Illinois State University | BSC 391 | Microbial Pathogens Exam 2

Coronybacterium diptheriae characteristics

Gram +/- variable, pleotrophic, classic one molecule pathogen, frequently colonizes humans

Diphtheria

infection of upper respiratory tract

Pseudomembrane formation in throat and mouth

Inflammation of throat, possible heart damage and neuron damage

Difficulty swallowing

Coronybacterium urealiticum

Opportunistic pathogen of the urinary tract

Produces urease, may cause renal calculi (kidney stones)

Regulation of tox gene by iron (coronybacterium)

Toxin: main virulence factor

AB receptor: binding and translocation on B

B binds to heparin: binding epidermal growth factor precursor

Catalytic group A: ADP ribosylation of diphthamide only found in EF2 molecules

Ceases de novo protein production

Toxin strongest in the throat, may spread to blood

Cardiac tissue and neurons susceptible

Repressed by iron: binds to promoter and inhibits transcription of toxin

How immunization against coronybacterium toxin works

Prevention: covered in TDaP vaccine, previously DPT

Protects against toxin

Listeria monocytogenes characteristics

Gram + rod, Intracellular pathogen, Moves from cell to cell efficiently

Listeria monocytogenes clinical manifestations

Causes health issues in pregnant women: bacteremia

Can transmit transplacentally: causes severe disease in newborns

Found in humans, mammals, birds, soil, plants, water

Listeria monocytogenes temperature fun fact

Motile at environmental temps but NOT body temp

Can grow at 4°C, allowing it to grow in food

How L. monocytogenes maintains membrane fluidity at low temperatures

Adjusts membrane fluidity though addition of branched structures in PM

Where is L. monocytogenes commonly contracted from?

Dairy, lunchmeat, or cabbage

Cellular invasion by L. monocytogenes and the proteins/genes essential in this process

Adherence: probably terminal galactose

Internalin: used for attachment and eliciting endocytosis

Listeriolysin O: degrades endocytic vesicle

Actin comet: caused by Act A

Pushes bacteria into adjacent cells

covered by double membrane in new cell

Phospholipase C and listeriolysin O: involved in release of double vesicle

Serotyping

relies on immunodetection of common antigens on bacterial surface

O serotyping

identifies various forms of O-antigen

H serotyping

identifies various forms of flagellum, Not always produced

K serotying

identifies various forms of capsule, Not always produced

Virotyping

Relies on presence of virulence factors that are linked with specific diseases

ETEC

enterotoxigenic E. coli

Clinical manifestations of ETEC

Causes travelers diarrhea, severe dehydration

ETEC pathogenesis

Produce AB toxin called LT-I or LT-II (labile toxin)

Stored in periplasmic space, but bile salts release

Interact with G protein, causing cAMP accumulation

No permanent cell damage

Cause efflux of water into lumen of intestines

Uses CFA I and II as adhesins to bind to glycoproteins

Produce bundle-forming pili

Fimbriae that clump together

EAggEC

enteroaggregative E. coli

EAggEC pathogenesis

Form clusters

GVVPQ fimbraie resemble curli

Named for distinctive amino acid sequence

Produces EAST: enteroaggregative stable toxin

Forms pores in host cell

Calcium floods in and calcium-dependent phosphorylation is disrupted

Efflux of water into lumen of intestine

No true tissue pathology

EPEC

enteropathogenic E. coli

EAST

enteroaggregative stable toxin

EPEC pathogenesis

Causes true tissue damage

Attaching and effacing eae gene products are important virulence factors 

Microvilli: long where there's no bacteria and short or nonexistent where bacteria are bound

This damages tissue 

BFP (bundle-forming pilus) involved in initial binding: encoded by genes on a plasmid  

Tir protein: inserted into host cell membrane and acts as binding target for intimin

Microvilli in EPEC

long where there's no bacteria and short or nonexistent where bacteria are bound

BFP (bundle-forming pilus) involved in initial binding in EPEC

encoded by genes on a plasmid

Tir protein in EPEC

inserted into host cell membrane and acts as binding target for intimin

EHEC

Enterohemorrhagic E. coli

EHEC pathogenesis

Causes dysentery (bloody diarrhea) and hemolytic uremic syndrome (HUS)

Causes true pathology

Uses Tir and intimin to bind and cause damage to host cells

Shiga toxin cause HUS:

AB toxin that spreads though blood stream and binds to globotrioacyle ceramide on host cells

Present in gut and glomerulus of kidney

High density in children

Clinical manifestations of EHEC

HUS causes renal damage and is life-threatening if not caught early

Where is EHEC found?

