Yersinia pestis (Plague)

Last updated: September 17, 2024

Yersinia pestis (Plague)

Noor

Noor

Cholinomimetics: Direct agonists
Plasmodium species (Malaria)
Babesia
Giardia lamblia
Entamoeba histolytica (Amebiasis)
Cryptosporidium
Acanthamoeba
Naegleria fowleri (Primary amebic meningoencephalitis)
Toxoplasma gondii (Toxoplasmosis)
Trypanosoma brucei
Trypanosoma cruzi (Chagas disease)
Trichomonas vaginalis
Leishmania
Loa loa (Eye worm)
Toxocara canis (Visceral larva migrans)
Onchocerca volvulus (River blindness)
Ascaris lumbricoides
Anisakis
Angiostrongylus (Eosinophilic meningitis)
Ancylostoma duodenale and Necator americanus
Strongyloides stercoralis
Guinea worm (Dracunculiasis)
Wuchereria bancrofti (Lymphatic filariasis)
Trichinella spiralis
Enterobius vermicularis (Pinworm)
Trichuris trichiura (Whipworm)
Echinococcus granulosus (Hydatid disease)
Diphyllobothrium latum
Paragonimus westermani
Clonorchis sinensis
Schistosomes
Pediculus humanus and Phthirus pubis (Lice)
Sarcoptes scabiei (Scabies)
Coccidioidomycosis and paracoccidioidomycosis
Histoplasmosis
Blastomycosis
Pneumocystis jirovecii (Pneumocystis pneumonia)
Candida
Mucormycosis
Aspergillus fumigatus
Sporothrix schenckii
Cryptococcus neoformans
Malassezia (Tinea versicolor and Seborrhoeic dermatitis)
Viral structure and functions
Varicella zoster virus
Cytomegalovirus
Epstein-Barr virus (Infectious mononucleosis)
Human herpesvirus 8 (Kaposi sarcoma)
Herpes simplex virus
Human herpesvirus 6 (Roseola)
Adenovirus
Parvovirus B19
Human papillomavirus
Poxvirus (Smallpox and Molluscum contagiosum)
BK virus (Hemorrhagic cystitis)
JC virus (Progressive multifocal leukoencephalopathy)
Poliovirus
Coxsackievirus
Rhinovirus
Hepatitis A and Hepatitis E virus
Hepatitis D virus
Influenza virus
Mumps virus
Measles virus
Respiratory syncytial virus
Human parainfluenza viruses
Dengue virus
Yellow fever virus
Zika virus
Hepatitis C virus
West Nile virus
Norovirus
Rotavirus
Coronaviruses
HIV (AIDS)
Human T-lymphotropic virus
Ebola virus
Rabies virus
Rubella virus
Eastern and Western equine encephalitis virus
Lymphocytic choriomeningitis virus
Hantavirus
Prions (Spongiform encephalopathy)
Bacterial structure and functions
Staphylococcus epidermidis
Staphylococcus aureus
Staphylococcus saprophyticus
Streptococcus viridans
Streptococcus pneumoniae
Streptococcus pyogenes (Group A Strep)
Streptococcus agalactiae (Group B Strep)
Enterococcus
Clostridium perfringens
Clostridium botulinum (Botulism)
Clostridium difficile (Pseudomembranous colitis)
Clostridium tetani (Tetanus)
Bacillus cereus (Food poisoning)
Listeria monocytogenes
Corynebacterium diphtheriae (Diphtheria)
Bacillus anthracis (Anthrax)
Nocardia
Actinomyces israelii
Escherichia coli
Salmonella (non-typhoidal)
Salmonella typhi (typhoid fever)
Pseudomonas aeruginosa
Enterobacter
Klebsiella pneumoniae
Shigella
Proteus mirabilis
Yersinia enterocolitica
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Serratia marcescens
Bacteroides fragilis
Yersinia pestis (Plague)
Vibrio cholerae (Cholera)
Helicobacter pylori
Campylobacter jejuni
Neisseria meningitidis
Neisseria gonorrhoeae
Moraxella catarrhalis
Francisella tularensis (Tularemia)
Bordetella pertussis (Whooping cough)
Brucella
Haemophilus influenzae
Haemophilus ducreyi (Chancroid)
Pasteurella multocida
Mycobacterium tuberculosis (Tuberculosis)
Mycobacterium leprae
Mycobacterium avium complex (NORD)
Mycoplasma pneumoniae
Chlamydia pneumoniae
Chlamydia trachomatis
Borrelia burgdorferi (Lyme disease)
Borrelia species (Relapsing fever)
Leptospira
Treponema pallidum (Syphilis)
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Coxiella burnetii (Q fever)
Ehrlichia and Anaplasma
Gardnerella vaginalis (Bacterial vaginosis)
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Mechanisms of antibiotic resistance
Integrase and entry inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Protease inhibitors
Hepatitis medications
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Neuraminidase inhibitors
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Antimalarials
Anti-mite and louse medications
Introduction to the immune system
