ICVA NAVLE Exam Questions

Correct answer: Viral disease

Causes of cataracts in horses include: 

• Penetrating wounds to the sclera/cornea, which damage the lens or attachments
• Traumatic-induced uveitis
• Anterior uveitis of any cause
• Lacerations to the eye
• Lens luxation
• Senility
• Developmental abnormalities (congenital or hereditary) +/- nutritional/toxic insult or inflammatory causes (Belgians and Morgans may be predisposed)

The Bovine Viral Diarrhea virus (BVD) has been associated with cataract formation in cattle. Still, to date, no viral infectious causes have contributed to the development of cataracts in our equine patients.

Correct answer: Pneumonyssoides caninum

Nasal tumors in dogs can be epithelial, nonepithelial, or miscellaneous in origin. They have a low metastatic rate overall. The most common metastatic region is the brain, followed by the lymph nodes, lungs, and liver. Males are more predisposed. Most patients present with unilateral epistaxis. Some may have intermittent sneezing, sometimes paroxysmal, triggering the epistaxis. They may have other signs, including crusty nares, snuffling, swelling in the facial area, or neurologic signs depending on where the tumor spreads, and seizures can also occur.

Chest radiographs to rule out mets should be performed. Anesthesia and skull radiographs may be warranted in addition to advanced diagnostics such as CT/MRI/endoscopy or rhinoscopy.

The differential diagnoses for unilateral nasal epistaxis and discharge are plentiful. They may include fungal diseases such as aspergillosis in dogs. Nasal foreign bodies, polyps (cats), and nasal mites (Pneumonyssoides caninum) may cause sneezing, rhinitis, and decreased smell (though they are much less likely to trigger epistaxis). Other parasites that trigger nasal discharge and epistaxis include Ehrlichia, leishmania, and even the lungworm (Capillaria aerophila) or Cuterebra.

Correct answer: 1–1.5 L of colostrum

Luckily, unlike calves, foals are immunocompetent when born. However, they have no exposure yet to foreign antigens and require colostrum to obtain the antigenic protection developed from the mother’s immune system, passed on in the colostrum. Foals, thus, are born without IgG. IgM is produced in utero, so they should have sufficient levels at birth. Normally, if they receive appropriate colostrum, within one to two weeks, foals will start to produce their own IgG, which can be detectable in the blood at that time, peaking around two to three months of age.

Colostrum provides the foal with temporary immune protection by providing cytokines, immune mediators, antibodies, and a few mononuclear cells. However, IgG doesn’t cross the placenta, so this is only obtained after birth via the colostrum.

Normal, acceptable levels of IgG for neonates, if sufficient colostrum has been ingested, will be 800–6000 mg/dL. If the foal fails to obtain this degree of protection, either because they do not ingest appropriate quantities or absorb it properly, it is called a Failure of Passive Transfer (FPT).

There are no obvious clinical signs of FPT (unless, as in this case, it is known that the foal hasn’t been nursed sufficiently or at all). However, within the first one to two weeks of life, foals who develop septicemia, pneumonia, septic arthritis, or enteritis suggest that they may have FPT. Failure of Passive Transfer (FPT) occurs in the neonate (zero to three weeks of age). The peripheral white count will be normal. B and T cell functions and counts will be appropriate. Serum IgM will be low; Serum IgG < 800 mg/dL is diagnostic; Serum IgA will be low. They will respond appropriately to vaccinations. However, they may have a secondary immunodeficiency. If they develop secondary infections and are well controlled, the prognosis is good.

Reasons for FPT:

1. Mother rejects the foal/prevents suckling
2. Colostrum is poor quality, lacking sufficient antibodies
3. Mare isn’t producing enough milk, fails to have milk letdown, or has agalactia
4. Foal cannot stand due to weakness or confirmational deformities and, therefore, cannot search and find the udder
5. Failure to latch on properly, poor suckle reflex
6. If the mare had early milk letdown before foaling and the colostral milk has already been emptied (uncommon)

FPT may be managed with a foster mare or via commercial colostrum products if readily available. Ideally, we want the foal to receive a minimum of 1–1.5 L of colostrum (measuring sugar/BRIX refractometer scale > 23%), ideally within the first six hours of life, though the mare naturally produces milk rich in antibodies for up to the first 48 hours post birth. If the mare isn’t producing sufficient milk or rejects the foal, or the foal cannot nurse due to musculoskeletal issues or other reasons, bottle feed with an appropriate equine milk replacer, starting with 10% of its body weight divided into six to ten smaller feedings throughout the day.

12 hours after you have started colostrum, check the foal’s IgG levels. Those with ≤ 400 mg/dL should be given additional high-quality colostrum; if unavailable, they can be given 1–2 L of equine plasma IV. Foals with lgG levels between 400–800 mg/dL are considered at high risk for sepsis, but this is just the overall IgG level and doesn’t reflect specific pathogen protections or lack thereof. Foals who nurse and receive colostrum within the first two hours after birth will have measurably sufficient IgG levels by about six hours post. By 18 hours, the levels usually peak.

