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MICROBIOLOGY > LECTURE 6 (Gram -ve bacteria) > Flashcards

LECTURE 6 (Gram -ve bacteria) Flashcards

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1
Q

Describe Neisseria

A
  • “kidney bean” appearance
  • Aerobic, gram -ve diplococci, non-motile, non-spore forming bacteria
  • Normal inhabitants of the human respiratory tract
  • Rarely cause disease
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2
Q

What are the similarities and differences between Neisseria gonorrhoeae and Neisseria meningitidis?

A

SIMILARITIES:
- pathogens for humans
- typically found associated with/inside polymorphonuclear cells
- both require aerobic atmosphere with added CO2 and enriched medium for optimal growth

DIFFERENCES:
- Meningococci have POLYSACCHARIDE CAPSULES, gonococci do not
- Meningococci rarely have plasmids, most gonococci do

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3
Q

Describe the Neisseria outer membrane structure

A
  • Composed of Lipid A, Core and lacks O-antigen
  • Outer membrane differs from other gram -ve bacteria
    [polysaccharide chains are shorter lacking the variable O-antigen. Short chain is called LIPOOLIGOSACCHARIDE (LOS)]
  • Has the same endotoxic power as other gram -ve bacteria (despite lacking O-antigen)
  • Pili, OMPs and LOS are antigenic
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4
Q

Why is the Oxidase test a key test for identifying Neisseriae?

A

Neisseriae produce oxidase and give positive oxidase reactions

LAB CORRELATION: When bacteria are spotted on a filter paper soaked with oxidase, the Neisseriae rapidly turn dark purple

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5
Q

Describe the growth characteristics of Neisseria Gonorrhea?

A
  • Grows well on chocolate agar + on specialised medium enriched to ensure its growth + require CO2 supplementation
  • Small, smooth, non-pigmented colonies appear after 18-24 hrs + are well developed after 48 hrs
  • Possess numerous pili
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6
Q

Do Gonococci have any capsules? (YES/NO)

A

NO

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7
Q

Describe the antigenic structure of Gonococci

A
  • PILI (Fimbriae) = hairlike appendages that enhance attachment to host cells + resistance to phagocytosis
  • POR = form pores through cell membrane
  • OPA PROTEINS = attachment to host cell receptors
  • RMP PROTEINS = associates with por in the formation of pores in the cell surface
  • LIPOOLIGOSACCHARIDE = lack O-antigen + cause mucosal cell death
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8
Q

What is Gonorrhea?

A

A sexually transmitted disease caused by Neisseria Gonorrhea

EPIDEMIOLOGY:
- highest rates in women 15-19 years old + men 20-24 years old
- major reservoir is asymptomatic patients
- newborns can be infected during birth

PATHOGENESIS:
- Not normal inhabitants of respiratory + genital flora -> PILI and OPA proteins allow initial attachment of bacteria to receptors on epithelial cells -> Gonococci attach mucous membranes of Genitourinary tract, eye, rectum and throat producing ACUTE SUPPURATION (discharge of pus) leading to tissue invasion
- Organism’s IgA protease can hydrolyse secretory IgA -> block attachment to mucosa
- Porin A in cell wall inactivates the C3b component of complement -> “serum resistance” (resistant to antibodies + complement)

SYMPTOMS:
WOMEN:
- Painful/burning sensation when urinating
- Vaginal bleeding
- Purulent vaginal discharge
MEN:
- Burning sensation during urination
- A white, yellow or green discharge from the penis
- Painful/swollen testicles

COMPLICATIONS:
- In women, ascending infection of uterine tubes (SALPINGITIS/PID) -> STERILITY (unable to have kids)
- Disseminated gonococcal infections (DGI) [most common cause of septic arthritis in sexually active adults]

LAB DIAGNOSIS:
- Specimens [pus + secretions taken from urethra, cervix, rectum, conjunctiva, throat or synovial fluid]
- Smear [reveal diplococci within pus cells]
- Culture
- Nucleic acid amplification test [important for screening population]

TREATMENT:
- CEFTRIAXONE (250mg) intramuscularly as a single dose or 400mg of oral CEFIXIME as a single dose
- ADDITIONAL THERAPY: 1g AZITHROMYCIN orally in a single dose with 100mg of DOXYCYCLINE orally twice daily for 7 days
[patients who do not complete course of treatment have risk of continued transmission + selection of resistant strains]

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9
Q

What is Disseminated gonococcal infections (DGI)?

A

Occurs when the sexually transmitted pathogen Neisseria gonorrhoeae invades the bloodstream and spreads to distant sites in the body

COMMON MANIFESTATIONS:
- Arthritis
- Tenosynovitis
- Pustules in the skin

It is the most common cause of septic arthritis in sexually active adults

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10
Q

What is Gonococcal Ophthalmia Neonatorum?

