Spore-forming bacilli include members of the genus Bacillus.
These are aerobic rod-shaped bacteria.
Spore-forming bacilli also include members of the genus Clostridium.
These are anaerobic rod-shaped bacteria.
Genus Bacillus
The genus Bacillus consists of Gram-positive, endospore-forming, motile rod-shaped bacteria.
They are mostly saprobic in nature.
They are aerobic and catalase positive.
Members of this genus serve as a source of antibiotics.
Their primary habitat is soil.
Two species of significant medical importance include:
Bacillus anthracis
Bacillus cereus
Bacillus anthracis - Introduction
Bacillus anthracis consists of large, block-shaped rods.
It produces central spores, which develop under nutrient-deficient conditions.
Its virulence factors include a polypeptide capsule and exotoxins.
There are three types of anthrax:
Cutaneous anthrax – spores enter through the skin, leading to a black sore (eschar); this is the least dangerous form.
Pulmonary anthrax – occurs through inhalation of spores.
Gastrointestinal anthrax – results from ingestion of spores.
Bacillus anthracis - Anthrax Pathogenesis and Clinical Presentations
Cutaneous anthrax has a mortality rate of about 20%.
Virulence factors include:
Capsule – provides antiphagocytic properties.
Toxin – causes oedema and death.
Inhalation anthrax is associated with high mortality.
Gastrointestinal anthrax also carries a high mortality rate.
The anthrax toxin is the major virulence factor of Bacillus anthracis and is composed of three proteins:
Lethal factor (LF)
Edema factor (EF)
Protective antigen (PA)
PA combines with either LF or EF enzymes to facilitate their translocation across the plasma membrane.
The combination of PA + LF forms lethal toxin (LeTx).
The combination of PA + EF forms edema toxin (EdTx).
Once the bacteria secrete a large amount of anthrax toxin, antibiotic treatment becomes far less effective.
At this advanced stage of anthrax pathogenesis, disrupting the biological activity of the toxin may be a more effective approach.
Bacillus anthracis - Diagnosis
Specimens used for diagnosis of anthrax include:
Aspirate or swab from a cutaneous lesion
Blood culture
Sputum
Laboratory investigations involve:
Gram stain
Culture
Identification of the isolate
Control and Treatment of Bacillus anthracis
Treatment options for anthrax include penicillin, tetracycline, or ciprofloxacin.
Vaccines are available and include:
Live spores and toxoid vaccines used to protect livestock.
Purified toxoid vaccine administered to high-risk occupations and military personnel, requiring annual boosters
Bacillus cereus - Introduction
Bacillus cereus is a common airborne and dustborne organism, and the usual methods of disinfection and antisepsis are ineffective against it.
It can grow in foods, with spores that survive cooking and reheating.
Ingestion of toxin-containing food leads to symptoms such as nausea, vomiting, abdominal cramps, and diarrhea, typically lasting about 24 hours.
There is no specific treatment for B. cereus food poisoning.
It is being increasingly reported in immunosuppressed individuals.
Bacillus cereus - Pathogenesis and Clinical Presentations
Emetic form:
Incubation period is less than 6 hours.
Causes severe vomiting.
Illness usually lasts 8–10 hours.
Presents as gastroenteritis.
Diarrhoeal form:
Incubation period is greater than 6 hours.
Leads to diarrhoea.
Illness usually lasts 20–36 hours.
The Genus Clostridium - Introduction
The genus Clostridium consists of Gram-positive, spore-forming rods.
They are anaerobic and catalase negative.
The genus includes about 120 species.
They produce oval or spherical spores, which form only under anaerobic conditions.
Members are capable of synthesizing organic acids, alcohols, and exotoxins.
They are responsible for wound infections, tissue infections, and food intoxications.
Important species of medical significance include:
Clostridium tetani
Clostridium botulinum
Clostridium perfringens
Clostridium difficile
Introduction to Tetanus
Clostridium tetani is the causative agent of tetanus.
