242 Disease of pulmonary parenchyma Part B Flashcards
How does BB cause infection, and who is likely to get pneumonia?
- BB creates its opportunity to infect by secreting exotoxins that cause dysfunction of mucociliary escalator
- both dogs and cats are susceptible
- ## Infection causes severe pneumonia in immunocompromised or young animals.
What does S. equi subspecies zooepidemicus cause?What can be done to identify pneumonia?
- Streptococcus equi Subspecies Zooepidemicus causes necrotising hemorrhagic pneumonia in dogs and recognised to affect cats
- Illness can become rapidly life threatening
- Likely cause severe fatal hemorrhagic pneumonia in kenneled dogs, shelters and research colonies.
- Airway lavage can be used for identifying infection and guide appropriate antimicobial therapy.
- Dogs that dye acutely, or with evidence of pneumonia, should undergo necropsy with bacterial culture
What are mycoplasma?
How are mycoplasma identified?
- How is mycoplasma treated?
- Mycoplasma are fastidious microbes that lack a cell wall and can be pathogenic and commensal organisms.
- opportunists and contribute to morbidity when present as co-infetion with other respiratory pathogens.
- Special culture or PCR must be requested to identify Mycoplasma spp. 81.8% Se with Sp of 78.9%
- treat with macrolides, tetracyclines, chloramphenicol, and fluoroquinolone antimicrobials but NOT antimicrobials that interfere with cell-wall synthesis (e.g. beta-lactams) .
What mycobacterial species cause pneumonia? How does mycobacterium present? What tests of mycobacterium help diagnose?
- tuberculosis (i.e. M. tuberculosis, M. bovis, M. microti) and non-tuberculosis type (M. avium complex, M. fortuitum) cause pneumonia
- Pneumonia can be primary manifestation of mycobacteria infetion or a component of DIC
- Mycobacterium often is granulomatous, and rads demonstrate lymphadenomegaly and pleural effusion in addition to interstitial- alveolar pulmonary infiltrates.
- BAL or FNA samples often yield low numbers
- culture and PCR have been used, but tuberculosis-type mycobacteria are notoriously slow growing.
Yersinia Pestis Pneumonia (Plague)
- In midwestern and far-western US, especially New Mexico and Colorado
- rare but has important zoonotic potential
- dogs are resistant and seldom have respiratory signs.
- rodents are natural reservoir of Gram-negative coccobacillus Yersinia pesis
- cats can be infected by ingestion of bacteremic rodents or rabbits or via bite of infected fleas.
- cats develop suppurative lymphadenitis in submandibular and cervical node.
Cytology: of exudate or LN aspirate reveals bipolar, safety-pin-shaped Gram-negative rods.
Treatment: fleas and antimicrobials immediately. Aminoglycosides, fluorquinolones, chloramphenicol, and tetracyclines
What are the viral infections implicated in infectious pneumonia of dogs or cats?
- Avian influenza
- canine distemper virus
- canine herpesvirus
- canine infectious hepatitis
- canine influenza (H3N8 and H3N2)
- Caine parainfluenza virus
- canine respiratory
- coronavirus
- feline calicivirus
- feline herpesvirus
- FIP/coronavirus.
How can viral pneumonia be diagnoses?
- infection is presumed
- targeted serologic or PCR tests used for confirming infection
- Many pathogens of canine infectious resp disease complex or cause feline upper resp infection.
How is Canine Influenza Virus (CIV) H3N8 and H3N2 diagnosed?
- Serologic diagnosis
- unvaccinated dogs are assumed naieve to CIV
- Ab formation lags behind CS, resulting in false-negative tests early in the disease course. - Antigen identification
- Influenza A nucleoprotein is shared between CIV and human infections allowing use of human point-of-care enzyme-linked immunosorbent assay influenza test.
- The test is only positive during viral shedding.
- shedding occurs early in disease (peaks at 2-3 days post-infection) and is inconsistent, resulting in false-negative tests - Virus isolation
- gold standard method
- depends on virus being present which is possible during first several days of illness - Polymerase chain reaction (PCR) identification
- Real-time PCR conducted on samples from nasal or pharyngeal swabs to identify nucleic acid sequences.
- Samples will be only positive during viral shedding, which can lead to false-negative test results.
What is the common agent causing protozoal pneumonia?
How does it manifest?
How is it identified?
How is it treated?
- toxoplasma is most common cause of pneumonia
- cats are reservoir host for Toxoplasma gondii and often infected without displaying clinical signs.
- also involve GIT, CNS, abdominal viscera, heart, eyes, or resp tract.
