bacterial meningitis and encephalitis in ruminants

Vet Clin Food Anim 20 (2004) 363–377

Bacterial meningitis and encephalitis inruminants

Gilles Fecteau, DMVa,*, Lisle W. George, DVM, PhDb

aDepartment of Clinical Sciences, School of Veterinary Medicine, University of Montreal,

CP 5000 St-Hyacinthe, Quebec J2S 7C6, CanadabDepartment of Medicine and Epidemiology, University of California, Davis, CA 95616, USA

Meningitis

Definition and etiology

Meningitis, an inflammation of one or more of the three covering layersof the meninges (dura mater, arachnoid, and pia mater) in the centralnervous system (CNS), may be classified by duration (acute or chronic),structures that are affected (meningitis, meningoencephalitis, or meningo-ventriculitis), location, (cerebral, cerebrospinal or spinal), cause (bacterialor viral), or histopathologic lesions (suppurative or nonsuppurative). Thecollective role of the meninges is to support, protect, and contribute to theirrigation of the nervous system. The dura mater is the most external layerand is mainly collagen, blood vessels, and neural terminations. It is thethickest and most resistant of the three meninges. In the skull, the duramater is adherent to the skull but is unattached to the vertebrae. The gapsbetween unattached meninges and the vertebral column form the epiduralspace. The pia arachnoid, which consists of the internal meningeal layer, isattached to the nervous tissue by fine trabeculae. The arachnoid surroundsa mass of capillaries to form the choroid plexus. Unlike the pia mater, thearachnoid does not follow all depressions of the nervous tissue.

The spaces that form between the arachnoid and the pia mater containthe cerebrospinal fluid (CSF), which is a clear fluid containing mainly waterand electrolytes. The CSF protects and nourishes the CNS. The fluid isproduced in several sites that include the lateral ventricles, the choroidplexus, and the pia arachnoid. The fluid is formed by the combined physio-logic mechanisms of ultrafiltration and active transport. Reabsorption of

* Corresponding author.

E-mail address: [email protected] (G. Fecteau).

0749-0720/04/$ - see front matter � 2004 Elsevier Inc. All rights reserved.

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364 G. Fecteau, L.W. George / Vet Clin Food Anim 20 (2004) 363–377

CSF occurs at the arachnoid villi and at the dural reflections over the cranialand spinal nerves. The two most clinically important cisternae are thecisterna magna and lumbosacral cistern, both of which may be used tocollect CSF from a living animal.

Bacterial meningitis has been described in adult cattle but seems to bea clinical entity of importance in neonates [1–4]. Bacterial suppurativemeningitis can also result from direct extension through the calvarium, asmay occur with conditions that include otitis interna, sinusitis, and infectedskull fractures or after bacteremia. The following section describes neonatalbacterial suppurative meningitis (NBSM).

Bacterial sepsis and NBSM are often linked. In human medicine, thefrequency with which NBSM occurs in neonatal sepsis cases has decreasedin recent years from 1 in 4 cases to 1 in 20 cases. In developed countries, thecase fatality rate from NBSM is 3%, which is lower than the 25% to 30%rate that was reported 20 years ago [5]. Such statistics are not currentlyavailable in domestic animals, but a reported case fatality rate of 100% [6]indicates that the prognosis is poor in cattle. The reported prevalence ofseptic meningitis in necropsied calves has been as high as 43% [7]. The trueincidence of the disease in cows remains to be studied, however.

Pathogenesis

Gram-negative bacteria, Escherichia coli in particular, are reported to bethe most common meningeal pathogens in bovine neonates [6,8–10]. In sheepand goats, E coli, Pasteurella, Streptococcus, Staphylococcus pyogenes, andArcanobacterium pyogenes have been cultured from meningitis cases [11,12].Some E coli virulence factors may be of importance in the development ofNBSM, because the successful meningeal pathogen would have overcomesequential host defenses mechanisms to reach the CSF and replicate.

E coli bacteria found in meningitic calves are nonhemolytic, synthesizeshydroxymate and colicin V, and has expressed the 31a surface antigen,antibody resistance, aerobactin production, and fimbriation [13].

