lect 27-36 Flashcards
(105 cards)
MORAXELLA AND
CHLAMYDIA characterstics
-moraxella BCL 2
-clamydia BCL 2/3
* Moraxella
* Gram negative, strict aerobes: small clusters
* Chlamydia: large reticulate bodies.
* Obligate intracellular parasites
* Genome reduction – rely on host metabolic machinery rather than having their own!
* Biphasic development
chalmdia mechanism on cells
- Elementary bodies (EB) bind to cell surface
- Endocytosis occurs, formation of
inclusion bodies - Organism becomes metabolically active
- Reticulocyte bodies (RB) divide
- RB then differentiate back into EB
- EB escape by lysis or extrusion and infect other cells
MORAXELLA AND
CHLAMYDIA natural habitat
Moraxella
* Found on the mucous membranes of mammals
* Don’t survive well outside of host
* May be transmitted by insects
* Chlamydia
* Elementary bodies somewhat resistant to environmental conditions
* Can survive for several days outside hose
* Avian GI tract is natural site for C. psittaci
* Asymptomatic infections are common
moraxella and chamydiaceae virulence
- Moraxella
- Type IV pilli
- Cytotoxin
- Transferring and lactoferrin binding proteins
- Chlamydia
- Virulence genes comprise ~10% of their genome!
- Various secretion systems (type II, III and V) – secretion of effector
molecules involved in cellular invasion - Cytotoxin – slows down cell cycle, the organism wants to control when
the cell dies/ruptures
moraxella bovis
- Cause of infectious bovine keratoconjunctivitis (pink eye)
- Incubation period of 2 days – 3 weeks
- Clinical signs:
- Copious watery lacrimation
- Blepharospasm, photophobia, in severe cases eye ruptures.
- Cattle are the reservoir
- Transmission via mechanical vectors (insects)
-treat: topical antimicrobials
-control: fly control
Chlamydia psittaci
-causes pistattcosis (brids)
-* Clinical signs:
* Nasal and ocular discharges
* Conjunctivitis
* Green-yellow feces
* Inactivity, anorexia
-if acute: * Hepatomegaly
* Serofibrinous polyserositis
* Petechial hemorrha* Hepatomegaly
* Serofibrinous polyserositis
* Petechial hemorrhages on liver and spleen
necrotizing hepatitis
-fecal-oral or vetrical transmission
-reportable disease in USA
Chlamydia psittaci
zoonosis
- This is an important zoonoses
- Infection through exposure to aerosolized organisms
- In people pneumonia is the most common presentation
- Varies from very mild to severe acute and fulminant
- Culture negative endocarditis
- Persons at risk
- Pet birds/pigeon fanciers
- Veterinarians
- Zoo keepers
farmers,
Chlamydia abortus sheep
- Cause of enzootic abortion of ewes “EAE”
- Abortions typically occur without prior signs
- Typically occur in last month of pregnancy
- Infection remains latent until 3-4 months
-vaginal discharge after abortpion
-common in Uk and USA - Can affect up to 60% of animals in naïve flocks
- Control:
- Isolate aborting animals and clean up abortuses
-zoonosis to people: abortions, avoid eweing lambs
Chlamydia pneumoniae
people
- Cause of respiratory tract infections
- Laryngitis, pharyngitis, fever, headache
- May or may not cause pneumonia
- 2-5% of individuals have asymptomatic infections
- Affects people of all ages
- Those in crowded settings are at highest risk
- Students, military, nursing homes, hospitals, prisons
- Quite common, koala conjuctivitis.
Chlamydia suis
- Associated with infections of the reproductive and respiratory tract
- Conjunctivitis, rhinitis, pneumonia
- Return to estrus, inferior semen quality
- Can survive up to 30 days in environment
- Treatment
- Antimicrobials
- Tetracyclines
-control: cleaning and management
Chlamydia trachomatis
people
- Sexually transmitted disease
- Often no overt clinical signs
- Can cause reproductive system damage and lead to infertility
- Burning on urination or discharge
- Transmitted from mothers to newborns
- Conjunctivitis, pneumonia
- Treatment: Azithromycin
Resistant drug for moraxella and chlamydiaceace
- Moraxella and Chlamydia
- No standardized methods available for determining or interpreting
antimicrobial susceptibility - For Chlamydia this is impossible!