It is a common resident of soil and the gastrointestinal tracts of animals.
It causes tetanus (lockjaw), which is a neuromuscular disease.
The disease is seen most commonly among IV drug abusers and neonates in developing countries.
Pathology of Tetanus
Spores of Clostridium tetani usually enter the body through accidental puncture wounds, burns, umbilical stumps, frostbite, or crushed body parts.
An anaerobic environment at these sites is ideal for the growth of vegetative cells and the release of toxin.
The main virulence factor is tetanospasmin, a neurotoxin that:
Causes paralysis by binding to motor nerve endings.
Blocks the release of neurotransmitters responsible for inhibiting muscle contraction.
Leads to uncontrolled muscle contractions resulting in spastic paralysis.
Death most often occurs due to paralysis of respiratory muscles.
Pathogenesis of Tetanus
Tetanus toxin, produced by Clostridium tetani, is responsible for the symptoms of tetanus.
The toxin is taken up into the terminals of lower motor neurons and transported axonally to the spinal cord and/or brainstem.
From there, it moves trans-synaptically into inhibitory nerve terminals, where it blocks vesicular release of inhibitory neurotransmitters, leading to disinhibition of lower motor neurons.
This results in muscle rigidity and spasms, often presenting as:
Trismus (lockjaw)
Dysphagia
Opisthotonus
Rigidity and spasms of respiratory, laryngeal, and abdominal muscles, which can cause respiratory failure.
Similar to botulinum toxin, tetanus toxin is taken up into nerve terminals of lower motor neurons, which activate voluntary muscles.
It is a zinc-dependent metalloproteinase that targets synaptobrevin/vesicle-associated membrane protein (VAMP), a protein necessary for neurotransmitter release via synaptic vesicle fusion with the neuronal plasma membrane.
The initial symptom of local tetanus infection may be flaccid paralysis, due to interference with acetylcholine release at the neuromuscular junction, resembling the effect of botulinum toxin.
However, unlike botulinum toxin, tetanus toxin undergoes extensive retrograde axonal transport, reaching the spinal cord or brainstem.
From the CNS, the toxin is transported across synapses and taken up by inhibitory GABAergic and/or glycinergic neurons that regulate lower motor neuron activity.
Once inside these inhibitory nerve terminals, tetanus toxin cleaves VAMP, preventing the release of GABA and glycine.
This leads to functional denervation of lower motor neurons, causing hyperactivity, increased muscle contractions, and ultimately spastic paralysis.
Treatment and Prevention of Tetanus
Antitoxin therapy with human tetanus immune globulin (TIG) is used to inactivate circulating toxin, but it cannot counteract toxin already bound to nerve tissue.
Infection control is achieved with penicillin or tetracycline.
Muscle relaxants are administered to help manage spasms and rigidity.
Clostridial Food Poisoning
Clostridium botulinum causes a rare but severe intoxication, most often associated with home-canned foods.
Clostridium perfringens causes a mild intestinal illness and is recognized as the second most common form of food poisoning worldwide.
Clostridium botulinum - Introduction
Botulinum Food Poisoning
Botulism is an intoxication that occurs due to inadequate food preservation.
It is caused by Clostridium botulinum, a spore-forming anaerobe that commonly inhabits soil and water.
Pathogenesis of Botulinum
Spores of Clostridium botulinum may be present on food at the time of gathering and processing.
If adequate temperature and pressure are not achieved during processing/preservation, air may be expelled but spores remain.
Anaerobic conditions (created in improperly sealed/processed foods) favor spore germination and vegetative growth.
The growing bacteria release a potent neurotoxin (botulin).
The botulin toxin is absorbed from the gut and carried to neuromuscular junctions, where it blocks release of acetylcholine, the neurotransmitter required for muscle contraction.