Ground beef, apple cider, leafy greens, water near livestock

EIEC

Enteroinvasive E. coli

EIEC phylogeny and relatedness

Virtually identical to an extremely close relative Shigella

Does not produce toxin associated with shigella

UPEC

Uropathogenic E. coli

What is a common cause of urinary tract infections (UTIs)?

UPEC

What type of infection does cystitis refer to?

Infection of the bladder

What type of infection does pyelonephritis refer to?

Infection of the kidney with fever

How is UPEC typically acquired?

By self-inoculation from the lower GI tract

What is a characteristic feature of UPEC that aids its movement?

It is motile and produces flagella

What do type 1 fimbriae bind to in the host?

Mannose in host structures in the lower urinary tract

What do pyelonephritis-associated pili bind to?

Structures in the kidney

Why is UPEC considered dangerous and damaging?

It can cause severe infections like cystitis and pyelonephritis

Type 1 fimbriae in UPEC

bind mannose in host structures in lower urinary tract

Pyelonephritis-associated pili in UPEC

bind to structures in kidney

Diseases caused by Salmonella

enteritis, septicemia, typhoid fever

Salmonella pathogens

S. typhi, S. typhimurium, S. enterica

What are common symptoms of enteritis?

Vomiting and regular diarrhea

How does the onset of enteritis compare to staph or bacillus?

Longer onset than with staph or bacillus

How long can symptoms of enteritis last?

Up to 10 days

How is enteritis commonly contracted?

From eggs or poultry (live chickens)

Is there a vaccine for enteritis?

Yes, a vaccine has been developed for chickens

What do cells invade in enteritis?

The intestines

What mechanism do M-cells of Peyer's patches use?

Cells antigen collection mechanism

What type of tissue is involved in enteritis?

GALT tissue

What serious condition can enteritis lead to?

Septicemia

Septicemia

infection of intestines spreads to endothelium

Usually only a problems for immunocompromised host

What causes typhoid fever in humans?

S. typhi

What type of disease is typhoid fever?

Febrile disease

How do bacteria invade the body in typhoid fever?

They invade macrophages and are carried to the liver and spleen.

What can result from the accumulation of bacteria in organs during typhoid fever?

Organ failure and death

What role does LPS play in typhoid fever?

It has a major role in intoxication.

What is S. typhimurium used as in research?

A model system for human typhoid.

What does S. typhimurium cause in mice?

Typhoid

What is a key component of the virulence factors of Salmonella?

LPS, particularly Lipid A

What type of genetic elements are found in Salmonella typhimurium that contribute to virulence?

Plasmids

What do the Inv genes in Salmonella encode?

Invasion and intracellular reproduction

What is the hyperinvasive locus in Salmonella referred to as?

Hil

What are pathogenicity islands?

Large gene clusters involved in virulence

What does the acid tolerance response in Salmonella allow the bacteria to do?

Survive time in the stomach

Salmonella survival in macrophages

Catalase and superoxide dismutase degrade H2O2 and reactive oxygen radicals so killing is prevented

Regulates intracellular genes by using PhoP/PhoQ system

Oxygen, metals, pHs

What is the role of the sensor in the two-comp regulatory system in salmonella?

Acts as a membrane bound receptor for specific conditions.

What does the sensor typically autophosphorylate in salmonella?

A histidine on the inside of the membrane.

What is the role of the affector in the two-comp regulatory system in salmonella?

Activated by phosphorylation of the sensor.

What does the affector act as in the two-comp regulatory system in salmonella?

A transcriptional regulator.

How does the two-comp regulatory system in salmonella affect gene expression?

It can alter gene expression of many genes based on environmental conditions.

In what type of bacteria is the two-comp regulatory system more important?

In bacteria that experience a range of conditions.