If multiple hours (more than two) pass before the foal receives any colostrum, the risk of infection skyrockets. It is recommended to administer a dose of broad-spectrum antibiotics, such as ceftiofur at 4.4 mg/kg IV q 12 hours.

Ensure to prevent any common means of entry for pathogens by ensuring appropriate umbilical care. Dip the umbilicus in 1% chlorhex or 2% iodine (or what is currently recommended by scientific evidence, as this changes periodically). Further, if meconium has not yet passed after obtaining colostrum, perform an enema. Bottle/bucket feed the foal until 1) the mom produces sufficient milk, 2) a nurse mare/foster is obtained, or 3) rear the orphan with other foals.

Correct answer: Incorporation of the cavernous tissues into the sutures

When performing a PU surgery (Perineal Urethrostomy), you want to place this patient in dorsal recumbency because he requires both a cystotomy and PU. Pull the pelvic limbs forward in dorsal recumbency, improving access to the perineal area. Avoid excessive dorsal dissection; this prevents damage to the vessels and nerves that service the urethral muscle. Take a hemostat, or 5-8 French catheter, and place it in the urethra to ensure that you are maintaining adequate width. Close the urethra with a simple interrupted pattern, with the first layer in the corpus spongiosum and urethral mucosa. You can then use a simple continuous to close the subcuticular layers and the skin. Make sure to avoid entering the cavernous tissue to minimize bleeding intra and postoperatively. 

Correct answer: Malocclusion will be a lifetime battle, even with surgery

Dental disease in chinchillas can manifest with dysphagia, ptyalism, less fecal output, poor coat quality, and decreased appetite. Abscessation may occur on premolars and molars, secondary to tooth overgrowth. Some animals may develop ocular and/or nasal discharge, which occurs either because apices overgrow into the nasal cavity or impinge the nasolacrimal duct.

Malocclusion will be lifelong. Surgical correction, restoring a normal occlusal plane to the teeth, rarely resolves underlying genetic factors, pre-existing dietary factors, and other parameters. As a result, while the dental procedure will provide relief, and set the stage for healthier oral living, it will likely reoccur. As a result, owners need to be well-informed that this may happen in the future in order to prepare financially and emotionally. Moving forward, client education about improving diet and overall health and minimizing pain is essential.

The prognosis is still guarded to grave, even with surgery — again, because they will have lifelong struggles with the disease. Further, due to the chinchilla's short clinical crowns, surgical correction may be limited, despite attempts to address occlusal surface abnormalities.

Finally, owners should be informed that there is a genetic component and that these animals should not be bred.

Correct answer: Radiographs

Pododermatitis, aka bumblefoot, commonly occurs in older birds. The term refers to any degenerative or inflammatory condition of the foot and can range from mild redness to bone changes.

Common causes include:

• Inappropriate perching provided
• Injury to one leg causes shifting weight to the other and different pressure on the foot
• Obesity
• Arthritis (hip, stifle, tarsal joint)
• Dietary deficiencies, including vitamin A
• Fractures

Generally, pododermatitis is progressive. Hyperemic lesions become ulcerated and, when untreated, can cause abscessation and osteomyelitis. When caught in the initial stages, treatment can prevent debilitation. Initial changes may include flattening and smoothing out of the skin on the digital and metatarsal pads. Over time, it will become proliferative and ulcerative and permit bacterial growth, and when untreated, it can then progress to bone infection and septic arthritis.

Clinical signs will vary depending on the stage of the disease, but birds may show reluctance to move, lameness, depression, and anorexia. Diagnosis relies on a combination of clinical signs, physical exam findings, and radiographs (identify fractures, osteopenia, or other abnormalities). Further, if lesions have progressed and secondary infection is suspected, antimicrobial therapy should be held until appropriate culture and sensitive results are obtained. While not necessary for the diagnosis, bloodwork can help evaluate the body systemically for any other underlying conditions.

Treatment includes padding bandages if needed, pain management, antimicrobial therapy if warranted, weight loss, diet revisions when needed, and improved sanitation of perches and the feet. Some require surgical debridement if let go too long without care.

Correct answer: Atrophic Rhinitis (AR)

Many porcine diseases cause vague clinical signs. Numerous respiratory pathogens and other conditions can trigger conjunctivitis. These include CSF, PRV, PRRSV, and other viral infections. Further, bacterial diseases such as Chlamydia and Mycoplasma also create red and inflamed conjunctiva.

However, Atrophic Rhinitis (AR) commonly causes (among other clinical signs) ocular discharge but not conjunctivitis. Early in the disease, AR causes sneezing, snorting, snuffling, and varying degrees of nasal discharge from serous to mucopurulent. In extreme cases, often in acute growers, epistaxis may arise. This can then progress to chronic changes in the nose, causing distortion and atrophy to the nasal turbinates, facial bones, and nasal bones in affected swine. While similar disease entities have been described in goats and dogs, this is species-specific. It can develop in any pig older than one week. This condition is becoming less prevalent in the U.S. through early weaning programs, vaccinations, and age-related segregation management practices. However, it is a globally recognized disease.