Before invading the meninges, the pathogen must colonize host mucosalepithelium. Bacterial omphalophlebitis or severe enteritis may lead tobacteremia without previous mucosal colonization. In calves, hematogenousbacteria survive because of inadequate colostral transfer.

The means of access of the pathogen into the meninges is poorlyunderstood. Specific mechanisms may include the development of a sus-tained and high-grade bacteremia in the highly perfused dural venoussystem and choroid plexuses, adherence of fimbriae of some strains of E coli,phagocytosis of the pathogens by circulating monocytes, and endocytosisthrough the microvascular endothelial cells [14]. Environmental growthconditions that may influence the ability to invade brain microvascularendothelial cells (microaerophilic, pH, newborn bovine serum, magnesium,and iron) have been studied in vitro [15].

365G. Fecteau, L.W. George / Vet Clin Food Anim 20 (2004) 363–377

Bacteria survive and proliferate in the poorly defended CSF. Comple-ment is essentially nonexistent in CSF, which, when combined with lowspecific antibodies, leads to inadequate opsonization of meningeal patho-gens. Despite an early influx of leukocytes into the CSF in bacterialmeningitis, the host defense system remains suboptimal, because opsonicactivity is deficient [16].

The sequelae of meningitis are associated with the release of cytokinesand the direct effects of bacterial invasion [16]. Bacteria may releaseendotoxins and lead to inflammatory infiltrates that cause thromboses ofthe arachnoidal or subependymal veins. Congestion or hemorrhagic in-farction may follow, with subsequent necrosis of nerve cells [5]. Inflamma-tory changes in the subarachnoid space may affect the choroid plexus,decreasing the absorption of fluid and potentially creating hypertensivehydrocephalus.

Risk factors

Calves with failure of passive transfer (FPT) have a high risk fordeveloping neonatal sepsis and subsequent bacterial meningitis.

Clinical presentation

Calves with NBSM are often presented because they have lost theirsuckling reflex and appear lethargic. Previous treatment for undifferentiateddiarrhea is common. According to two different studies, approximately 30%of critically ill neonatal calves are bacteremic [17,18]. Fever is usuallypresent unless some nonsteroidal anti-inflammatory drug (NSAID) has beenadministered or if the animal is in an extremely cold environment. Thecalves have an extended head and neck (Fig. 1). Attempts to flex orreposition the neck result in a tonic extension and thrashing of the limbs.Hyperesthesia is common. With time, a profound depression state develops,

Fig. 1. (A, B) Calf with septic meningitis secondary to septicemia. The animal is severely

depressed, prefers to remain in a decubitus position, and maintains an extended neck when

standing, which is rigid when manipulated. The presence of fibrin in the anterior chamber of the

eye is suspected.


and the animal eventually becomes comatose and nonresponsive or maydevelop tonic-clonic seizures. Dysfunction of cranial nerve VI results innystagmus and strabismus. Dysfunction of cranial nerve VII leads to facialpalsy. Spinal reflexes are described to be exaggerated. Concurrent findingsinclude hypopyon, arthritis, omphalophlebitis, and diarrhea.

Diagnosis

The presumptive diagnosis of bacterial meningitis is based on thedemonstration of FPT, presence of a septic focus (eg, omphalophlebitis,septic arthritis), and presence of the clinical signs described previously. Thedefinitive diagnosis is based on an abnormal CSF analysis result orhistopathologic lesions on postmortem examination, however.

Collection of CSF from the lumbosacral space is easy and safe inruminants. Suppurative CSF can be obtained from the lumbosacral cisternof animals with bacterial meningitis. Puncture of the cisterna magna isunnecessary for the confirmation of bacterial meningitis.

Normal values and standard techniques for CSF collection and analysisare presented in another article in this issue. The CSF should be examinedvisually to determine turbidity and color. Turbidity indicates the presence ofinflammation or epidural fat contamination during the procedure. NormalCSF is clear and colorless. Small amounts of blood contamination result ina pink-tinged specimen. Xanthochromia, a yellow coloration of the CSF,reflects previous in vivo blood contamination. After aspiration, the CSFspecimen should be placed in serum tubes or in tubes containing ethyl-enediaminetetraacetic acid (EDTA). Normal CSF does not contain fibrin-ogen and, consequently, does not clot. Dilution of small-volume samples byexcessive EDTA could result in spuriously low cell and protein counts.