Cytokines
Innate immune system
Complement system
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation, differentiation, and contraction
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
Antibody classes
Somatic hypermutation and affinity maturation
VDJ rearrangement
Contracting the immune response and peripheral tolerance
B- and T-cell memory
Anergy, exhaustion, and clonal deletion
Vaccinations
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Iron deficiency anemia
Beta-thalassemia
Alpha-thalassemia
Sideroblastic anemia
Anemia of chronic disease
Lead poisoning
Hemolytic disease of the newborn
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Autoimmune hemolytic anemia
Pyruvate kinase deficiency
Paroxysmal nocturnal hemoglobinuria
Sickle cell disease (NORD)
Hereditary spherocytosis
Aplastic anemia
Fanconi anemia
Megaloblastic anemia
Folate (Vitamin B9) deficiency
Vitamin B12 deficiency
Diamond-Blackfan anemia
Acute intermittent porphyria
Porphyria cutanea tarda
Hemophilia
Vitamin K deficiency
Bernard-Soulier syndrome
Glanzmann's thrombasthenia
Hemolytic-uremic syndrome
Immune thrombocytopenia
Thrombotic thrombocytopenic purpura
Von Willebrand disease
Disseminated intravascular coagulation
Heparin-induced thrombocytopenia
Antithrombin III deficiency
Factor V Leiden
Protein C deficiency
Protein S deficiency
Antiphospholipid syndrome
Hodgkin lymphoma
Non-Hodgkin lymphoma
Chronic leukemia
Acute leukemia
Leukemoid reaction
Myelodysplastic syndromes
Polycythemia vera (NORD)
Myelofibrosis (NORD)
Essential thrombocythemia (NORD)
Langerhans cell histiocytosis
Mastocytosis (NORD)
Multiple myeloma
Monoclonal gammopathy of undetermined significance
Waldenstrom macroglobulinemia
Microcytic anemia: Pathology review
Non-hemolytic normocytic anemia: Pathology review
Intrinsic hemolytic normocytic anemia: Pathology review
Extrinsic hemolytic normocytic anemia: Pathology review
Macrocytic anemia: Pathology review
Heme synthesis disorders: Pathology review
Coagulation disorders: Pathology review
Platelet disorders: Pathology review
Mixed platelet and coagulation disorders: Pathology review
Thrombosis syndromes (hypercoagulability): Pathology review
Lymphomas: Pathology review
Leukemias: Pathology review
Plasma cell disorders: Pathology review
Myeloproliferative disorders: Pathology review
Free radicals and cellular injury
Necrosis and apoptosis
Ischemia
Hypoxia
Amyloidosis
Inflammation
Wound healing
Atrophy, aplasia, and hypoplasia
Hyperplasia and hypertrophy
Metaplasia and dysplasia
Oncogenes and tumor suppressor genes
Choanal atresia
Laryngomalacia
Allergic rhinitis
Nasal polyps
Upper respiratory tract infection
Sinusitis
Laryngitis
Retropharyngeal and peritonsillar abscesses
Bacterial epiglottitis
Nasopharyngeal carcinoma
Tracheoesophageal fistula
Congenital pulmonary airway malformation
Pulmonary hypoplasia
Neonatal respiratory distress syndrome
Transient tachypnea of the newborn
Meconium aspiration syndrome
Apnea of prematurity
Sudden infant death syndrome
Acute respiratory distress syndrome
Decompression sickness
Cyanide poisoning
Methemoglobinemia
Emphysema
Chronic bronchitis
Asthma
Cystic fibrosis
Bronchiectasis
Alpha 1-antitrypsin deficiency
Restrictive lung diseases
Sarcoidosis
Idiopathic pulmonary fibrosis
Pneumonia
Croup
Bacterial tracheitis
Lung cancer
Pancoast tumor
Superior vena cava syndrome
Pneumothorax
Pleural effusion
Mesothelioma
Pulmonary embolism
Pulmonary edema
Pulmonary hypertension
Sleep apnea
Respiratory distress syndrome: Pathology review
Cystic fibrosis: Pathology review
Pneumonia: Pathology review
Tuberculosis: Pathology review
Deep vein thrombosis and pulmonary embolism: Pathology review
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Obstructive lung diseases: Pathology review
Restrictive lung diseases: Pathology review
Apnea, hypoventilation and pulmonary hypertension: Pathology review
Lung cancer and mesothelioma: Pathology review

Flashcards

Yersinia pestis (Plague)

0 of 10 complete

Transcript

Watch video only

Yersinia pestis is a Gram-negative coccobacillus which belongs to a family of bacteria called the Enterobacteriaceae.