Diseases caused by Yersinia pestis

Plague: transmitted to host by bite of infected insects

Rodents that carry fleas

Three forms: bubonic, pneumonic, septicemic

Bubonic plague:

Bacteria invade macrophages and accumulate in lymph nodes

Buboes: extremely inflamed lymph nodes that may burst

Not typically host-host transmission

Pneumonic plague: most dangerous form

Bacteria invades alveolar macrophages of lung

Lung tissue damage, may cough up blood and bacteria

Can transmit host-host, causing quick spread

Septicemic plague: infection of bloodstream

Causes clotting and vascular damage leading to tissue necrosis

Diseases caused by Y. enterocolitica

enterocolitis frequently in children

Mimics appendicitis

Y. pseudotuberculosis characteristics

rare in humans

Usually causes disease in the immunocompromised

The importance of specific plasmids in virulence

Have a large plasmid (70-75 kb) that carries general virulence genes

Pestis: 2 additional plasmids

110 kb Fra: antiphagocytic surface protein forms protein capsule

9.5 kb: plasminogen activator protease

YST (Yersinia stable toxin): produced by enterocolitica, similar to ETEC

The mode of transmission of Yersinia infections

YopH and yopE injected into host directly by Type 3 secretion system

Molecular syringe built by bacterium

Allows direct injection of bacterial proteins into host

YopH: protein kinase, interferes with signal transduction

YopE: stops actin polymerization

The secretory system used by Yersinia to inject proteins into host cells

Type 3 secretion system:

Similar to flagellum structure

Injects material from cytoplasm inside inner membrane

Sometimes, certain openings allow injection of molecules that are located in periplasmic space or gaps between bacteria and host cells

Temperature role in regulating virulence of Yersinia

Y. pestis: always ready to go

Enterocolitica and pseudotuberculosis: temp regulated

Lag in ramping up virulence

The specific molecular causes of dysentery

Kill mucosal cells by competition for micronutrients

Meaning the pathogen damages intestinal lining by taking nutrients those cells need

Tissue damage to host by inflammation and cell death

Can spread by invading macrophages

Invade M cells and underlying macrophages

Dysentery

direct pathology of tissue

The processes of attachment and invasion of host cells by Shigella and the molecules responsible for each step

IpaD: attachment

IpaB: internalization

IpaC: lyses vesicle

IcsA: polymerizes actin

IcsB: lyses double vesicle

Types of fimbriae used by K. pneumoniae and role in virulence

Uses type 1 and 3 fimbriae:

Type 1: binds mannose

Type 3: binds damaged tissue

The most common diseases caused by Klebsiella

Pneumonia (nosocomial) or UTI (makes urease):

where can someone get Klebsiella in a hospital

patient intubation

What does it mean that klebsiella is an Environmental organism

associated with plant roots, fixes nitrogen

Serratia marcescens

Opportunistic pathogen, can cause nosocomial pneumonia

Proteases: degrade host tissue

Cause corneal ulcers in contact wearers

Orange/pink pigment called prodigin

Fimbrial expression of Serratia and how Serratia bind to medical plastics

Hydrophobic cell surface: adheres to medical plastics

Fimbrial subunits rotate to expose hydrophobic domain toward hydrophobic surface of plastic

Type 1 and 3 fimbriae evolved from common Serratia fimbriae

The role of urease in Proteus virulence and also in other infections and the importance of motility in Proteus infections

P. mirabilis: most common

Primarily UTIs

Proteus swarms: highly motile

Very strong urease producer: renal calculi (kidney stones)

H. pylori characteristics

Gram - spiral

motile by spiral motility

Humans are reservoir

Clinical manifestations of H. pylori

most significant, causes gastric ulcers

Acquired in life, more common in adults

Urease role in H. pylori poathogenesis

very important, allows localized pH change

The progression of gastric ulcers in h pylori

Pathogen penetrates mucus layer of stomach and invades epithelium

Tissue damage caused by LPS, urease products, and cytotoxin VacA that damages epithelium

Successfully treated with antibiotics

Diseases caused by H. influenzae

Otitis media, bronchitis, epiglottitis, sinusitis, meningitis, Purulent keratoconjunctivitis, severe septicemia, Disseminated rash, edema, high fever, septic shock

H. influenzae characteristics

Gram - opportunistic pathogen, associated with respiratory tract

where is H. parainfluenzae most commonly found

most common bacteria in human saliva