Bacillus anthracis

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ANTHRAX

-Microscopy:Gram-positive rods with endospores

-Symptoms: (3 clinical forms) cutaneous, gastrointestional, and inhalational

-Cutaneous: painful papule develops into ulcer then into necrotic eschar. Painful lymph node infection, fever and edema may develop (systemic spread). Mortality is 20%.

-Gastrointestional: Ulcers in mouth and esophagus, or nausea, vomiting and malaise, systemic spread, sepsis, edema. Mortality near 100%.

-Inhalational: Fever, shortness of breath, cough, headache, vomiting, chills following 0-2 month latency. Edema, fever, and shock with near 90% mortality.

-Transmission: Direct contact with animals or contaminated soils, ingestion of contaminated meat, inhalation of spores.

-Pathogenesis: B. anthracis can invade macrophages and remain hidden. Capsule. Bacteria usually spreads to the lymph nodes. Produces exotoxins. Lethal Factor: stimulates TNF (tumor necrosis factor) and cytokine release from macrophage. Edema Factor: Stimulates adenylate cyclase, causing edema.

-Treatment: Ciprofloxacin, penacillin, chloramphenicol, doxycycline

-Prevention: vaccine

Bacillus cereus

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Gastroenteritis

-Microscopy: Gram-positive rods with endospores

-Symptoms: (emetic form) vomiting, nausea, cramps lasting <1 day, (diarrheal form) diarrhea, nausea, cramps, lasting >1 day

-Transmission: contaminated food: rice (emetic) or meat, vegetables, sauces (diarrheal)

-Pathogenesis: heat stable enterotoxin (produced in food), heat labile exotoxin (produced in GI tract): activates adenylate cyclase.  Cereolysin (hemolysin) and lecithinase

-Treatment: symptomatic 

Clostridium botulinum

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Botulism

-Microscopy: endosporing gram positive rods

-Symptoms: blurred vision, dry mouth, abdominal pain

-Complications: flaccid paralysis, asphyxiation

-Transmission: contaminated foods (toxin present) or entry through a wound

-Pathogenesis: Anaerobic. Botulism toxin is AB type exotoxin.  When ingested or produced internally, it enters circulation and blocks release of acetylcholine at neuromuscular junctions.  Flaccid paralysis.

-Treatment: Antibiotic (metronidazole), antitoxins, and respiratory support. 

Clostridium difficile

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Pseudomembrane Colitis

-Microscopy: endosporing, gram-positive rods

-Symptoms: watery diarrhea, severe colitis with pseudomembrane formation

-Transmission: endrogenous

-Pathogenesis: overgrowth of bacteria as a result of change in natural microbiota, usually after taking antibiotics.  C. difficile then produces exotoxins that attract white blood cells, stimulate cytokine release, produce inflammation, necrosis of tissue, and may cause hemorrhage.

-Treatment: Discontinue antibiotic, use vancomycin and/or metronidazole to eliminate C. difficile.

Clostridium perfringens

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Gas gangrene

-Microscopy: endosporing gram-positive rods

-Symptoms: asymptomatic infections, or pus formation in wounds progressing to muscle inflammation, cellulitis, and gangrene (rapid bacterial growth, gas pockets, and tissue death).

-Transmission: contaminated soil or water

-Pathogenesis: exotoxins (lethal toxin, tissue degrading enzymes), rapid bacterial growth damages tissues, shock and death may result from bleeding and hemolysis.

-Treatment: surgical debridement of affected tissue, high dose of penicillin.

Clostridium tetani

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Tetanus

-Microscopy: gram positive, endosporing rods

-Symptoms: spastic paralysis of facial muscles, progresses to other skeletal muscles

-Transmission: wound infection

-Pathogenesis: tetanus toxin (exotoxin) blocks inhibitory neurotransmitter release

-Treatment: antitoxin to neutralize circulating toxins, vaccine

Mycobacterium tuberculosis

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Tuberculosis

-Microscopy: gram positive rods, acid-fast

-Symptoms: malaise, night sweats, cough, weight loss, sputum may be bloody

-Transmission: respiratory (aerosol) from infected humans (reservoir)

-Pathogenesis: mycolic acid in cell wall causes resistance to lysomal degradation, intracellular pathogen, allows it to evade immune system, tissue damage caused by host immune response, (cytokines, complement, granuloma formation)

-Treatment: Ethambutol and Isoniazid and Rifampicin and Pyrazinamide (2 months), then INH and Rifampicin (4-6 months)

Mycobacterium leprae

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Leprosy

-Microscopy: gram positive rods, acid-fast

-Symptoms: tuberculoid: hypopigmented skin lesions, lepromatous: destructive skin lesions on trunk, face, nose, neuropathy

-Transmission: aerosols or contact with nasal secretions, contact with armadillos

-Pathogenesis: intracellular pathogen, survives in phago-lysosome.  Immunopathogenesis

-Treatment: Dapsone and rifampicin (and clofazimine for leptomatous form)

Mycobacterium avium complex

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MAC disease

Common in immunocompromised patients

Tissue, blood crowded with Mycobacteria, organ functions imparied

Corynebacterium diphtheriae

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Diphtheria

-Microscopy: club shaped, irregular, gram positive rods, parallel (palisade) arrangement

-Symptoms: pharyngitis, pseudomembrane in throat

-Complications: myocarditis, neurotoxicity

-Pathogenesis: diphtheria exotoxin: inhibits EF-2, kills cell 

-Transmission: respiratory

-Treatment: Antitoxin, penicillin, erythromycin

-Prevention: vaccine

Listeria monocytogenes

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Listeriosis

capable of growing from 1-45°C

-Microscopy: gram positive rods

-Symptoms: muscle aches, nausea, diarrhea, fever

-Transmission: food borne (soft cheese and cabbage)

-Pathogenesis: intracellular pathogen, produces invasins that allow them to enter host cells and macrophages, hiding from immune system.  Produce exotoxins (cytolysins).  Lyses phagosomes and escape into cytoplasm. Hemolysins and other immune responses cause tissue damage.

-Complications: meningitis, disseminated disease in immunocompromised due to importance of cell-mediated immunity to fighting infection, serious infections in neonates: early onset (disseminated abcesses and granulomas), late onset (meningitis)

-Treatment: penicillin or ampicillin

Erysipelothrix rhosiopathiae

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Erysipeloid

-Microscopy: gram positive rods (long thin filaments)

-Symptoms: purplish inflammatory lesion, commonly on hands

-Transmission: handling of infected animals, zoonotic (butchers, farmers etc.), common in pigs

-Pathogenesis: capsule resists phagocytosis, inflammation (mediated by hyaloronidase)

-Treatment: Penicillin, Clindamycin

Nocardia

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-Microscopy: acid-fast,gram positive, rods (filamentous)

-Transmission: soil microbes, infection through inhalation and wounds, immunocompromised are most at risk.

-Symptoms: pulmonary disease, cutaneous infections 

Propionibacterium acnes

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Acne

-Microscopy: gram positive rods

-Symptoms: black heads, or white heads (puss filled follicles) with areas of inflammation

-Transmission: endogenous 

-Pathogenesis: growth in follicles causes inflammation (due to glycoprotein) and attracts white blood cells

-Treatment: Clindamycin and benzoyl peroxide

Actinomyces israelii

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Actinomycosis

-Microscopy: gram positive rods (filamentous), acid-fast

-Symptoms: swelling, draining lesion (cervicocranial), abcesses can also form elsewhere

-Pathogenesis: immunopathogenesis, granuloma, abscess, pus formation

-Treatment: debridement, Penicillin, Erythromycin, or Clindamycin