A

An infection of the eye in newborns when a neonate is infected with genital gonorrhoea during passage through a birth canal

PATHOGENESIS:
Initial conjunctivitis rapidly progresses + if left untreated results in blindness

PREVENTION:
Instillation of tetracycline, erythromycin or silver nitrate into the conjunctival sac of newborns

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11
Q

Why are repeated gonoccal infections common?

A

Since protective immunity to reinfection does not appear to develop as part of the disease process due to the antigenic variety of gonococci

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12
Q

Describe Neisseria Meningitidis

A
  • Produce medium-sized smooth colonies on blood agar after overnight incubation
  • Most important disease-producing serogroups are A, B, C, W-135 and Y
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13
Q

Describe the Antigenic structure of Meningococci

A
  • Outer membrane + LOS = play major roles in organism virulence
  • Two porin proteins (POR A and POR B) = control nutrient diffusion into organism + interact with host cells
  • OPA proteins = attachment to host cell receptors
  • Lipid A = toxic effects
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14
Q

What are the three virulence factors that Meningococci have?

A
  • Polysaccharide capsule = enables organism to resist phagocytosis by polymorphonuclear leukocytes (PMNs)
  • Endotoxin = causes fever, shock
  • IgA protease = cleaves secretory IgA -> helps bacteria attach to membranes of upper respiratory tract
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15
Q

What is Meningitis?

A

An infection and inflammation of the fluid and membranes surrounding the brain and spinal cord caused by Neisseria Meningitidis

EPIDEMIOLOGY:
- Transmitted by airborne droplets/direct contact
- Carriers are asymptomatic
- Group A meningococci are most likely to cause epidemics + Group B meningococci cause many cases in developed countries since not present in the vaccine

PATHOGENESIS:
- Exclusively human parasite
- Meningococcal pili attach to surface proteins in NASOPHARYNGEAL epithelium -> organism can enter bloodstream + spread to meninges, joints or be disseminated throughout the body (meningococcemia)

SYMPTOMS:
- Sudden fever
- Purplish rash
- Headache + Stiff neck
- Nausea + Vomiting
- Increased sensitivity to light
- Confusion
- KERNIG’S SIGN [severe stiffness of hamstrings causes inability to straighten the leg when the hip is flexed to 90 degrees]
- BRUDZINKI’S SIGN [severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed]

COMPLICATIONS:
- Acute purulent meningitis
- Fulminant meningococcemia [endotoxin-induced sepsis + coagulopathy]

LAB DIAGNOSIS:
- Specimens = blood + spinal fluid for culture [lumbar puncture for spinal tap]
- Smear = shows neisseriae within polymorphonuclear leukocytes or extracellularly
- Culture = blood specimens are cultured without polyanethol sultanate + CSF is cultured on chocolate agar at 37 degrees with 5% CO2

TREATMENT:
- Penicillin G
- If allergic to penicillin, CEFOTAXIME or CEFTRIAXONE

PREVENTION:
- Vaccines containing capsular polysaccharide groups A, C, Y and W-135 at age 11 with boosters at 16
- Vaccine at 9 months for anyone at high risk of meningococcal disease

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16
Q

What are Enterobacteriaceae and what four metabolic processes do they have in common?

A

Large, heterogenous group of gram-negative rods whose natural habitat is the intestinal tract of humans and animals

COMMON METABOLIC PROCESSES:
- All facultative anaerobes
- All ferment glucose
- None have cytochrome oxidase (OXIDASE-NEGATIVE)
- Reduce nitrates to nitrites as part of their energy-generating processes

17
Q

Describe Enterobacteriaeceae

A

Short, gram-negative, oxidase-negative rods with rounded ends that contain flagella showing motility of the agar surface called “swarming”

PATHOGENESIS:
contain endotoxin in their cell walls

ANTIGENS:
- Contain “O antigen”
- H antigen is on the flagellar protein [only flagellated organisms have H antigens]
- Capsular/K polysaccharide antigen is prominent is heavily encapsulated organisms

LAB DIAGNOSIS:
- Hugh and Leifson agar (glucose test) = a +ve test turns it from green to yellow
- Triple sugar iron agar (TSI) = differentiate gram -ve rods due to ability to ferment glucose, lactose and produce hydrogen sulphide
- MacConkey’s agar = non-lactose fermenters form colourless colonies whereas lactose fermenters form coloured colonies

18
Q

What is Escherichia Coli?