AR is caused by toxin-producing bacteria, either Bordetella bronchiseptica or Pasteurella multocida (primarily type D). A gram-negative, aerobic rod, Bordetella bronchiseptica, easily colonizes porcine nasal passages. Under normal healthy conditions, it remains non-pathogenic. However, in pigs, up to 12 weeks, it can cause severe suppurative bronchopneumonias and losses secondary to septicemia. Lesions generally appear mild, and a progressive form of AR doesn’t usually develop.

However, compare this to the less widespread Pasteurella multocida, where nasal mucosa insults increase nasal colonization. This can occur secondary to other primary infectious agents such as viral diseases or other bacteria or via trauma, and it can be found together with B. bronchiseptica as well. The toxigenic form of P. multocida causes significant dermonecrotizing toxin release that causes severe damage to the turbinates with atrophy and bony changes. Generally, lesions arise before 16 weeks of age but can occur in any naive animal. These lesions persist for life, and some may go on to develop facial deformities such as snout shortening or snout deviation.

Diagnosis is made via history, clinical signs, gross necropsy findings if decreased, and isolation and identification via culture. Nasal swabs early in the infection course, especially from nursery-aged animals, are most rewarding.

Differentials for rhinitis include PRRS, PRV, inclusion body rhinitis (cytomegalovirus), and high dust or ammonia levels.

Control is either depopulation and restocking known AR-free herds or attempts to control the disease. Elimination from a herd can be achieved and tested via PCR.

PRV, AKA Aujesky’s disease, is a significant disease player in the swine industry. It was eradicated in the U.S. in 2004. It consists of three overlapping clinical syndromes affecting either the nervous, the reproductive, or the respiratory systems. PRV is an alphavirus subfamily of Herpesviridae. It can persist in a carrier (latent state) and easily be destroyed by many disinfectants.

Transmission occurs via contact and exposure to saliva, nasal excretions, urine, and feces. The virus can survive in carrier pigs’ tonsils for several weeks and in the CNS for months. Thus, stress can precipitate recrudescence and subsequent re-shedding. It spreads through direct contact, contaminated food/water, and aerosolization.

Clinical signs vary depending on the age of the pigs affected and the immune status of the dam. Younger appear more affected, while older pigs are more resistant.

Sudden death in the very young may be the only clinical sign. Nursing piglets often show neurological signs. You may see very high fevers, conjunctivitis, anorexia, tremoring, depression, vomiting, foaming at the mouth, dog-sitting, paddling, blindness, seizures, coma, and death within one to three days.

Pigs three to nine weeks of age, already weaned, generally have respiratory signs predominate, such as nasal discharge, sneezing +/- cough, and labored breathing. The mortality in nursing pigs can reach 100% but is lower in this age group. Most survive unless they develop secondary bacterial pneumonia.

Ten weeks to market weight morbidity is high and respiratory signs also predominance. They may be febrile, sneeze, cough, have nasal discharge, have depression, or be anorexic. Some will also develop CNS signs. However, most recover in seven to ten days.

Breeding animals may have respiratory disease with full resolution, though, reproductive failure is possible, including mummified fetuses, stillbirths, or weak pigs,  in the second or third trimesters.

Swine are the natural domestic animal reservoirs. Vaccinations are highly effective, but all ages are susceptible if not vaccinated. In the commercial U.S. swine industry, the disease has been eliminated. However, a reservoir still exists in some feral populations and is prevalent in other countries. If other species, such as sheep, cattle, dogs, cats, or goats (not horses), are kept in close proximity to pigs, they are susceptible, and death usually occurs in aberrant hosts. Several wild rodents, rabbits, and fur-bearing mammals can become infected. It is not zoonotic.

There is no treatment, but weaned and older pigs do tend to recover.

PPRSV (Porcine Reproductive and Respiratory Syndrome Virus) is an enveloped RNA virus in the Arteriviridae family. The disease has two clinical phases, the first causing reproductive failure and the second, respiratory disease post-weaning. If a naive herd is infected, not all will develop clinical disease, leading to a persistently infected subpopulation and carrier animal state. Since eradicating Classical Swine Fever, PRRSV is considered the most costly disease in the global swine industry.

Disease transmission occurs via direct contact and through contaminated semen.  Aerosolization and fomite transmission also contribute to disease spread. It is not zoonotic. Experimentally, insect vector transmission can also occur.

Reproductive disease phase: Stillbirths and mummies incidence may be up to 25–35%, and over 10% may abort. Anorexia and lack of milk production can lead to higher preweaning mortality rates of piglets. This form can last one to four months, depending on the health of the pigs at infection and various facility characteristics.