- resp manifestations of interstitial pneumonia either acute or slowly progressive are most common.
- Serologic identification of specific IgM support active disease, but false-positive and false-negative tests occur.
- T. gondi tachyzoites are identified in airway lavage from animals with pneumonia.
- Rapid response to treatment with potentiated sulfonamides or clindamycin.
What systemic fungi can cause mycotic pneumonia?
- Systemic fungi (Blastomyces dermatitidis, Histoplasma capsulatum, and Coccidoides immitis)
- slowly progressive lower resp disease is primary manifestation, but extrathoracic manifestations include weight loss and lymphadenopathy are common
- T-rads: variable and include nodular or miliary nodular interstitial lung patterns and hilar lymphadenopathy.
- Treatment: expensive & potentially toxic
- Interstitial mycotic infections do not result in early exfoliation of fungal elements into the airways, airway lavage is not sensitive technique for identification of fungal elements.
- Diagnosis confirmed from other sites (e.g. LN aspirates, impression smears of dermal lesions)
- Se & Sp urine fungal antigen tests available
What fungal agents are mostly in the US?
Blastomycosis, histoplasmosis, and coccidioidomycosis
What fungal agents are worldwide distribution? Where are the extrapulmonary infections?
Systemic aspergillosis:
- worldwide distribution
- located in bone, spine, LN, kidney, spleen, pancreas, liver
- Septate hyphae (2-3um) with parallel walls and dichotomous branching
- Dogs>cats
Cryptococcosis:
- worldwide distribution
- nasal cavity (cats), CNS, and eyes (dogs)
- Round to oval yeast (4-10 micron diameter) with thick clear capsule; narrow-based budding can be seen
- Cats>dogs
What is pneumocystis carinii? Who does it commonly affect? How is it diagnosed? How is it treated?
- pneumocystis carinii was originally a protozoon but now is considered a fungus.
- in immunocompromised hosts it can result in severe morbidity with high mortality due to pneumonia
- some immunocompromised small breeds, but most common miniature daschunds and cavalier king charles spaniels.
- most common in mini daschunds and in Pomeranians; IgG deficiency in Cavaliers
- most dogs are young, and present for lower respiratory disease signs, absence of fever despite severe pneumonia is a clue to this type of infection.
- Dx is complicated because the pathogens are not recovered easily by airway lavage and special stains such as Grocott-Gomori methenamine silver stain and required to visualise the organism when present.
- Potentiated sulfonamides appear to be the most effective therapy when administered early
What is aspiration pneumonia? What can make aspiration pneumonia harmful?
- aspiration pneumonitis and pneumonia result from inhalation of materials into lower resp tract.
- depending on volume and properties of the material (pH, tonicity, bacterial contamination, volume & size), the result is from minimal to fulminant pulmonary oedema, necrosis, and hemorrhage.
- Irritating chemicals cause pneumonitis
- Aspiration of polyethylene glycol can be harmful as these substances draw interstitial fluid into lungs
- Due to the low bacterial burden in stomach content infection is seldom important initially.
- Damage done to resp tract by acid irritant predisposes to secondary bacterial infection
What predisposes some animals to aspirate?
- Impaired conscious protection of the airways (GA< sedation, seizures, come)
- impaired unconscious protect of airways (laryngeal paralysis, surgical alteration of laryngeal anatomy, MG)
- impaired swallowing (achalasia, cranial nerve V deficits, rabies)
- regurgitation (megaesophagus, motility disorder, esophageal diverticulum)
- Gastric overdistension (overfeeding, ileus, GIT obstruction)
- Vomiting (primary GIT, pancreatic, uremia, hepatic disease)
- force feeding or administration of oral medications
What is the expected radiographic finding of aspiration pneumonia?
- patchy alveolar infiltrate
- some have interstitial pattern
- changes can lag behind aspiration due to fluid accumulation lagging in chemical lung injury.
- radiographs should include both lateral views.
- most affect lobes are right middle, right cranial, and caudal portion of left cranial.
How is aspiration pneumonia treated?
- Prevent aspiration in megaoesophagus by feeding elevated bowls, keep pet upright. Place Gastrotomy tube if regurgitating. H2 receptor antagonist or proton pump inhibtor increases pH of stomach content and lessen chemical lung injury due to aspiration but also increase gastric bacterial content
- Prokinetic drugs such as metoclopramide promote gastric emptying and tighten lower esophageal spincter
- Following aspiration, baseline thoracic rads should be obtained and O2 monitored.
- Dyspnea occurs after aspiration, bronchodilators could ameliorate acute bronchospasm.