After collection, the CSF specimen should be aliquoted for cytologic andchemistry analysis and for bacteriologic or viral cultures. Lumbosacral CSFtap culture was reported not to reflect adequately the organism present invivo. In one report, Ferrouillet et al [9] found in seven cases in which pre- andpostmortem culture results were available that there was no associationbetween the culture results in vivo and the culture results at post mortemexamination. Multiple explanations could be hypothesized to explain thisfact, one being that there was a delay between the in vivo procedures and thepostmortem culture. Moreover, all calves were treated in between the twocultures, suggesting that treatment may have modified the results.

CSF specimens should be submitted for laboratory analysis within anhour of collection [19]. If this is impossible, a sedimentation procedureshould be attempted to reduce artifactual lysis of white blood cells andreduction of glucose concentration. A sedimentation technique has beendescribed previously and may be helpful in practical situations. Using a 2-cm plastic cylinder placed on a clean glass slide, CSF, 1 mL, is allowed tosediment for 30 to 60 minutes. The supernatant is then removed, and the


glass slide is stained. The interpretation can be performed at a later time byqualified personnel [2,20].

Microscopic examination of CSF is essential for accurate diagnosis ofbacterial meningitis. There are three different studies examining CSFanalysis in calves suffering from meningitis [6,8,9]. The three studies agreedthat the number of nucleated cells and the protein concentration aremarkedly increased. The proportion of neutrophils may reach as high as80%. The ratio of CSF to plasma glucose concentration is less than 1 inanimals with bacterial meningitis because of bacterial metabolism of glucosein the CSF. Xanthochromia was frequent in one study and rare in another,whereas one author did not report this particular finding. Free orintracellular bacteria were observed in 45% of the specimens in Greenand Smith’s study [6].

The patient’s hemogram usually reflects the gram-negative bacteremia.Bacterial meningitis should be differentiated from other encephalopathies ofneonates. The condition can appear to be similar to several particularcongenital diseases and to acute diffuse cerebral edema caused by salt toxicity.

Treatment

Treatment of bacterial meningitis is difficult, and the mortality rate ishigh. The high mortality rate of calves correlates with that in human infants,which ranges between 3% and 13%, and has been reported to be as high as100% in meningitic calves [5,6]. Antimicrobials are the most importanttherapeutic modality for treatment of bacterial meningitis in calves.Selection of antimicrobial drugs should be based on sensitivity testing ofisolates from the CSF. This is rarely possible in farm animals, however,because isolation of the bacteria from the CSF may be difficult. In clinicalsettings, therapeutic delays that await bacteriologic results could increasethe mortality rate in patients with fulminant bacterial meningitis.

The physicochemical properties (lipid solubility, molecular weight, pro-tein binding, and ionization) and the pharmacokinetics of a drug influenceits penetration through the blood-brain-barrier (BBB). The CSF-to–bloodconcentration ratio is an indicator of the penetration of a drug into theCNS. These ratios are described for several antimicrobials used in humanmedicine and laboratory animals. In farm animals, however, little is knownabout these numbers [21]. Another key factor to consider is the suboptimalimmune response in the CSF (lack of complement and antibody), whichimplies that to be effective, an antibiotic needs to reach the minimalbactericidal concentration (MBC). The antibiotic concentrations in the CSFshould be compared with the MBC value for the targeted pathogens ratherthan using the standard minimum inhibitory concentration (MIC). A drugthat diffuses relatively easily into the CSF (eg, aminoglycosides) may not bethe best choice, because with standard dosing regimens, the concentrationsachieved only approximate the MBC for gram-negative bacteria causing


meningitis in human beings [21]. Conversely, the B-lactams, which diffuseless efficiently through the BBB, can reach effective therapeutic concen-trations in the CSF, because larger doses can be used without risk of toxicity[21]. The expected ratios of CSF antibiotic concentrations to bacterial MICs(MBC would be better but those numbers are not always available) are partof the equation. The data available on this matter are again lacking in farmanimals. One study available in calves presents the pharmacokinetic offlorfenicol. The maximum concentration of florfenicol achieved in the CSFafter a single intravenous (IV) dose of 20 mg/kg was 4.67 � 1.51 lg/mL. Theconcentration in the CSF remained above the MIC for Histophilus somni for20 hours [22].