It causes a disease called plague, which is transmitted by rodents, mainly rats, as well as prairie dogs, and their fleas.

Plague is highly contagious, and there have been three major pandemics in human history - one of them, known as the Black Death, killed up to one-third of the European population. Yikes!

Now, Yersinia pestis has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining.

Instead, like any other Gram-negative bacteria, it stains pink with safranin dye.

On Wright-Giemsa and Wayson staining it has a bipolar staining which means that only the poles of the bacteria stain, and the rest of it remains unstained, so the bacteria look like safety pins under the microscope.

Alright, now Yersinia pestis is non-motile, non-spore forming, facultative anaerobic which means it can survive in both aerobic and anaerobic environments and facultative intracellular which means it can survive both inside and outside the cells.

It’s oxidase and urease negative which means it doesn’t produce these enzymes and catalase positive which means it produces an enzyme called catalase.

Also, it’s indole negative which means it doesn’t convert tryptophan into indole.

Yersinia pestis grows well on MacConkey agar, sheep blood agar, and chocolate agar.

MacConkey agar is used to identify if a bacteria ferments lactose or not, and it contains a pH sensitive dye and lactose.

So, if a bacteria ferments lactose, it means that it’s able to ferment lactose and produce acid which causes the pH sensitive dye to turn pink leading to formation of pink colonies.

Non-lactose fermenters, like Yersinia pestis, aren’t able to modify the PH sensitive dye, grow into colorless colonies.

Next, on sheep blood agar and chocolate agar, Yersinia pestis forms opaque, yellow colonies that look like fried eggs.

Finally, the triple sugar iron test, or TSI for short can be done to assess hydrogen sulfide production.

This medium contains three sugars - lactose, glucose and sucrose, as well as iron and a pH sensitive dye.

If the bacteria produces hydrogen sulfide, that reacts with the iron, and a black precipitate forms in the test tube.

Yersinia pestis doesn’t, so no precipitate forms.

Now, the pathogenesis of Yersinia pestis consists of two components - the transmission of bacteria from fleas and the host response to the bacteria.

First, fleas get infected with Yersinia pestis by feeding on a bacteremic host like rats, which then colonizes the flea midgut.

So, when the flea bites a human it regurgitates the bacteria into the bite wound.

So, once the bacteria gets inside the host, neutrophils and macrophages come to the wound site to kill the bacteria.

Now, the bacteria has a capsule which consists of a capsular antigen, called F1, with antiphagocytic properties.

But, inside the flea gut, it loses this capsule, so neutrophils can easily destroy the bacteria.

Sadly, macrophages are not as efficient in killing the bacteria so, if the bacteria is caught by macrophages it can survive inside them and get carried to lymph nodes where it replicates and cause lymphadenopathy.

Inside macrophages, it starts to use virulence factors to avoid destruction.

So, now it starts again to produce it’s capsular antigen F1.

Also, it has a type III secretion system, or T3SS for short, which is a collection of proteins that can dampen the immune response.

So, using T3SS it starts to inject inside the macrophage Yersinia outer proteins, or Yops for short, which block secretion of proinflammatory cytokines such as TNF-alpha and IL-8 and inactivate the macrophages leading to evasion of phagocytosis.

Key Takeaways

Yersinia pestis is a Gram-negative bacillus that grows well on blood, chocolate, and MacConkey agar. Its virulence factors include capsular antigen F1, which protects it from neutrophils, and Yops, which inactivates macrophages, as well as a siderophore which it uses for iron uptake. It produces a disease called plague, which has three forms - bubonic, septicemic, and pneumonic. Plague is diagnosed by identifying the bacteria in cultures from blood, bubo aspirate, and sputum or in a peripheral blood smear with Gram, Wright-Giemsa, or Wayson staining and also through serological tests and rapid antigen tests. Effective treatment of plague involves aminoglycosides like gentamicin and streptomycin.