Blockage of acetylcholine release leads to flaccid paralysis, often starting with cranial nerves and progressing to limb and respiratory muscles.
Early clinical signs include double or blurred vision, difficulty swallowing, and other neuromuscular symptoms; severe cases may progress to respiratory failure.
Infant and Wound Botulism
Infant botulism occurs when ingested spores germinate in the immature intestine and release toxin, leading to flaccid paralysis.
Wound botulism results when spores enter a wound, germinate, and produce toxin, causing food poisoning–like symptoms that may progress to classical botulism manifestations.
Botulinum toxin
Botulinum neurotoxin (BoNT) is considered the deadliest toxin known, with an LD₅₀ of only 1–3 nanograms per kilogram of body mass.
The hallmark effect is flaccid paralysis, caused by the irreversible inhibition of acetylcholine (ACh) release at the presynaptic nerve terminals of neuromuscular junctions (NMJs).
Routes of acquisition:
Food-borne botulism – ingestion of preformed toxin in improperly stored food.
Infant botulism – spores germinate in the immature gut, releasing toxin.
Wound botulism – spores germinate in devitalized tissue, releasing toxin into local circulation (often linked to illicit drug injection).
Iatrogenic botulism or bioterrorism – direct exposure to toxin.
Structure: BoNT is a protein toxin with a heavy chain and light chain linked by a disulfide bridge.
Serotypes: There are eight BoNT serotypes (A–H).
A, B, E, and rarely F, G, and H cause human disease.
Type A is the most potent, followed by BoNT/B.
Pathogenesis:
In infant botulism, weak immunity allows colonization by C. botulinum in the intestine or bronchioles, with toxin release.
Food-borne toxin is absorbed through the intestinal mucosa; in inhalation exposure, through the pulmonary epithelium.
BoNT enters circulation and binds to presynaptic motor and autonomic NMJs.
Mechanism of action:
The heavy chain promotes endocytosis of the toxin into the neuron.
The light chain is released into the cytosol, where it cleaves SNARE proteins (fusion complexes responsible for ACh vesicle exocytosis).
By disrupting SNARE, ACh release is blocked, preventing muscle contraction.
The outcome is flaccid paralysis, regardless of serotype.
Treatment and Prevention of Botulinum
Diagnosis involves determining the presence of botulinum toxin in food, intestinal contents, or feces.
Treatment includes:
Administration of antitoxin to neutralize circulating toxin.
Providing cardiac and respiratory support as needed.
Infectious botulism (e.g., wound botulism) can be treated with penicillin.
Prevention requires:
Practicing proper food preservation and handling methods, especially for canned foods.
Using preservatives to inhibit spore germination and toxin production.
Kappa toxin – collagenase, gelatinase; causes tissue necrosis, destruction of blood vessels and connective tissue.
Lambda toxin – protease.
Mu toxin – hyaluronidase.
Nu toxin – DNase, hemolytic, and necrotizing.
Phi toxin – hemolysin, cytolysin.
Gas Gangrene
Clostridium perfringens is the most frequent clostridia involved in soft tissue and wound infections, leading to myonecrosis.
Gas gangrene, also called clostridial myonecrosis, is a very serious infectious disease characterized by rapidly progressive destruction of soft tissue and production of gas within the tissues.
It is usually caused by traumatic injury, but spontaneous gas gangrene (SGG) is rarely reported.
Recognized risk factors include gastrointestinal diseases, cancer chemotherapy, lympho-proliferative disorders, radiation therapy, acquired immunodeficiency syndrome (AIDS), and neutropenic state.
Predisposing factors include surgical incisions, compound fractures, diabetic ulcers, septic abortions, puncture wounds, and gunshot wounds.
Clinical Manifestations of Clostridium perfringens
Soft Tissue Infections
Causes cellulitis, fasciitis, myositis, and myonecrosis.
Alpha toxins (present in all types) cause hemolysis, vascular leakage, liver toxicity, and cardiac dysfunction.