Practically, the chosen antimicrobial to treat meningitis in ruminantsshould have a good spectrum against gram-negative and gram-positivepathogens. The availability, formulation, and labeling of the antimicrobialfor farm animals are also taken into consideration (eg, residue, possible IVadministration, cost of prolonged therapy). The actual selection is oftenreduced to third-generation cephalosporin (ceftiofur, 5–10 mg/kg, adminis-tered by the IV or intramuscular [IM] route one to three times a day),sodium ampicillin (10–20 mg/kg three times a day by the IV route), orfluoroquinolones (enrofloxacin, 5 mg/kg, administered by the IV route twicea day) in countries where the drug is labeled for use, and trimethoprim-sulfonamide (5 mg/kg based on the trimethoprim administered by the IVroute two or three times a day). A combination of drugs is routinely used tobroaden the spectrum (ampicillin-ceftiofur or ampicillin-trimethoprim-sulfonamide). Note that all antimicrobial regimens described are empiricand derived from comparative medicine and clinical experience. Solidscientific evidence to corroborate those regimens in the treatment ofbacterial meningitis in ruminants is not available at the moment. Oneshould remember that the inflamed meninges increase the diffusion towardthe CSF and that diffusion decreases as the animal improves.

Intrathecal treatment does not improve the prognosis in human medicineand seems too complicated for farm animal medicine [5].

Duration of therapy is empiric; 14 days seems to be the minimum inhuman medicine [5,16]. Anti-inflammatory agents are indicated to improvethe patient’s attitude in general and also to control the secondary effects ofsepsis. The choice between steroidal and nonsteroidal anti-inflammatoryagents remains empiric in farm animals, however. In human medicine,steroidal anti-inflammatory agents are indicated in cases of meningitisassociated with Haemophilus influenzae. In all other situations, the questionremains unanswered [16].

General supportive measures are essential, and any concurrent diseasemust be treated adequately and aggressively, because the continuousbacteremia may arise from another site (septic arthritis or omphalophlebitis).

Because FPT could be a predisposing factor to septicemia, plasmatransfusion seems to be of interest in the treatment. Convulsions should be


treated appropriately. Diazepam (0.01–0.2 mg/kg) every 30 minutes shouldbe administered by the IV route until convulsions are controlled.

The use of lytic bacteriophage has been studied in chickens and calvesand shows some potential. In an experimental challenge model, calves thatreceived IM inoculation of bacteriophage had a delayed appearance of thebacterium in their blood and survived longer [23].

Prevention

An adequate volume of colostrum is essential for prevention ofmeningitis in neonates. Early recognition and prompt therapeutic interven-tion are also important for prevention of life-threatening meningitis.Reduction of the exposure to risk factors is important; thus, appropriatecare to colostrum feeding is essential, and early recognition and treatment ofany bacterial diseases are also important.

Specific meningitis

Thrombotic meningoencephalitis associated with Histophilus somni

Etiology and epidemiologyH somni (recently renamed, traditionally known as Haemophilus somnus)

was first isolated from the nervous tissues of a calf that had died ofencephalitis. H somni has been traditionally associated with a fatal septice-mic condition of feedlot cattle often showing neurologic signs; however, it isnow well recognized that the organism play a role in a broader complexcalled the H somnus disease complex or hemophilosis (which will no doubtbe renamed histophilosis) [24]. The bacteria is a gram-negative non–spore-forming coccobacillus organism that causes a diverse set of clinical signs thatinclude pneumonia, arthritis, mastitis, urogenital tract infection, abortion,and myocarditis [25]. Isolates from the genital tract (prepuce and vagina)harbor differences from isolates cultured from septicemic animals [26]. Theprevalence of H somni infection is high, but the occurrence of the clinicaldisease is relatively low. The case fatality rate for the nervous form of Hsomni encephalitis is, however, high. Feedlot cattle are more often affectedthan are pastured or dairy animals. Histophilosis has a worldwide distribu-tion. In this section, we describe the nervous form of histophilosis.

