L4 gram positive bacilli

what are the two main classifications for gram + bacilli

endospore formers and non endospore formers( which can further be divided into regular and irregular shape and staining)

what are the two types of endospore forming gram positive bacilli

bacillus which is aerobic and clostridium wich is anaerobic

eg:

• bacillus anrthicos/ anthrax

• bacillus cereus/ food poisoning in rice and ice

• clostridium perfringens/ gas gangrene often in battelfield

• clostridium tetani/ tetanus

• clostridium botulinum/ botulism, botox causes paralysis

• clostridium difficile/ AAD

what are the types of non endospore forming bacilli

can be first classified as either being of regular or irregular shape and staining

regular shape and staining:

• listeria

• erysipelothrix

irregular shape and staining

non- acid fast

• corynebacterium

• propionibacterium

acid fast

• mycobacterium

filamentous

• actinomyces

• nocardia

listeria monocytogenes/ listerosis

• Severe disseminated infection in immune compromised people and in pregnancy – transmitted to foetus).

• Usually acquired from contaminated foods (esp. cold meats, soft cheeses)

erysipelothrix

It is a zoonotic bacterium primarily found in animals, especially pigs, fish, and birds. Humans typically acquire it through occupational exposure (e.g., veterinarians, butchers, fish handlers) via skin abrasions or wounds.

While it is not a common human commensal, it can cause erysipeloid, a localized skin infection, and in rare cases, systemic infections like endocarditis or septicemia in immunocompromised individuals.

corynebacterium

non acid fast, irregularly shaped, non endospore forming bacteria

Normal flora of the skin – rare infections, except Corynebacterium diphtheriae – recent resurgence of diphtheria

Corynebacterium diphtheriae is a Gram-positive, non-motile, non-spore-forming, pleomorphic bacillus that is the causative agent of diphtheria. It belongs to the Corynebacterium genus,

Diphtheria Disease:

C. diphtheriae causes diphtheria, a serious upper respiratory tract illness that can lead to:

1. Pharyngeal/tonsillar diphtheria – Formation of a thick, gray pseudomembrane in the throat, causing difficulty swallowing, breathing issues, and potential airway obstruction.

2. Toxin-mediated complications – Systemic absorption of the diphtheria toxin can result in myocarditis, neuritis, and kidney damage

3. is vaccine preventable

mycobacterium

acid fast, irregularly shaped, non endo spore forming, gram positive bacilli

causes tuberculosis

Actinomyces

Gram-positive, filamentous bacteria

Characteristics

• Gram-positive, filamentous, branching rods

• Anaerobic or facultative anaerobic

• Non-acid-fast

• Part of the normal flora of the oral cavity, gastrointestinal tract, and female reproductive tract

Disease: Actinomycosis

• Chronic suppurative infection forming abscesses and draining sinuses with characteristic sulfur granules (yellow granules in pus).

• Common forms:

  • Cervicofacial actinomycosis ("lumpy jaw") – often due to dental infections or trauma

  • Thoracic actinomycosis – can mimic TB

  • Pelvic actinomycosis – associated with IUD use

• Treatment: Penicillin G (long-term), sometimes surgical drainage

no cardia

Characteristics

• Gram-positive, filamentous, branching rods

• Aerobic

• Partially acid-fast (due to mycolic acid in the cell wall)

• Found in soil (not part of normal human flora)

Disease: Nocardiosis

• Pulmonary nocardiosis – pneumonia-like symptoms, often in immunocompromised patients (e.g., HIV, transplant, corticosteroid use)

• Cutaneous nocardiosis – from trauma, causing skin infections

• Disseminated nocardiosis – can spread to the brain, leading to brain abscesses

• Treatment: Trimethoprim-sulfamethoxazole (TMP-SMX) (first-line), sometimes combined with other antibiotics

bacillus anthracis

gram positive bacilli, endospore fromer

anthrax

spores inhaled or ingested or contaminate a wound

is rapidly progressive, causes skin sores, vomiting and shock

is a bioterrorism agent

is common in areas where animal carcases arent disposed properly

clostridioides /clostridium/ difficile

is present infaeces of most neonates and up to 30% of hospital patients

its spores are widespread in the environment

• Gram-positive, rod-shaped

• Spore-forming – allows survival in harsh conditions

• Obligate anaerobe – cannot grow in oxygen-rich environments

• Toxin-producing strains – Toxin A (enterotoxin) and Toxin B (cytotoxin

c.difficile pathogenesis

• Normally found in low numbers in the gut microbiota.

• Disruption of normal gut flora (due to broad-spectrum antibiotic use, especially clindamycin, fluoroquinolones, cephalosporins) allows C. difficile to overgrow.

• Produces Toxin A (causes fluid secretion and inflammation) and Toxin B (cytotoxic, causing cell death).

clinical manifestation of c. difficile

• Mild to moderate diarrhea

• Pseudomembranous colitis – inflammation of the colon with formation of yellowish plaques (pseudomembranes)

• Toxic megacolon – life-threatening dilation of the colon

• Sepsis and perforation (in severe cases

  Toxin-producing strains cause antibiotic associated diarrhoea -

• during or after antibiotic treatment

• - mild to severe, intractable diarrhoea

• - most severe: pseudomembranous colitis

• • Disease is a consequence of disruption of the gut microbiome

c.difficile risk factors

Risk Factors

• Recent antibiotic use

• Hospitalization, hospital caare facilities

• Proton pump inhibitor (PPI) use

• Immunosuppression

• food contaminated with c difficile

• pH increasing agents

treatment for c.difficile

Antibiotics (metronidazole, vancomycin)