Myonecrosis (gas gangrene) is characterized by tissue necrosis and gas bubble formation.
Other toxins are pore-forming and contribute to necrosis.
Treatment includes antibiotics and surgical debridement.
Food Poisoning
Caused by enterotoxin released in the small intestine.
Enterotoxin alters intestinal membrane permeability, leading to fluid and ion loss (superantigen effect).
Symptoms include abdominal cramps and watery diarrhea.
Antibiotics are not used; treatment involves rehydration as the disease is self-limiting.
Pathology of Clostridium perfringens
Clostridium perfringens is not highly invasive; it requires damaged and dead tissue under anaerobic conditions for infection.
Such conditions stimulate spore germination, vegetative growth, and the release of exotoxins and other virulence factors.
Fermentation of muscle carbohydrates produces gas, leading to further tissue destruction.
Clostridial infections usually arise in traumatized tissue, though spontaneous cases can also occur.
Infection often involves deeper tissues such as muscle, leading to rapidly spreading infection along tissue planes and sepsis.
The infection may develop within hours to weeks after the initial trauma and inoculation.
Not all inoculations result in gas gangrene; both host and organism factors determine disease progression.
Immunocompromised patients and those with local tissue hypoxia (due to trauma or poor blood supply) are most at risk.
Only about 5% of wounds colonized with clostridia develop infection.
Host factors and wound location are crucial in determining whether clostridial myonecrosis develops.
Deep penetrating wounds in immunocompromised hosts have a higher risk of infection compared to superficial wounds in healthy individuals.
Proper cleaning and dressing of superficial wounds reduce the risk, whereas crush injuries or tissue ischemia increase the likelihood of infection.
Virulence depends on exotoxin production; C. perfringens produces 17 toxins, with alpha toxin (lecithinase) being the most pathogenic.
Alpha toxin, a phospholipase, breaks down cell membranes, induces platelet aggregation, thrombosis, and histamine release.
Additional toxins and enzymes include collagenase, hyaluronidase, hemagglutinins, and hemolysins.
Theta toxin causes vascular injury and leukocyte destruction, blunting the host’s inflammatory response.
Collagenase degrades connective tissue, enabling rapid spread across tissue planes and into deeper muscle layers.
Treatment and Prevention of Clostridium perfringens
Immediate cleansing of dirty wounds, deep wounds, decubitus ulcers, compound fractures, and infected surgical incisions is essential.
Surgical debridement of diseased tissue helps control infection spread.
Large doses of cephalosporin or penicillin are used for antimicrobial therapy.
Hyperbaric oxygen therapy is beneficial in suppressing anaerobic bacterial growth.
Currently, no vaccines are available for prevention.
Clostridium difficile-Associated Disease (CDAD)
C. difficile is a normal resident of the colon, usually present in low numbers.
It causes antibiotic-associated colitis when broad-spectrum antibiotics disrupt the normal gut microbiota.
The bacterium is relatively non-invasive, but antibiotic use allows it to overgrow.
It produces enterotoxins that damage intestinal lining.
It is a major cause of diarrhea in hospitals (nosocomial infections).
Cases are increasingly reported in community-acquired diarrhea as well.
Treatment and Prevention of Clostridium difficile-Associated Disease (CDAD)
Mild, uncomplicated cases improve with fluid and electrolyte replacement and withdrawal of the causative antimicrobials.
Severe infections are treated with oral vancomycin (sometimes fidaxomicin is also used).
Strict infection control precautions are required to prevent spread, especially in hospital settings.
Corynebacterium Species
General Characteristics
Found as free-living saprophytes in fresh water, salt water, soil, and air.
Present as part of the normal flora of humans and animals, often considered contaminants.
Nonmotile, non-capsulated, facultative anaerobes.
Commonly referred to as “diphtheroids.”
Corynebacterium diphtheriae is the most significant human pathogen.