PathogenesisThe unpredictability of experimental induction of histophilosis causes

serious complications in the development of the understanding of thedisease as well as in the effort to evaluate vaccine effectiveness [27]. Usingthe 43,826 strain, Little [27] was capable of inducing a septicemic thromboticmeningoencephalitis in 60% to 70% of challenged calves. Clinical signsdevelop rapidly, and death occurs in less than 36 hours. Necrotic lesions


were found in challenged animals in the small vessels and veins. Initiation ofthis process seems to be associated with exposure of the underlyingbasement membrane [28]. The coagulation cascade is then initiated, andthrombosis develops. The lesion allows the organism to reach differenttissues to cause the histologic lesions typical of the disease: small vesselthrombosis and secondary tissue necrosis with an important neutrophilicinfiltration commonly filled with bacteria.

The bacterium first colonizes the surface of a mucous membrane, thenproliferates locally, and eventually invades the host to cause bacteremia.Which mucous membranes (respiratory or genital) are most often infectedto give access to the host is still under debate. Interaction betweenendothelial cells and the bacteria results in collagen exposure to cause thedescribed lesion. Thrombosis is seen in the brain, lungs, and heart ofaffected cattle [27,29]. The serum antibody titer does not correlate to theoutcome of challenge infection [28], suggesting that humoral immunity doesnot provide complete protection against clinical disease.

Clinical signsIn the nervous form, multiple animals are commonly affected and sudden

death could be the first and only sign that some animals show. Respiratorydisease may precede the neurologic signs (7–14 days earlier). When clinicalsigns develop, neurologic impairment is often severe. Lateral recumbency,profound depression, and closed to semiclosed eyelids giving the animala sleepy look (where the term sleeper syndrome came from) are frequent.Blindness may or may not be present and could be unilateral or bilateral. Ananimal in lateral recumbency may progress to opisthotonos and convul-sions. If the animal is able to stand, ataxia and weakness are obvious. A highfever is observed frequently. Animals treated early in the disease process(while still standing) may recover; otherwise, the evolution is rapidly fatal(less than 24–36 hours). Retinal hemorrhages have been described inaffected cattle [30].

DiagnosisThe history and physical examination often lead to a presumptive

diagnosis of H somni meningoencephalitis; however, the final diagnosis isoften based on postmortem examination. Complete blood cell count (CBC)changes are nonspecific and reported to be consistent with gram-negativesepsis (leukopenia and neutropenia or neutrophilia with left shift) [4]. CSFchanges are reflective of bacterial infection combined with hemorrhage: thenumber of nucleated cells is increased (neutrophils), protein concentrationsare elevated, and xanthochromia and an increased number of red blood cellsmay also be present. One method recommended by some authors to assessthe CSF globulin concentration rapidly is the Pandy reaction (saturatedphenol). A mild to strong reaction is observed in cases of meningitis [1,2].


The organism can be cultured from different body fluids if the animal hasnot been treated (blood, CSF, and joint and pleural fluids) [31]. A selectivemedium has been developed, and the laboratory can be informed that Hsomni is suspected [32]. Serology testing exists but does not seem to beroutinely used to confirm the diagnosis. Asymptomatic animals may showspontaneous seroconversion; thus, acute and convalescent sera are necessaryto confirm the role of the organism in a particular case.

Necropsy findings related to the nervous forms are hemorrhagic infarcts inthe brain and spinal cord. The lesions are most often multiple and of varioussizes, with some being visible macroscopically. Histologically, vasculitis,thrombosis, and neutrophil infiltrates are the signature of the disease.

TreatmentTreatment of an affected animal should be attempted only if the animal is

believed to be in the early stages of the disease. Treatment of down animalsin advanced stages of neurologic impairment is unrewarding; thus, energyand emphasis should be directed toward early identification of possiblyaffected pen mates. H somni is susceptible to most commonly usedantimicrobials; moreover, antibiotic penetration is not a major concern,because the endothelial damage and infarcts lead to breakdown of the BBB[32]. Parenteral oxytetracycline is the most commonly recommendedtreatment for commercial animals. A conventional formulation at a dosageof 10 mg/kg administered intravenously twice a day for at least 3 days oruntil clinical signs indicate improvement may be used. A long-actingformulation at a dosage of 20 mg/kg given intramuscularly every 48 hoursfor a maximum of three treatments may also be used. After this regimen,procaine penicillin (20,000 IU/kg) should be given intramuscularly untilcomplete recovery.