The respiratory phase tends to occur in suckling piglets, and they may develop thumping respirations and conjunctivitis, with interstitial pneumonia on histopath being common. Piglets may be born viremic and serve as another source of transmission. This post-weaning phase may become chronic, causing decreased total weight gain and 10–25% mortality. Other infections may occur concurrently, including Streptococcus suis, Salmonella, Mycoplasma, and swine influenza, among others.

Gilts, sows, or boars may show reproductive abnormalities,  fever, lethargy, waxing and waning, anorexia, and sometimes respiratory distress or vomiting. Mild cyanosis of the ears, vulva, and belly can occur, as well as dyspnea in nursing animals (thumping). Signs may cycle depending on when animals are exposed and shed. Multiple strains may infect a single herd and are not fully cross-protective. 

Young, growing, and finishing pigs may show depression, stunted growth, fever, lethargy, and pneumonia. Sneezing and expiratory dyspnea also may occur along with stunted growth.

Control is key, but there isn’t a single control strategy that works. Ideally, establishing ‘herd immunity’ minimizes transmission and subsequent losses. But quarantine of boars for 60-90 days before introducing them to the females in a negative herd is critical. Vaccination may be utilized as a part of a control strategy. Still, it cannot be the only measure as they are not 100% effective. Depopulation and appropriate cleaning measures then, obtaining all new animals PRRSV free is an option. If one doesn’t want to depopulate, they can close the herd for a minimum of 200 days, stabilizing the herd. But the risk of re-infection is high, and biosecurity protocols must be airtight.

Diagnosis most commonly relies on ELISA measuring the IgG antibodies. However, it cannot assess the level of immunity or predict carrier state animals. Titers are evident seven to ten days post-infection and may persist up to 144 days. Test options also include virus isolation, immunohistochemistry, and PCR. Sampling oral fluid from entire pig populations has been used widely as a screening method.

Modified live vaccines provide some protection and may limit shedding, but no treatment exists. Prevention is paramount.  

Classical Swine Fever (CSF), aka hog cholera, is another febrile, highly contagious disease of pigs, with virulent strains causing almost 100% morbidity and mortality. It is reportable on the national and global level (OIE) World Organization of Animal Health.

CSF, eradicated in 1976 in the U.S., remains endemic in Asia, Central and South America, and the Caribbean (posing a threat to the U.S.) and sporadically throughout Europe. Disease origin is not understood. CSF is related to BVD (Bovine Virus Diarrhea) and sheep’s Border Disease (B.D.). It is less resilient in the environment than ASF. Still, it can survive some curing processes and frozen products for months to years.

As with many swine diseases, signs are often non-specific but can include depression, significantly elevated temperatures, lying down, and huddling with other sick animals, diarrhea, or constipation +/- vomiting. CNS signs may be seen, including seizures in young growers, with most dying within three weeks or less. Less virulent strains may also demonstrate conjunctivitis and emaciation. Helpful in the diagnosis is aiding of single or multiple infarcts in a normal-sized spleen along the border, lymph nodes with subcapsular hemorrhages, and pulmonary and renal cortical hemorrhages.  Leukopenia may also be present, but this must be differentiated from acute salmonellosis, erysipelas, and ASF. This is a reportable disease. Eradication, vaccination strategies, and legislation banning importations help control/prevent disease in various areas.

Primary transmission occurs via oro-nasal direct or indirect contact or ingesting contaminated foods. The tonsils are the initial source of viral replication. Airborne spread is possible experimentally and potentially can occur via semen and humans as fomites.

CSF crosses the placenta, causing infection in fetuses during pregnancy. Depending on the strain, time of infection, and virulence, we can see abortions and stillbirths. If a sow is infected at 50–70 days of gestation, live births with persistent viremia seem normal initially, then develop congenital tremors, termed "late-onset CSF." They shed tons of infected virus particles and serve as significant viral reservoirs. Further, congenital CSF can lead to mummification, congenital malformations, cerebellar hypoplasia, and more.

Laboratory diagnosis is required, as it mimics other diseases, and nothing is pathognomonic. Choosing the most appropriate testing method during an outbreak is key since control and prevention of spread are of the utmost importance.

Correct answer: Systemic use of macrolide antibiotics

Keratoconjunctivitis Sicca (KCS) or dry eye is most commonly secondary to an idiopathic aqueous tear film deficiency, a quantitative dry eye caused by an autoimmune dacryoadenitis with lacrimal and nictitans glands destruction.

Generally bilateral, KCS causes chronic conjunctivitis, superficial corneal vascularization, corneal pigment deposition, fibrosis, and often mucopurulent discharge (when left untreated).

Additional causes of this condition may include:

• Trauma
• Hereditary predisposition
• Cherry eye removal (rather than tacking)
• Use of systemic sulfonamide medications (potentiated sulfonamides)
• Distemper virus
• Synthetic retinoids that are sometimes used in the management of sebaceous adenitis

Correct answer: To initiate therapy with a behavior modification medication such as an SSRI or TCA

While many vets are comfortable dealing with behavior cases, many simply don’t have the time or energy to devote to these patients. These cases can require patience and more than just a 15-minute appointment. Can primary care veterinarians prescribe behavior modification drugs, of course, but research shows that treatment often falls short without behavior modification efforts in addition to medications.