- Aggressive O2 supplementation could worsen oxidative lung injury associated with chemical pneumonitis.
- secondary bacterial infection could require treatment with appropriate antimicrobials.
What causes pulmonary oedema?
What does it cause?
- not a disease, but a consequence of disease.
- Due to inc hydrostatic pressure, decreased oncotic pressure, impaired lymphatic drainage, or increased vascular permeability, fluid accumulate in the interstitium and the alveolar at a faster rate than it can be reabsorbed.
- accumulation of alveolar fluid + decreased lung compliance + airway compression resulting from oedema all INCREASE pulmonary vascular resistance. This causes hypoxemia from the ventilation-perfusion mismatch.
- Removal of alveolar fluid depends on active transport of sodium & chloride from luminal surface through epithelial cell and across the basolateral membrane. Water movement passively follows salt
- fluid removal requires active salt transport across epithelium, injury to epithelial cells and leads to oedema formation but impedes lungs ability to resolve oedema.
What is cardiogenic oedema?
- how is it treated?
- follows increased venous pulmonary hydrostatic pressure associated with left-sided heart failure
- diuretic administration, afterload reduction, and any specific therapy aimed at causing congestive heart failure.
What
- normally minute quantities of fluid and solutes leak from gaps between capillary endothelial cells and enter interstitial space. Tight junctions between alveolar epithelial cells prevent fluid entering the alveoli.
- Instead interstitial fluid moves into peribronchovascular space where it is removed by lymphatics and returned to circulation. Starlings equation for filtration across a semipermeable membrane describes factors that determine the amount of vascular leakage.
- In CHF or IV volume overload increased microvascular hydrostatic pressure leads to increased transvascular fluid filtration and pulmonary oedema.
- Capillary endothelial permeability is unchanged so the oedema contains little protein.
- noncardiogenic pulmonary oedema occurs when vascular permeability increasesas a result of direct or indirect lung injury, and so the fluid is protein rich.
What are some causes of non-cardiogenic pulmonary oedema?
- Neurogenic pulmonary oedema (seizures, electrocution, head trauma)
- Post-obstructive pulmonary oedema (strangulation, laryngeal paralysis, pulmonary re-expansion)
- Systemic disease predisposing acute resp distress syndrome (sepsis, shock, severe pancreatitis, virulent babesiosis, paraquat poisoning, envenomation, gastric/splenic/mesenteric torsion, parvoviral enteritis, uremia)
- Direct pulmonary injury (aspiration pneumonia, bacterial pneumonia, lung lobe torsion, smoke inhalation, parasitic pneumonitis, pulmonary contusion, hyperoxia)
- profound hypoalbuminemia (PLN, lymphangiectasia, liver failure)
- impaired lymphatic drainage (lymphangitis, lymphatic neoplasia)
- Miscellaneous causes (vasculitis, drowning, high altitude, air, embolus, pheochomocytoma)
What is the definition of ARDS?
“an acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue [with] hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space and decreased lung compliance.”
What are differences between the AECC and Berlin criteria in regards to ARDS on timing, oxygenation, PEEP requirement, Chest imaging, Origin of oedema
AECC: Acute onset
Berlin criteria: within 1 week of inciting event or new or worsening respiratory symptoms
Oxygenation:
AECC = PaO2/FiO2 ≤200 mm Hg (defined as acute lung injury if ≤300 mm Hg
Berlin =
- Mild: PaO2/FiO2 >200 mm Hg but ≤300 mm Hg
- Moderate: PaO2/FiO2 >100 mm Hg but ≤200 mm Hg
- Severe: PaO2/FiO2 ≤100 mm Hg
PEEP:
AECC = none
Berlin = Minimum 5 cm H2O PEEP required by invasive mechanical ventilation (noninvasive acceptable for mild ARDS)
Chest imaging:
AECC = bilateral infiltrates seen on frontal chest radiograph
Berlin = Minimum 5 cm H2O PEEP required by invasive mechanical ventilation (noninvasive acceptable for mild ARDS)
Origin of oedema:
AECC = Pulmonary artery wedge pressure <18 mm Hg when measured or no evidence of left atrial hypertension
Berlin = Respiratory failure not fully explained by cardiac failure or fluid overload (need objective assessment, such as echocardiography, to exclude hydrostatic oedema if no risk factor present)
What is the presentation of non-cardiogenic pulmonary oedema?
- CS can be rapid or delayed for up to 72 hours after inciting insult.
