Lymphadenopathy Flashcards
Ehrlichia chaffeensis & Anaplasma phagocytophilum
Lymphadenopathy
• Small Gram-negative, obligate intracellular bacteria
• Form characteristic microcolonies resembling *mulberries, termed *morulae
• Ehrlichia chaffeensis infect mostly *monocytes SO the disease is called *human monocytic ehrlichiosis
• Anaplasma phagocytophilum infect mostly *granulocytes
- Ehrlichia (animate), it is transmitted by the *Lone Star tick and the main animal reservoir are *white-tailed deer
- Anaplasmosis (animate) is transmitted by the *black-legged ticks. It uses the *white-footed mouse as its main animal reservoir
CLINICAL
• Acute symptoms (1-2 weeks after tick bite): fever, headache, muscle pain, malaise, chills, nausea, abdominal pain, cough, confusion, red eyes, rash (rare with anaplasmosis); lab results may show leukopenia, thromobocytopenia, and elevated serum transaminase levels
• Severe clinical presentations may include difficulty breathing, hemorrhage, renal failure or neurological problems
• Because of the same tick species being involved, it is possible for a person to get co-infected with either anaplasmosis, Lyme disease amd/or babesia.
DIAGNOSIS
- indirect fluorescent antibody (IFA) test
Francisella tularensis
Lymphadenopathy
• Small, gram-negative coccobacillus
• Non-motile
• Facultative anaerobe
• Facultative intracellular
• Non-spore-forming, yet survives well in the environment
• Facultative intracellular of macrophages
• Virulence due to polysaccharide capsule
• Arthropod bite
• Contact with infected animal tissue (e.g., skinning a rabbit, bite from infected cat/dog, handling a dead animal)
• Inhalation of aerosols or dust (e.g., lawn mower over rabbits)
• Ingestion of contaminated food or water
- bioterrorism risk!
CLINICAL
• non-specific and flu-like.
- They include headache, backache, fever, chills, malaise, and weakness.
DISEASES
*Ulceroglandular tularemia
• Most common
• Usually by insect bite or tissue exposure
• Ulcers/eschar
• Regional lymphadenopathy
*Pneumonic tularemia
• Due to aerosols; lawn mowers/laboratory exposure/bioterrorism
• Rarely occurs in nature
• Pneumonia; respiratory failure
• High mortality rate
*Typhoidal tularemia
• Systemic infection without lymphadenopathy or ulcer; sepsis, pneumonia
• Inhalation exposure or skin/mucosal contact
• High rate of mortality
• May be due to bioterrorism
Oropharygeal tularemia
• From consuming contaminated food/water; inhalation
• Exudative pharyngitis and cervical lymphadenopathy
Oculograndular tularemia
• Usually from butchering infected animal
• Conjuctival inflammation with preauricular lymphadenopathy
DIAGNOSIS
- antibody agglutination, direct fluorescent antibody, immunohistochemistry or PCR
Leishmania species
Lymphadenopathy
• Vector: female Phlebotomus sand fly
• Reservoir: humans, dogs, foxes, rodents; depends on geographic location & parasite species
- *The key stages that you should know are the infectious promastigotes (animate) and the amastigotes inside macrophages (animate).
DISEASES
*Cutaneous leishmaniasis
• Most common form; ~1 million cases worldwide annually
• Causes skin lesions that slowly heal & leave a scar (social stigma); may develop into mucosal leishmaniasis
• Due to infection of macrophages in the dermis
• Most cases in Afghanistan, Brazil, Iran, Peru, Saudi Arabia and Syria
*Mucosal leishmaniasis (espundia)
• Causes disfiguring lesions of mucous membranes & cartilage; death due to secondary bacterial infections
• Due to dissemination of parasites from the skin to the naso-oropharyngeal mucosa
• Usually due to L. braziliensis
• Most cases in Bolivia, Brazil and Peru
*Visceral leishmaniasis (kala-azar)
• Infects organs of the reticuloendothelial system (liver, spleen, & bone marrow) causing anemia, leukopenia, thrombocytopenia & splenomegaly
• Most severe form; may be fatal
• May develop post kala-azar dermal leishmaniasis (PKDL), a syndrome characterized by skin lesions after treatment
• Usually is caused by L. donovani and L. infantum
• Most cases in Bangladesh, Brazil, India, Nepal and Sudan; ~300,000 cases/year
DIAGNOSIS
• Microscopy or molecular techniques using specimens from skin lesions (cutaneous) or bone marrow (visceral)
• Serology for visceral leishmaniasis
Leptospira interrogans
Lymphadenopathy
• Spirochete with hooked ends
• Gram-negative, thin, highly motile, slow-growing obligate aerobes
• Infects various animals including rats, dogs, cattle & pigs
• Rodents are the primary reservoir; carriage but no disease
• Causes illness in dogs, cattle & pigs; also carriers; vaccine available
• Occupational exposure: farmers, mine workers, sewer workers, slaughterhouse workers, veterinarians and animal caretakers, fish workers, dairy farmers & military personnel
• Triathletes & adventure racers (fresh water or irrigation ditches)
DISEASE
• Biphasic illness
• Leptospiremic phase= fever, chills, vomiting, headache, anemia, conjunctival suffusion, hemorrhagic rash, generalized lymphadenopathy for ~1 week
• “Immune” phase = severe disease (5-15% of case) including aseptic meningitis, jaundice, hepatitis, impaired kidney function (Weil’s disease); 10% mortality
DIAGNOSIS
• IgM serology for diagnosis; microscopy is difficult
Trypanosoma brucei
Lymphadenopathy
• Vector: tsetse fly = Glossina; daylight hours
• Transmission: bite of infected tsetse fly (saliva); congenital
- I think you should know (animate) the term “trypomastigote” as these are found in humans and can multiple. I also think you should be aware that the *life cycle for T. brucei is slightly different from its cousin T. cruzi.
