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45 Cards in this Set

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Corynebacterium spp morphology

-small, pleomorphic, gram +


-in stained smears appear Chinese letter characters


-relatively slow growth in lab media

Differentiating factors of corynebacterium spp

-most are catalase +, oxidase -,


-non spore forming


-pathogenic bacteria are non motile


-cause pyogenic infections

chinese letter characters of corynebacterium spp

corynebacteriu spp pathogenesis and pathogenicity

-opportunistic pathogens


-pyrogenic organisms(with the exception of C. Bovis which can be isolated from teat canal of healthy cattle)

C. presudotuberculosis can surviv and replicate in

phagocytes

virulence in C. presudotuberculosis is linked to

-cell wall lipid and an exotoxin(phospholipase D(PLD)) and Corynebacteial secreted protease 40(CP40)


what may enhance survival and multiplication of corynebacterium spp

PLD

CP40 induces

strong immune response which may provide protection

What do C. pseudotuberculosis and C. ulcerans produce

diphtheria-toxin which the presence of in milk may have public implications

C.renale group are

-urinary tract pathogens and produce urease


-also posses fimbriae for attachment to urogenital mucosa

Diagnositc procedures of Corynebacterium spp

-animals species affected and clinical signs may suggest a specific infection


-suitable specimens for the lab: pus, exudate, affected tissue, midstream urine


-direct examination of gram stained smears may reveal corynebacteria


-culture media: blood agar, McConkey and CNA incubated up to 5 days at 37C


Corynebacterium spp identifying diagnostic procedures

-colonial characteristics


- presence of hemolysis


-absence of growth in McConkey, presences of growth in BAP and CNA


-typical corynebacterium polymorphism on gram stain


-biochemical tests

Caseous lymphadenitis is

a chronic suppurative condition of sheep, goat, and rarely cattle caused by C. pseudotuberculosis with organisms surviving in the environment for several months

Caseous lymphadenitis transmission route

-skin wounds, arthropod bites, or dips


-ruptured abscesses


-hematogenous spread causes abscesses in internal lymph nodes

caseous lymphadenitis clinical signs

-abscessation and enlargement of superficial and internal lymph nodes


-goats usually develop superficial, subcutaneous abscesses usually in the head and neck


-ill-thrift and pneumonia may be present


-visceral form may not be detected antemortem

caseous lymphadenitis

incubation period of caseous lymphadenitis

around 3 months

Caseous lymphadenitis diagnosis

-clinical (or postmortem) findings


-smears from lesions by gram stain


-isolation and identification of bacteria via submitted swabs to lab


-serological diagnosis:ELISA (individual and flock screen)


-interferon-gamma test as flock screen

Caseous lymphadenitis: Tx

susceptible to many antimicrobials but therapy is usually ineffective due to intracellular survival ability of bacteria and inability of drugs to penetrate into abscesses

caseous lymphadenitis: control

-import animals from countries/states/flocks free of caseous lymphadenitis


-animals should be subjected to pre-importation screening tests such as ELISA


-imported animals should be quarantines up to 3 months


-infected animals should be slaughtered


-contaminated buildings and equipment should be disinfected


-vaccines available

ulcerative lymphangitis is/caused by

- slow and chronic either lymphangitis of lower limbs or abscessation of pectoral region(also called pigeon fever)


-C. pseudotuberculosis in horses and rarely in cattle


-prevalent in fall and early winter

ulcerative lymphangitis is transmited by

skin wounds, arthropod bites or contact of infected animals

ulcerative lymphangitis

ulcerative lymphangitis

ulcerative lymphangitis clinical signs

-lymphatic vessels swollen and firm with nodules forming along their length


-edema develops in affected limbs and ulcerated nodules exude a thick odorless, greenish blood-tinged pus

ulcerative lymphangitis diagnosis

based on isolation and identification in the lab

Tx and control of ulcerative lymphangitis

-systemic antimicrobials may be combined with topical Tx


- affected animals should be isolated and contaminated areas disinfected

Bovine pyelonephritis causative agent

C. renale- which may be isolated from healthy cattle vulva, vagina and prepuce


Bovine pyelonephritis acquired by

stress of parturition and short urethra in cow may predispose to infection

Bovine pyelonephritis


-ascending infection from bladder to ureters can result in pyelonephritis with chronic infections possibly leading to extensive renal damage

Bovine pyelonephritis: clinical signs

-fever, anorexia and decreased milk production


-restlessness and kicking in the abdomen may indicate renal pain


-dysuria and blood tinged urine are present


-clinical signs may suggest UTI


-red blood cells and protein are present in the urine


- thickened ureter and enlarged kidneys may be detected by renal palpation and or ultrasonography: unilateral


-culture of C. renale frome urine is confirmatory

Bovine pyelonephritis: Tx

-antimicrobial tx based on susceptibility test, should start early for at least 3 weeks


-penicillin is usually good choice for high excretion in urine

Ulcerative balanoposthitis

-caused by C. renale


-characterized by ulceration around prepucial orifice with a brownish crust developing over the lesion


-similar lesion may happen on the vulva of ewes


-castrated sheep more prone


-untreated cases may progress to total occlusion of preputial orifice

C. renale may cause mucosal irritation and ulceration by

hydrolyizing urea into ammonia

predisposing factor of Ulverative balanoposthitis

high urea level in the urine due to high protein intake

ulcerative balanoposthitis

rhodococcus equi morphology

-gram positive rods or cocci


-salmon-pink, mucoid, non-hemolytic colonies


-aerobic, non motile


-CAMP test positive


-major respiratory pathogen of foals

Rhodococcus equi

Rhodococcus equi- suppurative bronchopneumonia epidemiology

-one of the most common causes of pneumonia in folas


-generally acquired by inhalation of dust


-may be present in high number in horse feces


-environmental influences-dry weather, poorgrass coverage


-high foal density


-only young foals susceptible

Rhodococcus equi- suppurative bronchopneumonia pathogenesis

-ability to survive and multiply in macrophage


-virulence is principally associated with a large??(not on slide)


-encodes several proteins most important VapA


-only equine isolates have VapA gene


-capsular polysaccharides, mycolic acids and exoenzymes

Rhodococcus equi- suppurative bronchopneumonia clinical signs

-usually less than 4 weeks old foals


-sudden onset of fever


-anorexia


-signs of bronchopneumonia


-could be insidious in 2-4 month old foals


-coughing, dyspnea, weight loss, exercise intolerance


-loud, moist rales on auscultation

Rhodococcus equi- suppurative bronchopneumonia

Rhodococcus equi- suppurative bronchopneumonia: diagnosis

-differentiating lower respiratory trac infections problematic


-WBC, fibronegen, radiography, ultrasonography,


-bacterial culture from tracheobronchial aspirate


-salmon color mucoid colonies on BAP, CAMP test


-PCR tests

Rhodococcus equi- suppurative bronchopneumonia: Tx

-combination of oral rifampin and a macrolide for up to 10 weeks


-severely affected foals have poor prognosis


-response to therapy monitored by radiography/ultrsonagrophy and plasma fibrinogen


-supportive therapy: rehydration and bronchodilatotory agents or expectorants

Rhodococcus equi- suppurative bronchopneumonia: control

-vaccines not aailable


-screening of foals twice a week clinical examination


-prevention of dust ihalation


-limit the foal density


-limited time spent indoor


-foaling at pasture may reduce the occurence


-passive immunization-hyperimmune plasma


-chemoprophylaxis-conflicting evidence and danger or resistance


-development of active immunization highly needed(aka vaccine)