Thus, consider referring to a board-certified veterinary behaviorist if:

1. There is human-directed aggression, especially with kids involved, or the aggression is severe or very unpredictable
2. Client-patient dynamic concerns, including a negatively impacted human-animal bond, and/or owners are considering behavioral euthanasia rather than attempting to train/treat
3. Client is in denial about the severity of the problem or the risks involved
4. Behavior-modifying medications can be used if an owner inquires about medicine and/or if the behavior is bad enough that you feel it is warranted. In these cases, you should always suggest a referral. Again, that isn’t to say general practitioners cannot prescribe these meds. Still, they should be used in conjunction with training and other modalities and monitored closely for dosing side effects and dose adjustments.
5. There are legal issues, i.e., if the dog bit someone or has other legal-related concerns
6. A known medical condition exists, and concern may be present for drug interactions, drug metabolism issues, drug effectiveness, as well as the interplay between any physical ailments, and behavioral issues
7. Inter-dog aggression, especially leading to injury of dogs/people

You may have already recommended various things to an owner, such as cooperative care training, muzzle training, exercise, and other things; you may have tried short-acting and long-acting medications and aren’t getting the response you or the owner would like — in that case, a referral is also appropriate. 

Any veterinarian can start behavior modification drugs from gabapentin (adjunctive) to trazodone, alprazolam, to SSRIs, TCAs, and others. But it is never wrong to refer to a veterinary behaviorist and it may be in the best interest of the pet.

Correct answer: Ventral thorax adjacent to the sternum; Yes

When extra heart sounds are ausculted (S3 or S4), we call it a gallop. Hearing these abnormal sounds usually indicates myocardial disease in the dog and cat. Often, animals can have a gallop (especially cats) without a heart murmur. We are most likely to appreciate the gallop rhythm when ausculting to the ventral thorax adjacent to the sternum (in dogs or cats).

S3 (ventricular gallop) happens early on in diastole. It is attributed to rapid ventricular filling associated with decreased compliance.

S4 (atrial gallop) happens later in diastole secondary to vigorous atrial contractions. This leads to increased resistance to emptying the ventricles or poor ventricular compliance, as we commonly see in cats with hypertrophic cardiomyopathy or high blood pressure.

S3 and S4 often blur together when animals are tachycardic, causing a summation gallop.

While cats may not have any evidence of a murmur or gallop at the time of clinical heart disease manifestation, some may show only a gallop. However, the presence of a gallop in the phase of a clinical cat with dyspnea and tachypnea should put CHF at the top of the differential list.

A gallop is more likely to be ausculted in a cat vs. an arrhythmia. However, it can still develop abnormal rhythms, which are less common than in our canine patients.

Correct answer: Near the entrance to the bladder

Despite excreting large amounts of calcium carbonates into the urine, urolithiasis in equine patients is relatively uncommon compared to sheep/goats or small animals. The exact etiology of urolithiasis formation in equines isn’t fully understood. Signs of urinary tract issues, including stones in any location within the tract (kidney, ureter, urethra, bladder), may include none, abdominal pain (often waxing and waning), dysuria, pollakiuria, hematuria, stranguria, incontinence, pyuria, maintaining a urination posture for longer than normal, and in working or exercise animals, not wanting to work/reluctance to move.

Given that horses secrete calcium, it is no surprise that calcium carbonate is the most commonly identified urolith.

The presence of hematuria after exercise is consistent with cystic calculi. In contrast, hematuria at the beginning of micturition usually signifies a distal urethral lesion. Hematuria that occurs throughout urination suggests a kidney issue or bladder issue. Finally, hematuria at the end of urination suggests a bladder problem or, in a male, a proximal urethral concern.

As in dogs and cats, nephroliths may be incidental or cause clinical disease.

Ureteral stones, though uncommon, are most commonly found near the entrance of the bladder and can usually be identified via transrectal or trans-abdominal ultrasound.

Urethral calculi are most commonly found at the point where the urethra narrows, at the ischial arch. Urethral stones may be palpable transrectally.

Cystolithiasis (bladder stones) are usually seen in geldings.

This patient’s differential includes any cause of dysuria, cystitis, urethritis, urethral strictures, bladder rupture, penis/preputial trauma, or cancer. Further, we must ensure that the patient is not obstructed. The passage of a urinary catheter may help dislodge any stones in the urethra and or confirm an obstruction.

Note that urine cultures are often negative in equine patients with stones in the urinary tract. However, 60% of cultures of the calculi will be positive. E. coli, Staph, and Strep species are the most commonly identified.

Remember that a urinalysis will not help determine if stones are present, as horses naturally have large amounts of crystalluria.

