Micro Unit 9: Gastrointestinal, Nervous, Urogenital Diseases

Normal flora of GI system

Lactobacillus, E. coli

Bacterial pathogens of the stomach

H. pylori

H. pylori - peptic ulcers

> dark stools, bloating, nausea, etc.

Peptic ulcer virulence factors

production of urease > production of ammonia, neutralizes the stomach acids

Peptic ulcer pathogenesis

bacterium tolerates stomach's acidic environment
> damages stomach lining, ulcers
> stomach perforation, risk of stomach cancer

Peptic ulcer mode of transmission

direct contact (body fluids) or vehicle (contaminated water); mucus membranes

Lower intestinal diseases

2 types
- infection
- intoxication

Infection

where the actual pathogen is ingested, colonizes and causes damage
- longer incubation, slower progression

Intoxication

where only toxins are ingested, cause damage
- rarely fever, quick symptoms

Lower intestinal disease mode of transmission

vehicle, foodborne

Intestinal disease treatments

- oral rehydration therapy
- antibiotics

Bacterial pathogens of the lower intestine

- S. aureus
- Shigella spp.
- Salmonella spp.
- E. coli
- V. cholerae
- C. difficile

Staphylococcal food poisoning

- typically only intoxication
- prevalent in salty foods or improperly prepared

Staphylococcal food poisoning virulence factors

heat-stable enterotoxin (exotoxin) which act as superantigen

Shigellosis

- from fecal-contaminated food/water
- hemolytic uremic syndrome, rectal bleeding, etc

Shigellosis virulence factors

- organism is invasive, spreads
- shiga toxin > hemorrhaging

Salmonellosis

- invasive organism, but doesn't spread to other cells
- can enter bloodstream > carrier
- infection or intoxication
- endotoxin from some strains
- poultry, contamination from animals

EPEC (enteropathogenic E. coli)

- traveller's diarrhea > severe dehydration

EHEC (enterohemorrhagic E. coli)

more severe infection; shiga-like toxin
- complications similar to shigellosis, ex. hemolytic uremic syndrome
- can't be treated with antibiotics
- fecal contamination

Cholera

- rice water stools

Cholera virulence factors

motile bacteria produces an A-B exotoxin
> activation of chloride channels > loss of ions + H2O

Cholera causes

- fecal contaminated food/water, poor sanitation or following natural disasters
- shellfish

C. difficile infections

- microbe is gram-pos and endospore forming
> colon perforation, septicemia, shock

C. difficile virulence factors

produces 2 cytolytic exotoxins > diarrhea, dehydration, abdominal pain

C. difficile causes

HAI, opportunistic (extended use of antibiotics)
- fecal contamination

Protozoan pathogen of lower intestine

Giardia lamblia

Giardiasis

symptoms 2-6 weeks, dehydration diarrhea, nausea, cramps, gas; asymptomatic
> chronic infections resistant to treatment

Giardiasis virulence factors

protist attaches to intestinal mucosa using an adhesive disk > blocks absorption of nutrients

Giardiasis treatment

anti-protozoan medication

Giardiasis prevention

filtration of water to remove cysts; boiling water ineffective

Hepatitis

acute liver inflammation leads to malaise, dark urine, grey stool, loss of appetite, etc

Hepatitis pathogenesis

> virus enters blood, spreads, reacts + inflames liver
> liver loses normal function, ex. breakdown of bilirubin > jaundice

Hepatitis A

- non enveloped RNA
- no further complications, clears
- vehicle food
- mucus membranes
- self-limiting
- attenuated + inactivated vaccines

Hepatitis B

- enveloped DNA
- 6-10% will develop cirrhosis > liver cancer
- direct + indirect contact
- parenteral, mucous membranes
- antivirals
- subunit vaccine

Hepatitis C

- enveloped RNA
- majority develop cirrhosis > liver cancer
- direct + indirect contact
- parenteral, mucous membranes
- antivirals
- no vaccine

Blood-brain barrier

prevents pathogen entry into nervous system

Meningitis

inflammation of the meninges

Encephalitis

inflammation of the brain tissue

Transmission of meningitis

> pathogens gain access to bloodstream after trauma, production of toxins, or spread from respiratory tract
> inflammation
> pathogens enter CNS (tight junctions become leaky)

Bacterial causes of meningitis

- Neisseria meningitides
- Streptococcus pneumoniae
- Haemophilus influenzae

Neisseria meningitides

- petechial rash
- gram-neg
- children + young adults
> sepsis, organ failure, death

Neisseria meningitides virulence factors

- endotoxins for attachment
- capsule
- enzymes to avoid immune system

Streptococcus pneumoniae meningitis

- gram-positive
- children without vaccine susceptible
> septicemia

S. pneumoniae meningitis virulence factors

- proteins for attachment + inflammation
- capsule

Haemophilus influenzae meningitis

- gram-negative
- chemicals to trigger inflammation, adherence, invasion; capsule