Use of NSAIDs is indicated to control pain, fever, and generalinflammatory reactions. Supportive care is extremely important, becauseneurologic impairment may predispose animals to trauma or make them lessprone to seek and compete for water and food.

Prevention and controlThe pathogenesis of H somni thrombotic meningoencephalitis is still not

well understood, which complicates control and preventive programs. Inparticular, the myocardial form of H somni has become more prevalent, andthe reason for this increase is unknown [25]. When a case is suspected orconfirmed, all other animals in contact should be monitored closely to detectnew cases at the earliest stage possible. Observations every 6 to 8 hours forthe following week have been recommended [4,25]. Mass medication onarrival has been evaluated in feedlots and does not seem to reduce the risk ofmortality associated with H somni [33]. Vaccines are available in NorthAmerica and are protective against the nervous form of the disease whenstudied in an experimental challenge model [28]. Field efficacy studies are


difficult to perform given the sporadic and unpredictable appearance of thenervous form of the disease.

Mycoplasma meningitis in calves

A particular clinical entity has been described in newborn calves andassociated with Mycoplasma bovis infection. Newborn calves (less than 1week of age) were presented with fever, depression, swollen joints, and, insome cases, nervous signs. Treatment was unrewarding, and most animalsneeded to be euthanized. Although the clinical signs and necropsy findingsrelated mainly to pneumonia and arthritis, fibrinous meningitis was found insome cases [34]. Otitis media/interna caused by M bovis is described in thearticle on brain stem diseases in this issue.

Frontal sinusitis

EtiologyAcute infection of the frontal sinus in adult cattle is commonly associated

with dehorning. Chronic sinus infection may be secondary to dehorning evenif the clinical signs appear weeks or months after the surgical procedure.The bacteria involved are various, and in one retrospective study of 12 cases,A pyogenes and Pasteurella multocida were most frequently cultured. Mixedbacterial infections consisting of anaerobic species, A pyogenes, P multocida,Proteus sp, Pseudomonas sp, and E coli were identified in 6 patients withsinusitis [35].

PathogenesisBacterial sinusitis is a common sequela of the dehorning of adult cattle.

Bacteria access the sinus through the surgical incision. Other causes ofsinusitis include facial fracture, sequestration of frontal bone, and bulletwounds. Ascending infection without a history of a dehorning procedure isalso possible.

Clinical signsIn acute cases, the sinus is still open and may reveal an abnormal

discharge. The animal is often febrile. Anorexia and lethargy are alsopresent. In chronic cases, the clinical signs are often more subtle. The animalhas a decreased appetite, is described as not performing well (eg, milkproduction, weight gain), and is occasionally febrile. Because it is most oftenunilateral, frontal sinusitis usually creates an asymmetric look of the headwith swelling observed over the affected sinus, head, and neck extension anda distressed and anxious expression (Fig. 2). Exophthalmia can be observedon the ipsilateral side. An abnormal nasal discharge may be observed.

DiagnosisIn most cases, the history and physical examination are enough to

establish a presumptive diagnosis. Radiographs could be helpful to evaluate


bone integrity and dental lesions. Sinus trephination could be performed toaspirate pus for cultural examination.

TreatmentTreatment consists of establishing chronic effective drainage in the

affected sinus combined with systemic antibiotic therapy using trephination.Anatomic sites for sinusotomy have been described and include the dorsalfrontal sinus, the postorbital diverticulum, the rostral frontal sinus, and theturbinate portion of the frontal sinus [36]. Dorsal frontal sinusotomy shouldbe performed on a line drawn between the caudal aspects of the orbits and 4cm from midline. Postorbital diverticulum sinusotomy is performed 4 cmcaudal to the dorsal rim of the orbit, immediately above the temporal crestof the frontal bone. Rostral frontal sinusotomy is performed caudal to a linedrawn between the centers of the orbits. Just rostral from the line describedfor the rostral frontal sinusotomy, the turbinate portion of the frontal sinuscan be trephined. Frontal bone distortion sometimes may influence thechosen site. After trephination, the sinus should be flushed with warm salinesolution and the patient should be treated with antibiotics. Antibiotictherapy should be initiated at the time of sinusotomy and continued forperiods ranging between 10 and 28 days. The preferred antimicrobial ispenicillin, because A pyogenes is the most frequent bacteria isolated from thesinus pus. The prognosis remains guarded in chronic cases (8 of 12 patientsrecovered in the study by Ward and Rebhun [35]).

