Bacterial InfectionsGRAM-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.
Pathogenesis:S. aureus and other virulent staphylococci possessa 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 inskin, lungs, bones, or heart valves, S. aureus causespyogenic inflammation that is distinctive for its localdestructiveness.
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.
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.
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.
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.
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.
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.
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%.
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.
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.
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.
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 sheeps 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.
Pathogenesis: Both species of Neisseria use antigenic variation to escape the immune response.
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.
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.
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 (swimmers ear) in healthy individuals, and severe external otitis in diabetics.
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.
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.
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.
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.
Chancroid (Soft Chancre):acute, sexually transmitted, ulcerative infectioncaused 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
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.
Granuloma Inguinale:Granuloma inguinale or donovanosis, is a chronicinflammatory disease caused by Calymmatobacteriumdonovani( 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.
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.