Other species may cause opportunistic infections in immunocompromised hosts.
Morphology
Gram-positive, non–spore-forming rods.
Often arranged in palisades or characteristic “L-V” shapes resembling Chinese characters.
Pleomorphic with club-shaped ends (coryneform).
Show beaded, irregular staining.
Contain metachromatic granules of polymetaphosphates.
Strains of Corynebacterium diphtheria
Based on generation time and toxin production, Corynebacterium diphtheriae is classified into three main strains.
Corynebacterium diphtheriae gravis – generation time about 60 minutes.
Corynebacterium diphtheriae intermedius – generation time about 100 minutes.
Corynebacterium diphtheriae mitis – generation time about 120 minutes.
Determinants of pathogenicity
Pathogenicity begins with colonization of the mucous membranes of the respiratory tract.
Toxin production varies depending on the biotype and lysotype of the strain.
C. diphtheriae: Agent of Diphtheria
C. diphtheriae is toxigenic and acts as the causative agent of diphtheria.
It has a worldwide distribution, but is rare in regions with strong vaccination programs.
The major virulence factor is the exotoxin (diphtheria toxin).
Not all strains of C. diphtheriae produce the toxin.
Toxin production occurs only in certain strains.
The diphtheria toxin is antigenic, stimulating an immune response.
Pathogenesis of Diphtheria
The pathogenesis of diphtheria depends on two main determinants:
The ability of a given Corynebacterium diphtheriae strain to colonize the nasopharyngeal cavity and/or skin.
The ability of the strain to produce diphtheria toxin.
Determinants of colonization are encoded by the bacterial genome, whereas toxin production is encoded by the corynebacteriophage.
Therefore, the molecular basis of virulence in Corynebacterium diphtheriae is the result of combined effects from two genomes.
Nontoxigenic strains are rarely associated with clinical disease.
These strains, however, may become highly virulent if they undergo lysogenic conversion to toxigenicity.
Toxigenic Corynebacterium diphtheriae
The gene for diphtheria toxin production is carried by a lysogenic phage.
The tox gene is regulated by iron concentration.
The diphtheria toxin consists of two fragments:
Fragment A (Active fragment):
Inhibits protein synthesis by blocking the transfer of amino acids from tRNA to the growing polypeptide chain.
Leads to cell and tissue death.
Fragment B (Binding fragment):
Binds to specific cell membrane receptors.
Mediates entry of Fragment A into the cytoplasm of the host cell.
Clinical Forms of Diphtheria
Respiratory diphtheria is acquired through droplet spray or hand-to-mouth contact.
Individuals who are not immunized are especially susceptible to respiratory infection.
Non-respiratory diphtheria includes other localized forms of the disease.
Systemic diphtheria occurs when the toxin spreads throughout the body, leading to more severe complications.
Skin and cutaneous diphtheria presents with localized lesions on the skin.
Diphtheria
Diphtheria is primarily a respiratory disease.
The incubation period ranges from 2 to 5 days.
Symptoms include sore throat, fever, and malaise.
The toxin is produced locally, usually in the pharynx or tonsils.
The toxin causes tissue necrosis and may be absorbed into the bloodstream, leading to systemic effects.
A tough grey-to-white pseudomembrane forms, which may obstruct the airway and cause suffocation.
Diphtheria is a contagious disease, transmitted by direct physical contact or by inhaling aerosolized secretions from infected individuals.
Psuedomembrane
Diphtheria is an upper respiratory tract illness that presents with sore throat, low fever, and the formation of an adherent membrane, known as a pseudomembrane, which typically develops on the tonsils, pharynx, and/or nasal cavity.
The diphtheria toxin, produced by Corynebacterium diphtheriae, has the potential to cause severe complications such as myocarditis, polyneuritis, and other systemic toxic effects.
In some cases, a milder form of diphtheria may occur that remains localized and restricted to the skin.
