhagic
mediastinitis.
• Frequently, anthrax meningitis develops due to
bacteremia.
• Inhalational anthrax rapidly leads to shock and
frequently death within 1 to 2 days.
 Gastrointestinal anthrax:
• Uncommon, caused by eating undercooked meat
contaminated with B. anthracis.
• Initially nausea, abdominal pain, and vomiting.
• Severe bloody diarrhea rapidly develops, and
mortality is over 50%.

12. Pathogenesis:
B. anthracis produces potent toxins and
a polyglutamyl capsule that is antiphagocytic.
Morphology:
 Anthrax lesions at any site are typified by
necrosis and exudative inflammation with
infiltration of neutrophils and macrophages.
 The presence of large, boxcar-shaped
Gram-positive extracellular bacteria in chains,
seen histopathologically or recovered in culture,
should suggest the diagnosis.

14. Nocardia:
 aerobic Gram-positive bacteria that grow in distinctive
branched chains.
 In culture, Nocardia form aerial structures with terminal
spores, resembling hyphae.
 Nocardia are found in soil and cause opportunistic
infections in immunocompromised people.
 Nocardia asteroides : causes respiratory infections.
 Nocardia brasiliensis : infect skin.
 A fifth of N. asteroides infections involve CNS,
presumably after dissemination from lungs.

15. Morphology:
 The diagnosis of nocardiosis depends on
identification of slender Gram-positive organisms
arranged in branching filaments .
 Nocardia stain with modified acid fast stains
(Fite-Faraco stain).
 At any site of infection, Nocardia elicit
a suppurative response with central liquefaction
and surrounding granulation and fibrosis.
 Granulomas do not form.

17. GRAM-NEGATIVE BACTERIAL INFECTIONS:
Neisserial Infections :
 Neisseria are Gram-negative diplococci that are
flattened on adjoining sides, giving the pair the shape
of a coffee bean.
 These aerobic bacteria grow best on enriched media
such as lysed sheep's blood agar ("chocolate" agar).
 The two clinically significant Neisseria are : Neisseria
meningitidis and Neisseria gonorrhoeae.
 N. meningitidis : cause bacterial meningitis, particularly
among people between 5 and 19 years old.
 N. gonorrhoeae : cause sexually transmitted disease,
gonorrhoea.

18. Pathogenesis:
 Both species of Neisseria use antigenic variation
to escape the immune response.

19. Whooping Cough:
 caused by Gram-negative coccobacillus Bordetella
pertussis.
 is an acute, highly communicable illness characterized
by paroxysms of violent coughing followed by a loud
inspiratory "whoop."
 B. pertussis vaccination has been effective in preventing
whooping cough.
Pathogenesis :
 B. pertussis colonizes the brush border of bronchial
epithelium and also invades macrophages.
 Pertussis toxin is an exotoxin composed of five distinct
peptides.

20. Morphology:
 Bordetella bacteria cause
laryngotracheobronchitis that in severe cases
features bronchial mucosal erosion, hyperemia,
and copious mucopurulent exudate .
 a striking peripheral lymphocytosis (up to 90%)
with hypercellularity and enlargement of mucosal
lymph follicles and peribronchial lymph nodes.

22. Pseudomonas Infection:
 Pseudomonas aeruginosa is an opportunistic aerobic
Gram-negative bacillus that is a deadly pathogen
of patients with cystic fibrosis, severe burns, or
neutropenia.
 Most patients with cystic fibrosis die of pulmonary
failure secondary to chronic infection with
P. aeruginosa.
 P. aeruginosa also causes corneal keratitis in wearers
of contact lenses; endocarditis and osteomyelitis in
intravenous drug abusers; external otitis (swimmer's
ear) in healthy individuals, and severe external otitis
in diabetics.

23. Pathogenesis:
 P. aeruginosa has pili and adherence proteins
that bind to epithelial cells and lung mucin.
 as well as an endotoxin that causes symptoms
and signs of Gram-negative sepsis.
 The organisms also secrete an exotoxin and
several other virulence factors.

24. Morphology:
 Pseudomonas pneumonia: necrotizing
inflammation distributing through the
terminal airways , with striking whitish
necrotic centers and red hemorrhagic
peripheral areas.
 Gram-negative vasculitis accompanied by
thrombosis and hemorrhage, although not
pathognomonic, is highly suggestive of
P. aeruginosa infection.

26. Plague:
 Yersinia pestis is a Gram-negative facultative
intracellular bacterium that is transmitted by
fleabites or aerosols.
 causes a highly invasive fatal systemic infection
called plague, also named Black Death.
 Y. enterocolitica and Y. pseudotuberculosis :
are genetically similar to Y. pestis ; these bacteria
cause fecal-orally transmitted ileitis and
mesenteric lymphadenitis.

27. Morphology:
 Y. pestis causes lymph node enlargement
(buboes), pneumonia, or sepsis, all with
striking neutrophilia.
 The distinctive histologic features of plague
include:
(1) massive proliferation of organisms.
(2) necrosis of tissues and blood vessels with
hemorrhage and thrombosis.
(3) neutrophilic infiltrates that accumulate
adjacent to necrotic areas.

28. Chancroid (Soft Chancre):
acute, sexually transmitted, ulcerative infection
caused by Hemophilus ducreyi.
Morphology:
Grossly:
 tender, erythematous papule involving external
genitalia.
 primary lesion erodes to produce an irregular ulcer .
 In contrast to primary chancre of syphilis, the ulcer
of chancroid is not indurated.
 The regional lymph nodes enlarged and tender in about
50% of cases

29. Microscopically :
• the ulcer of chancroid contains a superficial zone
of neutrophilic debris and fibrin.
• underlying zone of granulation tissue containing
areas of necrosis and thrombosed vessels.
• A dense, lymphoplasmacytic inflammatory
infiltrate is present beneath the layer of
granulation tissue.
• Coccobacillary organisms are sometimes
demonstrable in Gram or silver stains.

30. Granuloma Inguinale:
Granuloma inguinale or donovanosis, is a chronic
inflammatory disease caused by Calymmatobacterium
donovani( a minute, encapsulated, coccobacillus ).
The organism is sexually transmitted.
Morphology:
Grossly:
 a raised, papular lesion involving genitalia.
 eventually ulceration, and abundant granulation tissue
manifested grossly as soft, painless mass.
 Disfiguring scars in untreated cases.
 Regional lymph nodes are spared or show only
nonspecific reactive changes, in contrast to chancroid.

31. Microscopically:
 marked epithelial hyperplasia
(pseudoepitheliomatous hyperplasia).
 A mixture of neutrophils and mononuclear
inflammatory cells at the base of ulcer and
beneath the surrounding epithelium.
 The organisms are demonstrable in
Giemsa-stained smears of exudate as
minute encapsulated coccobacilli (Donovan
bodies) in macrophages.
 Silver stains (e.g., Warthin-Starry stain) may also
be used.

32. Typical histological pattern showing epithelial proliferation - pseudoepitheliomatous
hyperplasia.

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