- Moraxella catarrhalis intrinsically resistant to trimethoprim
- Probably best to avoid trimethoprim monotherapy for Moraxella spp. of
veterinary interest
rickettsiales characteritics
- Obligate intracellular parasites
- Bacteria are rod shaped
- Rickettsiaceae family are Gram-negative
- Anaplasmataceae family lack cell wall components of other
Gram negatives - Biocontainment level:
- Level 3 when working with infectious tissues
-level 2 if blood
-cant culture using normal methods
rickettsiales habitat
- These organisms are arthropod associated
- Replication of organism in tick (gut, ovaries, salivary glands)
- Sylvatic cycle
- Vector ↔ Reservoir
- Tick to tick transmission
- Transstadial
- Vertical (female → eggs)
- Horizontal (venereal)
tissue tropisms of rickettsiales
- Rickettsia – Vascular endothelium
- Anaplasma – Erythrocytes, platelets, leukocytes
- Ehrlichia – Leukocytes
- Neorickettsia – Leukocytes
Rickettsia rickettsii dogs
-rocky mountain spotted fever
-1980s from travelers west (trail fever)
-dogs and people
-high mortality
* Clinical signs:
* Fever most common
* Edema or extremities
* May develop petechial or ecchymotic haemorrhages
* Can get necrosis associated with vasculitis
* Seasonality – March-October
Rickettsia rickettsii vector and geographical
- Vectored by hard (Ixodidae) ticks
- West - Dermacentor andersoni, SK, AB
- East – Dermacentor variabilis SK, MB, ON
Rickettsia rickettsii human clinical
- Rash is classical
- Also see fever, headache, nausea, vomiting, injected conjunctiva
- Long term consequences related to vascular inflammation and thrombosis
- Hemorrhage or thrombosis of organs or brain
-treat docyclyline
Rickettsia prowezakii
-Epidemic Typhus (people)
* Clinical Disease
* Begins with flu like symptoms
* Rash, neurological signs (headache to coma)
* Untreated takes 2-3 months to recover fully
* Mortality rate variable (up to 40%)
* Spread by Pediculus humanus corporis
* Human body louse
* Human is reservoir
* Infected lice die within weeks
* Also associated with flying squirrels in southern USA
-disease in WWI with dirty + high density.
Anaplasma
marginale bovine
-bovine anaplasmosis
* In young animals (<1year) infection is usually subclinical
* Disease more severe the older the animal is
* >2 years = severe disease
* Severely affected animals
* Icterus, anemia (extravascular hemolysis!)
* Fever
* Decreased milk production
* Severe infections can be rapidly fatal
-treat: tetracyclines
-vaccination.
Anaplasma phagocytophilum dogs
- Canine granulocytotropic anaplasmosis
- Vectored by Ixodes ticks
- Mirrors distribution of Lyme disease
- Clinical signs are non-specific
- Pyrexia, lethargy, depression and anorexia
- Also reported to affect cats, small mammals, horses, mountain lions, coyotes
-treat: doxyclicine
-avoid: ticks, acaricides
Ehrlichia canis
- Multi-systemic disease
- Cause of canine monocytotrophic ehrlichiosis
- Depression, lethargy
- Bleeding and petechiation possible
- Lymphadenopathy and splenomegaly in ~20-25% of affected dogs
- Ocular signs
- Change in eye colour, blindness,
-neuro signs
-polyarthritis (lameness) - Vector:
- Dermacentor variabilis
- Rhipicephalus sanguineous
- Treatment: Doxycycline
Neorickettsia
helminthoeca dogs clinical
- Cause of Salmon poisoning in dogs
- Highly fatal disease of dogs found in California → B.C.
- Clinical signs
- Sudden febrile illness 5-7 days after eating parasitized fish
- Gradually become hypothermic 4-8 days after signs begin
- Marked anorexia and wasting
- Develop diarrhea and vomiting ~14 days after signs begin
- Hematochezia may occur before death
- Adult flukes (Nanophyetus
salmincola) in dog intestine -> metacercaria in fish muscle
Neorickettsia
helminthoeca dogs treatment
- Treatment”
- Tetracyclines
- Praziquantal
- Anti-trematode therapy
- Supportive therapy
- Fluids
- Anti-emetics
- Prevention:
- Vaccines not effective
- Preventing exposure most important
- Organism survives in rotting fish carcases for months