The disease progresses rapidly and is characterized as an acute, febrile infection that involves both local and systemic pathological changes.
A local lesion forms in the upper respiratory tract, resulting in necrotic injury to the epithelial cells.
This epithelial damage allows blood plasma to leak into the affected area, where it combines with a fibrin network.
The fibrin mesh becomes interlaced with rapidly growing C. diphtheriae cells, contributing to the structure of the pseudomembrane.
The resulting membranous network, known as the pseudomembrane, covers the site of the local lesion and can obstruct the airway.
This obstruction may lead to respiratory distress and, in severe cases, suffocation.
C. diphtheriae - Causative Agent of Diphtheria:
Corynebacterium diphtheriae is the causative agent of diphtheria.
Infection leads to the formation of a pseudomembrane in the upper respiratory tract.
The pseudomembrane is composed of white blood cells (WBCs), necrotic epithelial cells, fibrin, and the proliferating C. diphtheriae organisms.
Clinical Infections of C. diphtheriae:
Non-respiratory diphtheria can present as systemic or cutaneous disease.
In systemic infections, diphtheria toxin is absorbed into the bloodstream and distributed throughout the body.
The toxin targets vital organs such as the kidneys, heart, and nervous system.
Severe systemic involvement may lead to death, primarily due to cardiac failure.
The cutaneous form of diphtheria is more common in tropical regions.
It usually develops at the site of minor skin abrasions.
These lesions may become superinfected with Streptococcus pyogenes and/or Staphylococcus aureus.
Treatment of C. diphtheriae
Treatment of diphtheria requires both antitoxin and antibiotics.
The diphtheria antitoxin is produced in horses and administered to neutralize circulating toxin.
Antibiotics are ineffective against toxin already present in the circulation.
However, antibiotics play a key role in preventing further bacterial growth and toxin production.
Penicillin is considered the drug of choice for antibiotic therapy.
Laboratory Diagnosis of C. diphtheria
Microscopic morphology
Gram-positive, non–spore-forming rods, club-shaped, sometimes beaded
Appear in palisades, giving a “Chinese letter” arrangement
Contain metachromatic granules (Babes’ Ernst bodies) that stain more darkly than the rest of the cell and serve as food reserves
Cultural Characteristics
Loeffler’s slant or Pai’s slant: Demonstrates pleomorphism and metachromatic granules
Serum Tellurite or modified Tinsdale medium: Produces brown or grayish-black halos around colonies
Blood agar plate (BAP): After 24–48 hours at 37 °C, shows small, grey, translucent colonies with a small zone of β-hemolysis
Identification tests
Fermentation reactions: Glucose positive
Catalase positive
Urease negative
Non-motile
Toxigenicity testing
Elek test (Immunodiffusion test)
Detects toxin production
Organisms are streaked at right angles to filter paper saturated with antitoxin on media with low iron (to maximize toxin production)
Positive result confirms toxin production
Note: Identification of C. diphtheriae alone does not confirm diphtheria; toxin production must be demonstrated.
Schick Test
Used to detect the antitoxin level in blood (in previously infected or immunized individuals)
Method:
Inject toxin intradermally in one forearm
Inject the same amount of heat-treated toxin (control) in the other forearm
Observe for 24–72 hours, up to 6 days
Positive test: Redness and swelling → insufficient antitoxin present
Negative test: No reaction → sufficient antitoxin present, toxin neutralized
Treatment and Prevention of C. diphtheriae
Treatment
Administration of antitoxin (neutralizes circulating toxin)
Prevention
DPT immunization (combined vaccine for diphtheria, pertussis, and tetanus)
Listeria monocytogenes
Small, rod-shaped bacteria, sometimes appearing like “Chinese characters”.
No capsule and facultatively aerobic.
Exhibits tumbling motility at 25 °C, but not at 37 °C.
Can grow at low temperatures, including 4 °C.