DISEASE
- *Sleeping sickness = African trypanosomiasis
*Sleeping sickness: three phases
• Trypanosomal chancre→ picture
• Hemolymphatic stage
• Fever, lymphadenopathy, pruritus
• Meningoencephalitic stage
• Headaches, somnolence, abnormal behavior, and lead to loss of consciousness and coma
DIAGNOSIS
- microscopic examination of chancre fluid, lymph node aspirates, blood, bone marrow, or, in the late stages of infection, cerebrospinal fluid
Trypanosoma cruzi
Lymphadenopathy
• Vector: Reduviid bug = kissing bug = Triatomine; lives on walls of rural huts, feeds at night & bites around mouth & eyes; feeds on chickens
• Reservoir: Humans & animals (cats, dogs, guinea pigs, armadillos, raccoons, rats)
• Trypomastigotes in feces of triatomine bugs into bite wound or mucosal membrane
DISEASE
• *Chagas disease = American trypanosomiasis
*Chagas disease: acute phase
• Non-specific symptoms like malaise, fever, anorexia, lymphadenopathy, mild hepatosplenomegaly, and myocarditis
• *Chagoma = inflammation and swelling at the site of inoculation; if eyes inoculated, Romaña’s sign
• Parasitemia
*Chagas disease: chronic phase
- complications include a dilated esophagus or colon, leading to difficulties with eating or passing stool.
- more commonly, infected individuals may develop cardiac complications, which can include an enlarged heart (cardiomyopathy), heart failure, altered heart rate or rhythm, and cardiac arrest.
- During the chronic phase, the parasitemia is too low for diagnosis, but the amastigotes may be found in stained biopsy specimens. In people who have suppressed immune systems (for example, due to AIDS or chemotherapy), Chagas disease can reactivate and then the parasites found in the circulating blood. This occurrence can potentially cause severe disease.
DIAGNOSIS
Acute phase
• Peripheral blood smear to reveal trypomastigotes
Chronic phase
• Biopsy specimens stained with hematoxylin-and-eosin (H&E) or Giemsa to reveal amastigotes
• Serology testing using indirect fluorescent antibody (IFA) test and a commercial enzyme immuno assay (EIA) are available at CDC
Yersinia pestis
Lymphadenopathy
• Pleomorphic Gram-negative bacilli; can look like coccobacilli
• Bipolar staining; “*safety pins”
• *Facultative anaerobe
• Primarily animal pathogens
• *Oxidase-negative
• *Non-lactose fermenting
• Non-motile; non-spore-forming
• *Catalase positive
• *Flea (Xenopsylla cheopis) bites
• Contact with contaminated fluid or tissue
• Infectious droplets (direct & close contact)
• Contact with domesticated cats
• Slow-growing on blood agar & MacConkey agar
- bioterrorism!
VIRULENCE
• *F1 capsule: protects against phagocytosis
• Plasminogen activator (Pla)
• V and W antigens
• *Yops proteins (via T3SS)
• LPS endotoxin
DISEASE
*Bubonic plague
• Transmission by bite from infected flea; incubation period of 2-8 days
• Fever, headache, chills, weakness & one or more swollen, tender & painful lymph nodes (buboes)
• Without treatment, may lead to septicemic/pneumonic plague; 50% case fatality
*Septicemic plague
• Transmission by bites of infected flea or from handling an infected animal
• Fever, chills, extreme weakness, abdominal pain, shock & possibly bleeding into skin & other organs; gangrene of fingers, toes & nose
• 100% fatal without treatment
*Pneumonic plague
• Via inhaled droplets (incubation of 2-3 days), or untreated bubonic or bubonic/septicemic plague
• Can spread person-to-person
• Fever headache, weakness & rapidly developing pneumonia (shortness of breath, chest pain, cough & bloody mucous); respiratory failure & shock; untreated is invariably fatal
DIAGNOSIS
• Stained smears or culture from blood or of an aspirate from a bubo/CSF/sputum
• Serology using paired sera
• Report to CDC
