Week 14 Microbiology-Bacterial Diseases and Health

Tuberculosis

• Alveola macrophages ingest M. tuberculosis

• Survive ingestion by lung macrophages

  • Additional macrophages are recruited to the site

• Fibrous capsule surrounds the macrophages excluding lymphocytes-forming granulomas called tubercles

• When tubercles rupture, they release mycobacterium into airways

Ghon foci

Tissue calcifies when affected by tuberculosis

Ghon complex

Ghon foci with adjacent lymph nodes involved

Tuberculosis Causative organism

Mycobacterium tuberculosis

• acid fast rod

Tuberculosis transmission

• Vehicle—airborne

• latent infections can reactivate

Tuberculosis virulence factors

• Mycolic acid in cell wall prevents phagosome-lysosome fusion so they multiply in macrophages

• Ability to stimulate a strong cell-mediated response

Tuberculosis signs and symptoms

• Initial symptoms: minor cough and mild fever

• Later symptoms: difficulty breathing, chest pain, wheezing, coughing up blood, weight loss

Tuberculosis treatment

Rifampin, isoniazid

Tuberculosis prevention

• Tuberculin test

• Avoiding airborne M. tuberculosis

• BCG vaccine available in other countries

Tuberculin Skin Test-TST

Purified protein derivative—PPD

TST category 1

5-9mm bleb

TST category 2

10-14mm bleb

TST category 3

15mm bleb

Black Plague Causative organism

Yersinia pestis, gram negative rod

Black Plague Signs and symptoms

High fever, enlarged lymph nodes (buboes), skin hemorrhages, bloody sputum

Black Plague Pathogenesis

• Enters via infected flea bite

• Taken up by macrophages: produce virulence factors

Black Plague Transmission

• Endemic in rodents and other wild animals

• Bubonic plague— transmitted by fleas

• Pneumonic plague— person to person—coughs and sneezes

Black plague virulence factors

• Encoded on 3 plasmids and chromosome

• E.g. capsule, antiphagocytic, plasminogen activator (destroys clots), YOP interfere with phagocytosis

Black plague treatment

• Ciprofloxacin, gentamycin

Black Plague prevention

• Flea and/ or animal control

• Vaccine for high-risk individuals

Infection

Growth of a pathogen

• Penetrate intestinal mucosa and grow

• Incubation is from 12 hours to 2 weeks

• Fever

Intoxication

Ingestion of toxin

• Symptoms appear a few hours after ingestion

Enterotoxin

A toxin that targets intestinal mucous membrane cells Gastroenteritis

Gastroenteritis

Diarrhea, dysentery

Treatment of diseases lower digestive system

Oral rehydration therapy

Transmission of lower digestive system diseases

fecal-oral route for many diseases

Typhoid

Humans— the only host

• Spread from person to person

Can reside in the gall bladder— multiply free of competition

• Patient is a carrier

  • Mary Mallon

Typhoid causative agent

• Samonella enterica serovar Typhi

• Salmonella enterica serovar Paratyphi

• Gram negative rod

Typhoid transmission

Person to person fecal-oral transmission

Typhoid pathogenesis

• Cross intestinal epithelium via M cells

• Multiply in macrophages

• Carried in blood stream to other parts

• Peyer’s patches can be destroyed—intestinal rupture

Typhoid signs & symptoms

• Fever, severe headache, constipation abdominal pain

• Intestinal rupture, bleeding, shock, and death

Typhoid prevention

Attenuated and inactivated vaccines for typhoid

Typhoid treatment

Fluoroquinolones or combination antibiotic treatments

Cholera causative organism

Vibrio cholerae, slightly curved gram negative rod; alkali and salt tolerant

Cholera transmission

Vehicle, ingestion of food or water contaminated with feces— marine crustaceans

Cholera signs & symptoms

Abrupt onset; Diarrhea with large water loss; Rice water stools

Cholera Virulence factor

Cholera toxin (enterotoxin), an A-B toxin

Cholera treatment

Oral or IV rehydration; water and electrolytes

Cholera prevention

Purifying water, handwashing, vaccine—killing bacterium + B subunit toxoid

Cholera pathogenesis

Adhere to epithelial cells of small intestine, establish infection, and produce cholera toxin, an A-B toxin

AB toxin

B portion attaches to microvilli

A portion enters cells

• activates a G protein that turns on adenylate cyclase to convert ATP to cAMP

• High cAMP causes cell to secrete chloride ions

• Sodium and other ions follow, then water follows them

Lysogenic conversion

toxin encoded by bacteriophage

Sexually Transmitted Infections (STIs)

• Transmitted by sexual contact

  • Genital—Genital

  • Genital—oral

  • Genital—Anal

• Poorly transmitted by inanimate objects

• Prevented by condoms

• Bacterial infections are treated with antibiotics

Gonorrhea Causative agent

• Neisseria gonorrhoeae

• gram negative coccus

Gonorrhea mode of transmission

Direct contact

Gonorrhea Virulence

• Primary factor—fimbriae for attachment

• Protease that inactivates IgA

Gonorrhea Complications

Endocarditis, meningitis, arthritis, ophthalamia neonatorum

Gonorrhea prevention

Condom

Gonorrhea treatment

ceftriaxone plus either azithromycin or doxycycline

Syphilis causative agent

Treponema pallidum

Gram negative spirochete

Syphilis mode of transmission

Sexual contact, kissing, transplacental

Syphilis Virulence factors

lipoproteins that induce an inflammatory immune response

Syphilis Pathogenesis

Three distinct stages—primary,secondary, and tertiary

Syphilis Treatment

Penicillin G

Syphilis Prevention

Abstinence, monogamy, condoms

Syphilis primary stage

• A painless chancre at site of infection

• Firm margins and an ulcerated center crater

• Can go unnoticed in woman

chancre

a painless genital ulcer most commonly formed during the primary stage of syphilis

Syphilis Secondary stage

• 2 to 10 weeks after the primary stage

• Pathogen multiplies in the blood

• Skin and mucosal rashes including palms and soles

• Loss of hair, malaise, and fever

Syphilis Latent period

No symptoms

Syphilis Tertiary stage

• Gummas on liver, skin, bone, and cartilage

• Neurosyphilis- delusions, memory loss

• Cardiovascular syphilis—aneurysms

Congenital Syphilis

T. pallidum can cross placenta

• Can occur in absence of any signs or symptoms in mother, and at any stage of pregnancy

• Damage to fetus usually not until fourth month

• Spontaneous abortion, stillbirth, and neonatal death common

• Survivors develop signs, symptoms