Animals with chronic calculi issues may have weight loss or loss of body conditioning, ventral abdominal scalding, and scalding of the perineum, preputium, and hind legs. They may also have waxing and waning signs of mild colic. 

Correct answer: Clipping fins or gills underwater; > 110%

Gas supersaturation (ΔP - change in pressure), or gas bubble disease, refers to the presence of excess gas from the water environment entering an animal's bloodstream. As it comes out of the solution, the gas triggers gas embolisms. The increased gas could be either oxygen, carbon dioxide, or nitrogen.

Causes may include:

• Small pipe leaks (venturi effect)
• Pumping water from depths
• Waterfalls
• Sharp rise in water temperatures as it comes from the source to the tank
• Air shipping
• Submerged aquatic plants
• Spring water post thawing

Acute ΔP > 50-200 mm/HG leads to sudden death. Chronic low-level ΔP leads to stress-related disease and lower levels of mortality.

Younger fish (fry/fingerling) are considered more susceptible because those that dive deeper can sometimes escape the excess gas, but younger fish have not yet developed that ability.

Clinical signs may manifest as the presence of gas bubbles in gills, tissues, or eyes. Additionally, the swimbladder can become hyperinflated, and they can develop exophthalmos. Eggs may be seen floating.

Diagnosis is easy; simply clipping fins or gills underwater will release the gas. To then determine the degree of supersaturation requires using a saturometer to determine the total gas concentration. Levels of 100% saturation are dangerous. There are no other differential diagnoses.

Treatment consists of gas removal and aeration of the water source. Packed column degassers, which add oxygen, or remove nitrogen and carbon dioxide, can also be utilized. 

Correct answer: Etomidate 0.5–1.5 mg/kg IV

Etomidate is a nonbarbiturate hypnotic. It works by providing agonist activity at the GABA receptor. It does cause vasoconstriction of the cerebral vasculature. This causes a decrease in cerebral blood flow and decreased oxygen metabolism. When given at induction, it rapidly metabolizes, thus having a rapid onset, though without a premed may sting. The benefit of its use is that it has no adverse effects on the heart, meaning no cardiovascular depression occurs. Secondly, it has minimal adverse effects on the respiratory system. Thus, it is a safe option for patients who may not be completely cardiovascularly stable. If a patient is severely stressed, or Addisonian, it should be avoided as it can cause adrenocortical function suppression for two to six hours after use.

Propofol is a useful induction agent with a short onset of action and short duration. It fails to accumulate in the body, making it safe to use as a CRI for TIVA. It works on the GABAa receptor. It, too, reduces cerebral oxygen metabolism as well as intracranial pressure. However, it has dose-dependent cardiovascular depressant effects and causes vasodilation. Thus, hypotension can result. Further, it can also have a respiratory depressant effect, to the point of sometimes causing apnea. Because of the cardiovascular and respiratory changes, this medication should be reserved for hemodynamically and cardiovascularly stable patients.

Alfaxalone is a neurosteroid-type anesthetic that triggers CNS depression by binding directly to GABA receptors. Unlike propofol, it can be used IM, which can benefit some species (reptiles) or fractious animals. Intracranial pressure, cerebral oxygen demands, and cerebral blood flow are all diminished with this drug. It, too, can cause dose-dependent apnea and cardiopulmonary depression. Recovery can be rough with paddling, excitement, rigidity, or myoclonic activity. Because of the negative CV and respiratory effects, it is not recommended unless stable.

Dexmedetomidine is the most potent Alpha-2 agonist with potentially long-lasting effects. Unlike the other three drugs, it has analgesic properties as well. It is contraindicated in patients with cardiac, respiratory, liver, or kidney disease. Further, it should be avoided in patients with shock, debilitation, or stress associated with thermal injury. Because of this patient’s underlying heart disease as well as lack of full cardiovascular stability, this is not a safe option.

Correct answer: Anal sac abscessation

Anal gland disease generally occurs in small to medium-breed dogs. However, it can develop in any dog with atopy, obesity, seborrheic patients, dogs eating insufficient fiber, or other underlying disease causing diarrhea or constipation.

Anal gland impaction refers to sac distension without the ability to express them. They are usually mildly painful.

Anal gland sacculitis patients are painful on palpation (moderate to severe), and discharge can be liquid (brown), purulent, blood-tinged, or yellowish.

Anal gland abscessation causing often significant distension of the sac with purulent discharge. Often the overlying skin is erythematous, and evidence of cellulitis may be present. Dogs with this condition are usually painful and febrile.

Anal gland rupture is identified once a draining tract can be appreciated associated with the gland.

Differentials for anal gland sacculitis include flea allergy dermatitis, perianal tumors, tail-fold pyodermas, or perineal fistulae.

