Obligate intracellular bacteria- characteristics
gram negative (mostly)
small (don't need a huge genome because it uses host machinery) genomes
AT-rich genomes- don't know why this is but maybe it provides stability?
Must invade host cells and take over normal host machinery
Detection of intracellular bacteria
Culture: generally difficult but CAN be done, therefore not a routine diagnostic procedure: co-culture with eukaryotic cells
Microscopy: non-specific staining--> indicative but not diagnostic
Immunohistochemistry (antigen detection)
Immune responses: antibody or CMI
Genomic detection: PCR
Widely distributed, host-specificity, "parasites" and pathogens i.e. many species often reside without overt/apparent disease.
Pathogenic chlamydia include (major ones we'll look at)
Ch. psittaci: avian -multiple serovars
Ch. abortus- ruminant abortion
Ch felis- cat conjunctivitis and rhinitis
Chlamydia infection cycle
Infective form--> adherence to cell membrane (necessity)--> entry by endocytosis--> *prevention of phagosome-lysosome fusion--> replicative form (infective form redifferentiates to replicative form)-->division-formation of "inclusion" (rapid 24-48 hours)--> re-differentiation to infective form--> exit from infected cells
1 million BPs--> 1000 proteins
sophisticated infectious cycle.
Chlamydia developmental phases
Elementary body (EB): infective form, spore-like and dense. 300-500 nm (cf. staph=2000nm), some tolerance of environmental streses but not resistance-can survive on pasture
Reticulate body (RB): replicative form, non-infective, 2000nm (much more like typical coccus), divides by binary fission
Non synchronous differentiation-- mixed populations of EBs and RBs
Pathogenic mechanisms of Chlamydiae
Cytopathic effect: interferes with metabolism; cytolysis
"PAMP" effect: molecular components trigger innate inflammatory cytokines (IFN, ILs, TNF)
Acute inflammation: neutrophils and macrophages
Delayed-type hypersensitivity: indicated as cause of damage- contributes to inflammatory damage.
Secondary immunpathology: primary exposure may not result in serious pathology, but secondary might.
Latency and persistentce: adept at entering latent phase and persist without causing clinical disease features. This is important to consider in terms of control.
Enzootic abortion of Ewes (EAE)/Ovine Enzootic Abortion (OEA)
continually present in UK flock
1st exposure: ~30% abort; 2nd exposure: ~5% abort.
1st exposure is productive infection, 2nd is less productive. This example makes it difficult to back up the idea of seconday immunopathology. I.e. exposure CAN result in protective immune response.
C. abortus (OEA) pathogenesis
Ingestion/inhalation--> localisation to tonsils/LNs (live in many phagocytic cell types)-->dissemination (unknown tissues, cell types)--> placentitis (animals could just be slightly febrile or appear normal until end of infection. seems infection becomes reactived in late pregnancy)
Placentitis--> fetal infection--> abortion, stillbirth, weak lambs, subclinically affected lambs.
Placental lambs are heavily infected, contaminated environment (Elementary bodies)
C. abortus- tx and control
Closed flocks/OEA free-accrediation
Vaccines: mediavac, enzovax, cevac chlamydophila
ZOONOSIS: respiratory and abortion
non-specific in humans
fever, chills, headache, muscle aches, dry (non-productive) cough, malaise, penumonia, endocarditis/meningitis/ abortion
typically aquired via inahalation
NB: C. psittaci is a schedule 5 notifiable pathogen
Anaplasma spp and Ehrlichia spp.
Arthropod borne therefore geographically restricted.
Tick borne fever (TBF)
Tick hemolymph--> inoculation by tick bite--> infection of neutrophils
Show up on histology as light irregular purple staining in cytoplasm of neutrophil= inclusion bodies of anaplasma phagocytophilum.
Anaplasma phagocytophilum- TBF pathogenesis
Infection of neutrophils--> cytokine release/neutropenia
causes: 1) fever, abortion, decreased milk yield, decreased weight gain (non-specific signs, but indicative)
2) "immunocompromise"--> secondary infections--> tick pyremia (S. aureus introduced into tick bite wound), systemic pasturellosis, louping il, listeriosis
Persistent infection (reservoir).
Coxiella burnetti- Q fever
Asymptomatic in ruminants--> excreted in urine, feces, milk and placenta--> inhalation by human--> infects respiratory epithelium, endothelium and phagocytes--> flu-like syndrome, pneumonia and endocarditis
nb: coxiella burnetti causes occasional abortion storms- esp in goats
ZOONOSIS + ATCSA schedule 5
Porcine proliferative enteropathy
Diarrhea, hemorrhagic diarrhea, fatalities
Non-specific signs: reduced/variable weight gain, reduced feed conversion, variable or low slaughter weight
caused by Lawsonia intracellularis
Pathogenesis of Lawsonia intracellularis/ PE
ingestion--> invasion of ileal crypt enterocytes--> epithelial hyperplasia (mature epithelium replaced with immature non-differentiated epithelial cells)--> intestinal thickening.
highly prevalent pathogen- up to 95% seroprevalence at farm and animal levels. worldwide distribution.
Lawsonia has a lot of unique features and v. few conserved system: has flagella, has a type III and type V secrtion system
ABX: tylosin, tiamulin, tetracycline
vaccine: attenuated L. intracellularis strain (oral drench or in drinking water)