Forms small, smooth colonies on blood agar with a narrow zone of β-hemolysis.
Biochemical characteristics:
Fermentation positive
Catalase positive
Oxidase positive
Listeriosis
Listeriosis is a serious infection caused by ingesting food contaminated with Listeria monocytogenes.
The disease primarily affects pregnant women, newborns, and immunocompromised adults.
Prenatal transmission occurs when the organism crosses the placenta.
Postnatal transmission can occur through the birth canal.
Intrauterine infections are widely systemic and can result in premature abortion or fetal death.
Pathogenesis of Listeria monocytogenes
L. monocytogenes enters the body through the gastrointestinal tract after ingestion of contaminated foods such as cheese, fruits, or vegetables.
The bacterium possesses several adhesin proteins (Ami, FbpA, and flagellin) that facilitate binding to host cells, contributing to virulence.
Cell wall surface proteins, internalins A and B, interact with E-cadherin receptors on epithelial cells, promoting phagocytosis into the cells.
After phagocytosis, the bacterium is enclosed in a phagolysosome, where the low pH activates production of listeriolysin O.
Listeriolysin O, along with two phospholipases, lyses the phagolysosome membrane, allowing the bacteria to escape into the cytoplasm.
Inside the cytoplasm, the organisms proliferate, and the surface protein ActA induces host cell actin polymerization, propelling bacteria toward the host cell membrane.
This movement forms elongated protrusions (filopods), which are ingested by adjacent epithelial cells, macrophages, and hepatocytes, continuing the infection cycle.
L. monocytogenes can spread from cell to cell without exposure to antibodies, complement, or polymorphonuclear cells.
Other pathogens, like Shigella flexneri and rickettsiae, similarly exploit the host’s actin and contractile system to spread.
Iron is an important virulence factor; listeriae produce siderophores and obtain iron from transferrin.
Immunity against L. monocytogenes is primarily cell-mediated, due to the intracellular nature of infection.
Conditions of impaired cell-mediated immunity—such as pregnancy, advanced age, AIDS, lymphoma, and organ transplantation—are associated with increased susceptibility.
Immunity can be transferred by sensitized lymphocytes, but not by antibodies.
Symptoms of Listeriosis
Fever
Muscle aches
Gastrointestinal symptoms: Nausea and diarrhea
Pregnant women: Mild flu-like symptoms; may result in miscarriage, stillbirth, premature delivery, or an infected newborn
Lethargy and irritability
Neurological involvement: If infection spreads to the nervous system, can cause headache, stiff neck, confusion, loss of balance, or convulsions
Severe infections may lead to pneumonia, meningitis, or sepsis
Transmission of Listeria monocytogenes
L. monocytogenes is distributed worldwide in animals, plants, and soil.
Humans can be infected by direct contact with animals or their feces.
Transmission can occur through consumption of unpasteurized milk.
Contaminated vegetables are also a source of infection.
Infection can occur endogenously from the gastrointestinal tract.
Diagnosis of Listeria monocytogenes
Difficult to isolate due to slow growth and intracellular location.
Cold enrichment procedure: Specimens are held at 4 °C and periodically cultured to enhance recovery.
ELISA can be used for detection of bacterial antigens.
Treatment and Prevention of Listeria monocytogenes
Treatment:
Drug of choice: Ampicillin (Amp)
Alternative: Erythromycin
Supportive care for symptoms like fever, myalgia, and arthralgia
High-risk groups require prompt treatment:
Pregnant women – risk of transplacental or vaginal transmission to fetus
Newborns/infants – risk of granulomatosis infantiseptica, septicemia, meningitis, brain abscess
Elderly and immunocompromised – higher risk of severe disease
Mild gastroenteritis in healthy individuals is usually self-limiting
Prevention:
Ensure adequate cooking of foods
Consume pasteurized milk
Practice proper food hygiene to avoid contamination
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