Most cases respond to medical management - e-collar, pain medications, and broad-spectrum antibiotics. Some patients may need sedation to express impacted glands and flush them +/- infuse medications. Address any underlying causes such as diarrhea with diet changes, deworming, or environmental or food allergies. Ideally, culture should dictate antibiotic selection, and surgical intervention is only warranted when medical management fails. 

Correct answer: Aspergillosis

Likely, in addition to your findings above, the postmortem evaluation showed intralesional hyphae, making a diagnosis of fungal disease more likely and helping to narrow your focus.

Aspergillosis, though not contagious or zoonotic, is a ubiquitous fungal disease that can affect a wide array of species. In poultry, we can see both acute and chronic forms. The disease occurs in part due to toxins produced by the organism. 

Differentials for acute respiratory death include carbon monoxide poisoning, acute bacterial septicemia, and mycotoxicosis. Aspergillosis should always be ruled out as a cause of broiler chick early mortality. The granulomatous lesions of pulmonary aspergillosis help to differentiate it from other avian respiratory diseases, such as infectious bronchitis or infectious laryngotracheitis.

There is no effective treatment for aspergillosis. If exposure is prevented, spontaneous recovery can occur.

Key mitigation strategies for aspergillosis include the following:

1. Removing birds from contaminated areas
2. Limiting further exposure
3. Preventing aerosolization of spores
4. Improving ventilation and air exchange rates
5. Maintaining strict hygiene, cleaning, and disinfection protocols
6. Removing all contaminated or cracked eggs before incubation to prevent spread

Though challenging, diagnosis can be confirmed through clinical signs, gross and histological findings, epidemiological considerations, and culture/cytology in the air sac or tracheal lavage. Identifying the organism on histopath is also confirmative.

Infectious Bronchitis Virus (IBV) is a worldwide avian coronaviral disease. Chickens are the primary host, though the disease has been seen in peafowl and pheasants. It is transmitted via inhalation and direct contact, and morbidity in birds is usually 100%. Various strains lead to different clinical pictures, including decreased egg yields, poor egg quality, upper respiratory tract disease, and acute nephritis.  Respiratory lesions are not granulomatous but may contain serous, caseous, or catarrhal exudates when advanced and may be foamy within the air sacs, then develop cloudiness as the disease progresses.

Carbon monoxide poisoning occurs infrequently when poultry are exposed to exhaust fumes during transport or in hatcheries with poor ventilation. Cyanosis around the beak and face may be evident with a cherry red (bright pink) visceral appearance, especially in the lungs. Diagnosis occurs via blood analysis.

Infectious Laryngotracheitis (ILT) is a very contagious, generally acute herpesviral infection in chickens and pheasants. They often have severe coughing, dyspnea, and audible rales. However, some can have a subclinical disease, mild nasal or ocular discharge, conjunctivitis, or tracheitis. ILT is caused by Gallid herpesvirus I. It most commonly occurs in intensive production systems in the U.S. and other countries. Granulomas do not form in this respiratory disease, separating it from aspergillosis.

Correct answer: Cherry-red gums

Signs of significant heart disease include JDV (Jugular Vein Distension) and a palpable thrill in addition to an audible heart murmur, weak pulses, arrhythmias, dyspnea, tachypnea, failure to gain weight, and cyanosis or blue coloring to the lips/mouth indicating decreased oxygen levels. Cherry-red gums are found in cases of sepsis, several toxins, and heatstroke. 

You inform the owner that animals between birth and five days old can have a normal murmur until a portion of the heart fully closes (the ductus arteriosis). If the murmur continues after that time, it could still be physiologic (not related to structural disease) or could indicate an underlying abnormality, such as a Patent Ductus Arteriosis (PDA) or Ventral Septal Defect (VSD). The ductus arteriosus takes several days to close after birth, forming the ligamentum arteriosum.

Correct answer: Forbid feeding of feral cat populations

Cases of toxoplasmosis have greatly declined since the 1990s. However, we still see cases in the U.S. that can cause human abortions, encephalitis, systemic disease, or birth defects in people. Thus, it is a zoonotic disease about which we should educate the community and understand its cycle and transmission.

Feral cat populations and how entities handle them vary globally and locally. Some people favor feral cats because they provide rodent control. Knowing the infectious disease risks they carry, including rabies, toxoplasmosis, and Toxocara cati, others feel that these populations should never be allowed to survive. Still, others fall somewhere in between.

Feral cat populations can contaminate the environment with T. gondii oocytes. However, shedding is usually very short-lived. Cats are usually exposed early on in life and then tend to remain resistant to infection. Seroprevalence of Toxo, for example, doesn't always correlate well with environmental load or human infection levels.

Toxo is more likely spread via environmental contamination in urban areas than in rural areas due to ingestion of infected paratenic hosts.

The density of a cat population does not predict the risk for other species developing toxo.

Feeding commercially prepared, cooked diets to these groups of cats can help decrease predation on intermediate hosts, and this has the benefit of saving the bird species and may lessen the risk of environmental contamination. However, this reduces their ability to control varmint species that may be nuisances and can also carry and spread diseases. Preventing access to human food sources either in production areas/food storage areas or rearing areas can lessen the risk of environmental contamination and minimize the risk of entering the food chain.