A

The most common cause of urinary tract infection and gram -ve sepsis and is associated with “traveller’s diarrhoea”

19
Q

Describe Escherichia Coli

A

Bacteria that normally live in intestines of people and animals, but some are pathogenic

MORPHOLOGY:
- Gram -ve + motile
- Facultative anaerobe
- Non-sporulating
- Ferments lactose (distinguishes from Shigella and Salmonella)

ANTIGENS:
three antigens used for identification = O antigen (cell wall antigen), H antigen (flagellar antigen) and K antigen (capsular antigen)

SYMPTOMS:
- Begins with stomach cramps and watery diarrhoea which turns bloody within a few days
- Vomiting
- Nausea + Headaches
- Little/no fever

DIAGNOSIS:
- Physical examination
- Stool analysis
- Toxin detection (PCR)
- Blood test (CBC)
- Creatinine (kidney function)

TREATMENT:
- Mild: rest, fluid intake, rarely antibiotics
- In ICU: IV fluids + electrolytes, TMP-SMX or FLUOROQUINOLONES

20
Q

What are the virulence factors of Escherichia coli?

A
  • Mucosal interaction
    [mucosal adherence with pili -> ability to invade intestinal epithelial cells]
  • Exotoxin production
    [pore-forming cytotoxin, cytotoxic necrotising factor (CNF), Heat-labile and stable toxin, Shia-like toxin]
  • Endotoxin
    [lipid A portion of LPS]
  • Iron-binding siderophore
    [obtains iron from human transferrin or lactoferrin]
21
Q

Describe the MOA of Stx (Shiga) toxin

A

1) The A-B toxin binds to the cytoplasmic membrane, enters in an endocytotic vacuole and enters the Golgi network
2) Exiting to the cytoplasm, it combines at ribosome sites involved with tRNA binding
3) Interference with protein synthesis

22
Q

Why are newborns highly susceptible to sepsis?

A

Because they lack IgM antibodies

23
Q

Describe how E. coli causes UTIs

A

Pili virulence factor allows E. coli to travel up the urethra and infect the bladder (CYSTITIS) + move up to infect kidney (PYELONEPHRITIS) + usually occurs in catheterised patients

SYMPTOMS:
- burning during urination (dysuria)
- frequent urination
- feeling of fullness over the bladder

ADDITIONAL INFO: E. coli with enhanced potential to produce UTI are called UROPATHOGENIC E. COLI (UPEC)

24
Q

What are the 5 different types of E. coli?

A
  • STEC/EHEC (food poisoning)
  • ETEC (traveler’s diarrhoea)
  • EPEC
  • EAEC (watery diarrhoea with blood and mucous)
  • EIEC (profuse diarrhoea + high fever)
25
Q

Describe Shiga toxin-producing E. coli (STEC)/Enterohemorrhagic bacteria E. coli (EHEC)

A

Bacteria that comes from uncooked meat + raw milk and fruit + vegetables that enter the human stomach and begin producing toxins that cause serious illnesses

INCUBATION PERIOD:
3-8 days

SYMPTOMS:
- Stomach muscle spasms
- Diarrhoea
- Fever
- Vomiting

COMPLICATIONS:
- Haemolytic uremic syndrome (HUS)
- Acute renal failure
- Anemia
- Thrombocytopenia

26
Q

Describe Enterotoxic E. coli

A

It is the most important cause of “traveller’s diarrhoea” and endemic diarrhoeas in developing countries

TRANSMISSION:
- consumption of food and water contaminated by infected human/carriers
- uncooked foods such as salads/marinated meats
- direct person-to-person is UNUSUAL (since infecting dose is high)

PATHOGENESIS:
- due to HEAT-LABILE ENTEROTOXIN LT and HEAT STABLE TOXINS STa and STb
- initially attach to small intestine enterocytes using BUNDLE-FORMING PILI (Bfp) to form clustered microcolonies on enterocyte cell surface -> lesion progresses with degeneration of brush border, loss of microvilli and changes in cell morphology [ATTACHING AND EFFACING (A/E) LESION]
- not toxin mediated, symptoms result from invasive damages to intestinal walls

SYMPTOMS:
- watery diarrhoea with mucous but no blood
- deformation/destruction of microvilli

27
Q

Describe Salmonella

A

Gram-negative rods that do not ferment lactose but produce H2S. Salmonella have two serotypes: Typhoidal (causes typhoid + paratyphoid fever) and Non-typhoidal (causes Gastroenteritis + food poisoning)

THREE TYPES OF SALMONELLA INFECTIONS:
- Enterocolitis [invasion of epithelial and sub-epithelial tissue of small and large intestines + causes nausea, vomiting, headache, profuse diarrhoea, low grade fever]
- Enteric fevers [life-threatening, spread via oral transmission of contaminated food, water, toilets]
- Bacteria with focal lesions [commonly associated with S serotype choleraesuis + early invasion of bloodstream + intestinal manifestations absent + blood culture results +ve]

28
Q

What are the four serotypes of salmonella that cause enteric fever?