Early signs = exercise intolerance and tachypnea. moist cough could produce frothy foam - Resp distress and orthopnea can be observed, and animals demonstrate cyanosis or hemoptysis
- harsh, loud, bronchovesicular sounds are expected, and inspiratory +/or ed-expiratory crackles auscultated.
- lung sounds can be quiet when oedema is severe
- sinus tachycardia is common with cardiogenic oedema
-vagal stimulation associated with lung disease causes resp sinus arrhythmia
What is the likely radiographic changes that progress with oedema and ARDS?
- unstructured +/- peribronchial radiographic pattern that progresses with severity of oedema and produces alveolar pattern
- patchy infiltrates common
Why are the lungs a common site for metastasis?
- The pulmonary vascular bed receives the entire output from RV ->blood passes through small diameter, well-oxygenated capillary beds, making lungs ideal for metastasis.
- “Seed & soil” hypothesis
Where can pulmonary lymphoma be found? What is seen on t-rads?
- lymphoma affects lungs of cats and dogs either in conjunction with lymphoid and solid organs or without additional tumour burden.
- interstitial, alveolar, and mixed pulmonary infiltrative patterns are observed on T-rads with or without concurrent hilar and mediastinal lymphadenopathy.
What is Pulmonary lymphomatoid granulomatosis ?
Where does it affect?
What do t-rad demonstrate?
What is required for diagnosis?
- rare lumphoproliferative cancer, where atypical lymphoid cells infiltrate and destroy blood vessels.
- Other sites include lymph nodes, abdominal organs, and dermis
- leukocytosis with eosinophilia +/- basophlia documented in several affected dogs, but concurrent parasite infection present in some of the animals.
- T-rads demonstrate pulmonary masses +/- lobar consolidation
- Interstitial and alveolarinfiltrates are common as is tracheobronchial lymphadenoathy
- FNA or lavage suggest lymphoma, pulmonary biopsy is required to achieve a diagnosis because of the relationshp between granulomatous lymphoid infiltrates and vasculature defines the disease.
- Supportive care might be necessary for hypoxemic animals, but definitive treatment relies on chemotherapy.
What breeds does malignant histiocytosis (disseminated histocytic sarcoma) affect? Where does it affect?
- more common in dogs than cats.
- Bernese mountain dogs with genetic basis with polygenic mode of inheritance is suspected.
- Flat-coated retrievers, golden retrievers, and rottweilers
- lymphoma, malignant histiocytosis can affect any combinations of organs, bone marrow, CNS, abdominal viscera, and lungs.
What are the signs of histiocytosis (disseminated histocytic sarcoma)?
What is seen on x-ray and CT?
How is it diagnosed?
- Nonspecific signs such as lethargy and anorexia; cough and/or dyspnea
- Radiographs show thoracic lymphadenopathy (tracheobronchial and sternal nodes); pulmonary nodules (often large, and mostly right middle lung lobe) or interstitial infiltrate; and sometimes pleural effusion.
CT-> mild-moderate enhancing and heterogenous, poorly marginated, and bronchocentric.
Dx = histopath of tissue or suggestive clinical findings and supportive bone marrow cytologic features.
Tx = Chemo is largely ineffective and prognosis remains guarded to grave
What is a histiocytic lung disease in cats?
- Feline pulmonary Langerhans cell histiocytosis described in 7 cats
- rads show diffuse bronchointerstitial pattern with miliary to nodular opacities
How to dogs with primary neoplasia present?
- over half present with chronic, nonproductive cough.
- 1/3 of dogs present with no resp clinical signs.
- only 20-40% cats present with dyspnea
- Cough, tachypnea, cyanosis, and hemoptysis occur occasionally in dogs and cats
- other sigs such as weight loss, lethargy, and diminshed appetite +/- resp signs
- may present for lameness due to paraneoplastic osteopathy or in cats, metastises of pulmonary neoplasm to phalanges (lung-digit syndrome)
- Other signs include oedema of head & neck, ascites from tumour obstruction of flow through veins or lymphatics, vomiting, and diarrhea,
- pleural effusion or spontaneous pneumothorax leads to acute onset of resp distress.
What are the differential Dx for solitary or multifocal pulmonary nodules?
- arteriovenous malformation
- atelectasis
- Eosinophilic pneumonia
- fluid- filled bullae
- focal pneumonia
- focal bronchiectasis with mucus
- fungal granuloma
- foreign body granuloma
hematoma - metastatic pulmonary neoplasia
mucoid impaction - parasite granuloma
- primary pulmonary neoplasia (carcinoma)
- pulmonary abscess
- pulmonary cysts
- pulmonary parasites
- Pulmonary thromboembolism
- Tuberculosis
