Staphylococcus aureus and Streptococcus pyogenes are common Gram-positive bacterial infections that cause issues like skin lesions, pneumonia, and rheumatic fever. They produce toxins and adhere to host cells to cause illness. Gram-negative bacteria like Neisseria meningitidis, Bordetella pertussis, and Pseudomonas aeruginosa can lead to meningitis, whooping cough, and pneumonia through virulence factors and invasion of tissues. Yersinia pestis caused the bubonic plague through proliferation in lymph nodes and necrosis of tissues.

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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