A
  • Salmonella Paratyphi A (serogroup A)
  • Salmonella Paratyphi B (serogroup B)
  • Salmonella Choleraesuis (serogroup C1)
  • S Typhi (serogroup D)
29
Q

What are the most common salmonella serotypes?

A

Enteritidis & Typhimurium

30
Q

Describe Enteric (Typhoid) fever

A

Fever caused by Salmonella

PATHOGENESIS:
Ingestion of contaminated food or water -> Salmonella invade the small intestine + enter the bloodstream temporarily -> bacteria carried by white blood cells in liver, spleen and bone marrow where they multiply + re-enter bloodstream

INCUBATION PERIOD:
10-14 days

SYMPTOMS:
- Fever
- Red skin rash
- Hepatosplenomegaly
- Ulcers in the intestine
- Hyperplasia + necrosis of lymphoid tissue
- White coating of tongue
- WBC normal/low
- Headache, stomach pain, diarrhoea

DIAGNOSIS:
- Blood, stool + urine test
- WIDAL test (demonstration of Salmonella antibodies against O and H antigens)
- Differential medium culture
- Nucleic acid amplification test

TREATMENT:
- Ampicillin
- Trimethoprim-sulfamethoxazole
- A third generation Cephalosporin

31
Q

What is Shigella?

A

A gram-negative, facultative anaerobic, non-spore-forming, non-motile (no flagellar (H) antigens), rod-shaped bacteria

LAB FINDINGS:
- Does not ferment lactose (unlike E. coli)
- Does not produce H2S (unlike Salmonella)

EPIDEMIOLOGY:
- Only a human disease
- Transmitted via the focal-oral route
- Invade intestinal epithelial cells + release Shiga toxin which causes cell destruction

VIRULENCE FACTORS:
- Diarrhoea-inducing enterotoxin
- Type III secretion system = causes macrophage death
- Shiga-toxin stops protein synthesis in the host

PATHOGENESIS:
1) Shigella are taken up by M cells in the large intestine by endocytosis
2) Bacteria are quickly released from endosomes, leaving shigella free in the cytoplasm + bacteria multiply and enter the inferior and lateral aspects of the epithelial cells
3) Actin filaments form a tail + push bacteria to next cells where they multiply + macrophages that take up shigella are killed + release organism
4) Infected cells die and slough off + acute inflammatory response occurs with bleeding and abscess formation

INCUBATION PERIOD:
1-2 days

SYMPTOMS:
- Dysentery (GI disease)
- Abdominal pain
- Fever
- Watery + bloody diarrhoea
- Tenesmus (rectal spasm)

DIAGNOSIS:
- Specimen
- Culture
- Nucleic acid amplification test

TREATMENT:
- Ciprofloxacin
- Ampicillin
- Doxycycline
- Trimethoprim-sulfamethoxazole
- Azithromycin

PREVENTION:
- Sanitary control of water, food, sewage
- Isolation of patients + antibiotic treatment of infected individuals
- Detection of subclinical cases + carriers

32
Q

What is Klebsiella?

A

Non-motile, rod-shaped, gram-negative bacteria with a prominent polysaccharide capsule

ANTIGENS:
- Lipopolysaccharide (O antigen)
- Capsular polysaccharide (K antigen)

CLINICAL CORRELATION:
- responsible for hospital-acquired infections
- high level of antibiotic resistance (resistant to penicillins and cephalosporins)

TRANSMISSION:
- person-to-person contact
- surfaces

SYNDROMES:
- UTI
- Pneumonia
- Diarrhoea
- Wound infection

33
Q

What are Proteus?

A

A part of enterobacteriaceae family of gram-negative “swarming” bacteria and is commonly found in the human intestinal tract as part of the normal human intestinal flora

MORPHOLOGY
- Gram -ve
- Motile (has flagella)
- Urease +ve

PATHOGENICITY:
- Urease
[Urease hydrolyses urea to form ammonia which raises pH + form alkaline urine -> encourages formation of stones called “STRUVITE” composed of magnesium ammonium phosphate -> stones obstruct urine flow, damage urinary epithelium + trap bacteria within stone for recurrent infection}
- Motility
- Endotoxin

DISEASES:
- UTI
- Kidney stones

DIAGNOSIS:
- Culture

TREATMENT:
- Penicillins (for Proteus Mirabilis)
- Aminoglycosides + Cephalosporins (for P. Vulgaris and P. Panneri)
- Keeping urine at a low pH

MICROBIOLOGY (14 decks)

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