If refractory or severe(recurrent infections or unresponsive to antibiotics), consider faecal transplant

microbiome

microbial cimmunity that occupies a well defined habitat- includes viruses, bacteria and parasites

dysbiosis

an imbalance in the microbial community associated with disease

what are the causes for dysbiosis

overgrowth of members of the commensal microbiotae e.g., Enterobacteriaceae, in inflammatory bowel disease

loss of commensals (eg antibiotic therapy)- often accompanied by pathogen overgowth eg clostridioides difficile associated with colitis

loss of diversity- associated with inflammatory bowel disease, HIV, type I diabetes ,mellitus, overgrowth of a few species

pathobiont

a potentially pathogenic organism which under normal circumstances lives as a symbiont

what are the factors determining microbial community composition

environmental parameters

• eg oxygen tension(difference between upper respirartory tract and lower GIT),pH, temperatture,energy sources,

interactions between microbes

• competition and collaboration between microbes

• positive: cross feeding to help others grow is seen when two species of bacteria co exist

• negative; bacteria produce antibiotics/ bacteriocins/ that inhibit the growth of competing bacteria

rapid evolution

stochastic/ unpredictable forces

• eg dispersal

how to measure the microbiota and its function

through sequencing its genetic composition

there is new technology called next generation sequencing

• sequencing many genes in parallel

• this removes the need to sequence bacteria individually

composition of the gut microbiome

varies due to environmental changes eg what you eat

what are some factors influencing the gut microbiome

• geographical location

• host genetics

• exercise

• stress
  antibiotics

• age

• gastric motility

• antimicrobial peptides and igA

• gastric secretion

• diet

• mode of delivery: c section vs natural

obesity and the gut microbiota

there are two main bcteria to consider: firmicutes and bacteroidetes

• in obese individuals, there is a higher firmicutes to bacteroidetes ratio

• while in lean individual then is higher bacteroidetes to firmicutes

lean vs obese micorbiota transplant experiment

two test subjects where taken, one lean one obese

there microbiota was implanted in recipient mice, and both mouse groups had a low fat high fibre diet

it was observed that the mouse that received the obese twins microbiota displayed increased adiposity while the other mouse became more lean

how does a diet consisting of high plant fibre and low animal fat and protein impact metabolic health

• these plant fibres are indigestable to humans but gut bacteria can ferment them

• it is linked to increased metabolic health as well as daily defacation

how does a high animal fat and protein diet and low in fibre influence metabolic health

• aberrant microbiota related to metabolic diseases

what are some microbiome- directed interventions

• exercises

• individualised nutrition

• faecal mucrobiota transplantation

• prebiotics- nutrients that are degraded by and may change composition of the gut microbiota

• probiotics- live microorganisms that confer a healthbenefit when consumed in adequete amounts

• synobiotics

• postbiotics- functional bioactive compounds, generated during fermentation which may be used to promote health

Mycobacterium tuberculosis

• causes tuberculosis

• needs an acid fast cell wall to be seen as its a gram intermediate

• is the leading cause of death- 1.4 million deaths p.a

• around 30% of the population is infected but latent TB infection is pathogenic

• poverty and crowding increases the risk of TB

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Key Characteristics of Mycobacterium tuberculosis

• Acid-fast (Ziehl-Neelsen stain positive) due to mycolic acid in the cell wall

• Obligate aerobe – prefers high-oxygen areas (lungs)

• Slow-growing – takes 2-6 weeks to grow in culture

• Resistant to drying & disinfectants due to its waxy cell wall

• Can remain latent in the body for year

how is Mycobacterium tuberculosis transmitted

airborne aerosol droplets from infected individuals, coughing sneezing talking

no animal or environmental reservoir

direct human to human transmission

very low infectious dose 1-10 bacteria

how does TB enter body

• small droplet nuclei enter terminal airspaces

• phagocytosed by alveolar macrophages

• spread throughout body

• survive within macrophages- by evading killing

primary TB infection

• Usually asymptomatic or mild flu-like symptoms

• Bacteria multiply in alveolar macrophages

• Forms Ghon complex (infected lung area + nearby lymph nodes)

• Outcomes:

  • Latent TB (most cases): Bacteria remain dormant in granulomas

  • Progressive primary TB (immunocompromised patients): Leads to active disease

latent TB /dormant phase

• No symptoms, not contagious

• Bacteria are "walled off" inside caseating granulomas

• Can reactivate later (especially with immunosuppression)

secondary/ reactivation of TB

• Occurs when immune defenses weaken (e.g., HIV, diabetes, malnutrition)

• Commonly affects upper lung lobes (more oxygen)

• Symptoms:

  • Chronic cough, hemoptysis (bloody sputum)

  • Night sweats, weight loss, fever ("consumption"\

  • pathogenicity largely due to host inflammatory reaction to the bacterium which causes tissue destruction- no classic toxins produced

TB treatment

• multi drug therapy to prevent emergnece of resistant strains

• minimum treatment duration is 4-6 months for drug sensitiveTB

• usually INH (1 in 10^6 is resistant)and rifam (1 in 10^8 is resistant)

• MDR (multidrug resistant 1 in 10^14)

how does multi drug therapy work

• antibiotic resistance arises in TB as a consequence of chance spontaneous mutations in the chromosome

• antibiotics dont cause mutation, but they select for pre-existing resistant mutants

• by combining two or more drugs, chance of a particular strain being resistant is 10^14 which is extrememly rare thus the infection will be cleared

what happens if inappropriate treatment is administered

firstly antibiotic resistance of first antibiotic occurs

then this causes the resistant strain to be spread