Fig. 2. An 18-month-old heifer with severe chronic sinusitis after being dehorned 6 months

previously. The heifer had not grown as well as her herd mates and appeared depressed and

lethargic. Trephination confirmed sinusitis of the left and right frontal sinuses, with the left frontal

sinus being more severely affected. (Courtesy of P.D. Constable, BVSc, PhD, Urbana, IL.)


PreventionDehorning should be performed in calves using a hot iron. When done in

calves at an early age (months), the risk of frontal sinusitis is almostnonexistent. When dehorning is performed on adult animals, proper care toenvironmental conditions is necessary. Surgical procedures must be per-formed aseptically. Closed techniques, such as cosmetic dehorning, may besuitable in small ruminants and cattle that must return immediately ina dusty environment in which fly control is difficult.

Brain abscess

Etiology and pathogenesisBrain abscess is a relatively rare condition in cattle. Two different

pathogeneses are postulated to be of importance: extension of a localsuppurative process (eg, chronic frontal sinusitis) and hematogenous spread.The pituitary gland abscess constitutes a particular entity and is describedseparately. In all cases, A pyogenes is commonly the cause.

Clinical signsThe clinical presentation is often vague and somewhat chronic. Neuro-

logic lesions are asymmetric and related to the compression of the cerebralcortex. Specific described signs are vision loss in the contralateral eye,ipsilateral mydriasis, and generalized cortical signs, including corticalblindness. Depression, mania, head pressing, and coma have been observedand associated with irritation of nervous tissue. Circling and head tilttoward the lesion side may be observed. If the abscess is near the brain stem,other cranial nerve dysfunction may be observed. A single lesion oftencreates clinical signs that make localization of the lesion feasible. Converse-ly, multiple lesions of various sizes and locations create clinic signs that areoften confusing and difficult to explain.

DiagnosisThe diagnosis is based on clinical signs and CSF analysis, which may or

may not be abnormal depending on where the abscess is located (extraduralor not). Contrast MRI and electrodiagnostic techniques have been used toconfirm the diagnosis in bovine patients [37,38]. Most diagnoses are madepostmortem.

TreatmentRationale treatment would be based on long-duration antibiotic therapy

and supportive care. The prognosis is unknown, because no retrospectivedata are available at the moment, but must be considered grave.


Pituitary abscess

Etiology and pathogenesisPituitary abscess occurs sporadically in ruminants. The causative

bacterium is most often A pyogenes. The precise pathogenesis is still to bedetermined; however, it is routinely accepted that the complex capillary bedsurrounding the gland known as the rete mirabile is important in thedevelopment of the disease. Multiple other explanations have beenpostulated and reviewed [39].

Clinical signsThe clinical presentation is often variable and somewhat chronic.

Neurologic signs include depression, dysphagia, dropped jaw, blindness,and absence of the pupillary light reflex [40]. Male animals aged 2 to 5 yearsseem to be most at risk. The gender predilection may be explain by thetendency of male animals to fight and to incur head injury that mayeventually become infected. The use of a nose ring in male animals to helprestrain the animal may also predispose to sepsis. Bradycardia is frequentbut probably reflects inappetence rather than stimulation of the vagalnucleus in the brain stem.

DiagnosisThe diagnosis is based on clinical signs; CSF analysis, which may reveal

an inflammatory process (elevated protein concentration and pleocytosis);and postmortem examination. The CBC is nonspecific but should confirmthe presence of a chronic active inflammatory process.

TreatmentRationale treatment would be based on long-duration antibiotic therapy

and supportive care. The prognosis seems to be grave [40].

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