Viral causes of meningitis

herpes virus, influenza virus, measles virus
- less severe

Fungal causes of meningitis

Cryptococcus neoformans

Cryptococcosis

- asymptomatic in healthy ppl
- thick capsule
- anti-fungal drugs

Cryptococcosis mode of transmission

vehicle transmission where pathogen is found in soil + aerosolized pigeon droppings

Protozoan causes of meningitis

Naegleria fowleri

Naegleria fowleri

parasite in trophozoite form with enter thru nasal passages to CNS

Naegleri fowleri mode of transmission

submersion of head in freshwater

Naegleri fowleri detection

observation of cerebrospinal fluid

Naegleri fowleri treatment

anti protozoan drug + therapeutic hypothermia
- if infection caught early

Other bacterial disease of the nervous system

- Clostridium tetani
- Clostridium botulinum

Clostridium tetani - tetanus

- microbe is gram-pos, obligate anaerobe, endospore-forming
- localized or generalized

Localized tetanus

affects only the muscle groups at the site of injury > muscle spasms in that area

Generalized tetanus

spread throughout the body > lockjaw, muscle spasms (arched back), progresses to respiratory system

Tetanus virulence factors

tetanospasmin exotoxin

Tetanospasm

exotoxin which prevents the release of GABA, for muscle relaxation

Tetanus mode of transmission

- direct contact thru wounds
- vector biological transmission thru animal bites

Tetanus treatment

assisted breathing, wound debridement, antibiotic therapy, anti-toxins
- toxoid vaccine

Clostridium botulinum - botulism

- gram-pos, obligate anaerobe, endospore-forming
- 3 types

Foodborne botulism

- foodborne vehicle transmission (honey, improper canning, etc)
- mucous membranes (GI)
- infants or immunocompromised

Inhalation botulism

- airborne vehicle transmission
- mucous membranes (respiratory)

Iatrogenic botulism

- direct contact transmission
- parenteral (rare after use of toxin)

Medical usage of botulism toxin

- to treat various medical conditions, ex. cerebral palsy, multiple sclerosis, etc
- cosmetic purposes to remove wrinkles, prevent excessive sweating

Botulism virulence factor

botulism A-B toxin

Botulism treatment

anti-toxins

Viral diseases of the nervous system

rabies virus

Furious rabies

individual shows signs + symptoms such as agitation, hydrophobia, excessive salivation

Paralytic rabies

where the muscles progressively become paralyzed leading to coma

Rabies progression

> incubate weeks to years
> replicates + moves along neuron
> disrupts normal neurotransmitter function in brain
> moves to other tissues

Rabies mode of transmission

vector biological transmission thru animal bites; parenteral

Normal flora in urogenital system

Staphylococcus aureus

Rabies treatment

inactivated vaccine to slow progression of pathogen; antibodies

Cystitis

inflammation of the bladder

Urethritis

inflammation of the urethra

Pylonephritis

infection of the kidneys

Glomerulonephritis

inflammation of the glomeruli

Female risk for urogenital infections

- typically caused by fecal contamination
- shorter urethra > increased bladder infection

Male risk for urogenital infections

enlarged prostate or kidney stones > impact drainage of urine, increases bladder infections

Bacterial causes of cystitis

E. coli, Pseudomonas aeruginosa, Klebsiella spp.

Cystitis symptoms

dysuria, pyuria, hematuria, bladder pain
- treated with antibiotics
- can lead to kidney infection, back pain

Bacterial causes of reproductive diseases

Neisseria gonorrhoea, Treponema pallidum,

Neisseria gonorrhoea > gonorrhea

typically asymptomatic
> can spread thru body, different organs

Gonorrhea in women

pelvic pain + discharge
- can spread to endometrium + fallopian tubes > PID

Gonorrhea in men

burning during urination + discharge

Treponema pallidum > Syphilis

tissue damage caused by lipoproteins from bacteria > inflammation, further invasion
- 3 stages

Syphilis primary stage

formation of painless lesion called chancre

Syphilis secondary stage

skin rash, many forms
- bacterium can enter a latent phase

Syphilis tertiary phase

formation of granulomatous lesions (gammas) from chronic inflammation
> severe tissue damage in cardiovascular or nervous system

Human Papillomavirus

some serotypes asymptomatic, self-limiting or lead to genital warts or cancer

HPV treatment

removal or use of topical medications, chemotherapy
- vaccine for some serotypes

HPV detection

testing only done for women; Pap smears
- biopsy for confirmation

Pap smear

looking for cells with enlarged nuclei (koilocytes)