By controlling the intermediate host populations, you further minimize the environmental contamination and lessen the chance of transmission to new cats.

By forbidding the feeding of feral cat populations, you may encourage more urban wildlife interfaces and increase the risk of environmental contamination, especially in urban areas.

Really, the biggest way to lessen the risk of transmission is to have people not handle feral cats, keep their pet cats indoors, cook meat to the appropriate temperatures, practice proper hygiene, and more. 

Correct answer: Myobia musculi

Rats tend to be more resistant to ectoparasites versus mice. However, there are fur mite species in mice. If rats do develop ectoparasites, we can see Polyplax spinolosa or the spined rat louse, Demodex nanus, and Radfordia ensifera (rat fur mite). However, mice seem more likely to be infected and clinical for ectoparasites.

Clinical signs of Myobia musculi, pictured here, consist of alopecia and self-barbering.  

Polyplax serrata, the house mouse louse, leads to more significant disease with anemia, dermatitis, pruritus, and, if heavily infested, death.

Syphacia obvelata is an internal parasite, the mouse pinworm. It is a commensal nematode that feeds on mice bacteria inhabiting their GIT (Gastrointestinal Tract). If overgrowth occurs, clinical signs may develop and be seen via tape prep on the rectal area and viewing under the microscope. 

Mites and lice are treated with ivermectin and topical products, as with other species. 

Correct answer: Requires tech-savvy users

AAHA suggests that when you are researching possible office management software options, you should consider the following: 

1. Ensure the technology is a fit for you and your staff. This would include the type of software. (Is it cloud-based or use in-house servers? What is the ability for backup, and what happens if you lose power? What kind of hardware do you need, and will you need to purchase additional equipment? Suppose you are switching from paper records to your first computer management software (beyond just billing and scheduling). In that case, you want to choose a product that your doctors and staff are willing to use, feel comfortable using, and is user-friendly. Some products have ideal features from the billing and inventory side, while others may focus on patient records, providing readability and ease of use. If your staff already does computer records, changing from one program to one that may be slightly less intuitive but offers more, with proper training, may be right for you.
2. Ideally, you want to improve the practice's efficiency, including improving workflow, maintaining inventory, and managing schedules for doctors and clients. Software that provides templates for SOAPs and discharges also may help alleviate the burden and time constraints of medical record keeping. Finally, software that provides reminder services for clients for appointments and other tasks and permits communication with clients by text and email further helps improve efficiency. 
3. Improve the client's experience by providing a means to share educational information with the client, such as handouts on medications or discharge paperwork. Some software permits online appointment booking, saving the client from having to call the office. Client reminders help with compliance. 
4. Grow and monitor your practice's success can be achieved with software that permits various types of reports. Some allow doctor comparisons, while others may help demonstrate client statistics such as demographics or preventative care plan participants. 
5. Plan for the future. It is key to choosing a software program that will continue to have the IT support needed for its lifetime. Further, in the cell phone era, apps are huge. A program that can be used with a phone app, providing a patient portal with the ability to check on pet medications, order refills, order pet food, and schedule appointments, is key. Additionally, see what other options the program may have. Does it have templates and the ability to do preventative care plans? Can it be linked with a Cubex drug dispensing system? While you may not want to use all the software's features today, think ahead about what you may do in the future. 
6. Practicing advanced diagnostics. Having blood machines and other diagnostics integrated with the software so that results are automatically loaded into the patient's record may be something you really want vs. having to scan the documents later. 
7. Consider the partnership. It may not be just about the software but the support the software provides. Some companies have no 24/7 support, and for you, that may be okay, but for 24-hour practices, all-day support is paramount. Further, price, how often updates are developed, and how well they fit your budget are things to consider.

Each software program has its pluses and minuses. Read reviews, ask around, see what people like and dislike about each type of program, and go from there.

Correct answer: 0.5% cidofovir

Conjunctivitis in dogs can occur for various reasons, including secondary to keratoconjunctivitis sicca (dry eye), trauma, entropion, trichiasis, parasites, foreign body (usually unilateral), or canine distemper virus.

Generally, regardless of the cause, we presume a secondary bacterial component when initiating therapy and treatment with a broad-spectrum topical antibiotic. First-line examples include tobramycin or Neomycin-bacitracin-polymixin B. However, the latter (polymyxin B) is contraindicated in cats, as some may develop an allergic reaction (hypersensitivity to full-blown anaphylaxis). Once you see this reaction once, you will never want to see it again. Caution should be used with antibiotic choice to ensure appropriate antimicrobial stewardship.

Conjunctivitis can be painful; some people may reach for topical anti-inflammatory pain relief such as Flurbiprofen. In contrast, others may elect oral pain management.

0.5% cidofovir is a topical antiviral medication most commonly used for cats with feline herpes virus.